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Abe, Toshiaki; Saigo, Yoko; Hojo, Masayoshi; Kano, Tetsuya; Wakusawa, Ryosuke; Tokita, Yumi; Tamai,
Makoto (2006): Protection of photoreceptor cells from phototoxicity by transplanted retinal pigment epithelial
cells expressing different neurotrophic factors. In: Cell transplantation, Jg. 14, H. 10, S. 799–808.
Abstract Transplantation of cells or tissues and the intravitreal injection of neurotrophic
factors are two methods that have been used to treat retinal diseases. The purpose
of this study was to examine the effects of combining both methods: the
transplantation of retinal pigment epithelial (RPE) cells expressing different
neurotrophic factors. The neutrophic factors were Axokine, brain derived-
neurotrophic factor (BDNF), and basic fibroblast growth factor (bFGF). The
enhanced green fluorescence protein (eGFP) gene was used as a reporter gene.
These genes were transduced into RPE cells by lipofection, selected by antibiotics,
and transplanted into the subretinal space of 108 rats. The rats were examined at 1
week and 3 months after the transplantation to determine whether the transduced
cells were present, were expressing the protein, and were able to protect
photoreceptors against phototoxicity. The survival of the transplanted cells was
monitored by the presence of eGFP. The degree of protection was determined by
the thickness of the outer nuclear layer. Our results showed that the degree of
photoreceptor protection was different for the different types of neurotrophic factors
at 1 week. After 3 months, the number of surviving transplanted cell was markedly
reduced, and protection was observed only with the BDNF-transduced RPE cells. A
significant degree of rescue was also observed by BDNF-transduced RPE cells in
the nontransplanted area of the retina at both the early and late times. Lymphocytic
infiltration was not detected in the vitreous, retina, and choroid at any time. We
conclude that the transplantation of BDNF-transduced RPE cells can reduce the
photoreceptor damage induced by phototoxicity in the transplanted area and weakly
in the nontransplanted area.
Schlagwörter Animals; Brain-Derived Neurotrophic Factorbiosynthesisgeneticsphysiology; Cell
Survival; Cell Transplantation; Ciliary Neurotrophic
Factorbiosynthesisgeneticsphysiology; Dermatitis,
Phototoxicpathologyphysiopathologyprevention & control; Fibroblast Growth Factor
2biosynthesisgeneticsphysiology; Gene Expression Regulation; Genes, Reporter;
Green Fluorescent Proteinsanalysisgenetics; Lightadverse effects; Nerve Growth
Factorsbiosynthesisgeneticsphysiology; Pigment Epithelium of
Eyechemistrycytologymetabolismtransplantation; Rats; Rats, Long-Evans; Rats,
Sprague-Dawley; Retinal Rod Photoreceptor Cellscytologyphysiology;
Transduction, Genetic

Albrecht-Buehler, G. (1977): Phagokinetic tracks of 3T3 cells: parallels between the orientation of track
segments and of cellular structures which contain actin or tubulin. In: Cell, Jg. 12, H. 2, S. 333–339.
Abstract Phagokinetic tracks were used to determine the current direction of migration in 3T3
cells. Comparing this direction with the orientation of actin or tubulin-containing
cellular structures by indirect immunofluorescence, the following results were
obtained. First, the main actin-containing bundles were located at the bottom and
tail end of 3T3 cells and ran parallel to the current or preceding direction of
migration. Second, the 3 micrometer long rod-like structure (primary cilium), which
contains tubulin and which has been observed by other investigators in
transmission electron microscopy (Barnes, 1961; Sorokin, 1962; Wheatley, 1969)
and in indirect immunofluorescence (Osborn and Weber, 1976), was oriented
predominantly parallel to the substrate and to the current movement direction. It
seems possible that the primary cilium has a role in the directional control of a
migrating 3T3 cell, and that the main actin containing bundles act as substrate-
attached rails along which the nucleus and bulk cytoplasm slide during
displacement of the cells.
Schlagwörter Actins; Cell Line; Cell Movement; Cilia; Fluorescent Antibody Technique;
Glycoproteins; Microtubules; Tubulin
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Albrecht-Buehler, G. (1997): Autofluorescence of live purple bacteria in the near infrared. In: Experimental cell
research, Jg. 236, H. 1, S. 43–50. Online verfügbar unter doi:10.1006/excr.1996.3688.
Abstract We have developed a novel microscope with which to study the fluorescence of
cells in the near-infrared region (lambda = 750-2500 nm). For one of its first
applications we report on the autofluorescence of live purple bacteria,
Rhodospirillum rubrum, and suggest that the autofluorescent component is
bacteriochlorophyll. The rapid fading of the autofluorescence of fixed bacteria and
of purified bacteriochlorophyll suggests that the live bacteria are able to regenerate
their pigment with a time constant of approximately 20 s.
Schlagwörter Bacteriochlorophylls; Infrared Rays; Microscopy, Fluorescence; Rhodospirillum
rubrum; Time Factors

Allen, Karen Miller (1983): Artificial lighting and health. A selected bibliography. Monticello Ill.: Vance
Bibliographies (Architecture series--bibliography, A-1087).
Schlagwörter Fluorescent lighting; Physiological effect; Bibliography.; Health aspects; Electric
lighting

Amick, Charles L. (1947): Fluorescent lighting manual. 2nd ed. Fluorescent lighting (Hg.). New York: McGraw-
Hill.
Schlagwörter Fluorescent lighting.

Arai, Takao; Tani, Satoshi; Isoshima, Akira; Nagashima, Hiroyasu; Joki, Tatsuhiro; Takahashi-Fujigasaki, Junko;
Abe, Toshiaki (2006): [Intraoperative photodynamic diagnosis for spinal ependymoma using 5-aminolevulinic
acid: technical note]. In: No shinkei geka. Neurological surgery, Jg. 34, H. 8, S. 811–817.
Abstract OBJECTIVE: The fluorescence-guided resection using 5-aminolevulinic acid (5-
ALA) is a well established method for the treatment of brain tumor, especially
malignant glioma. However, there is no report on photodynamic diagnosis (PDD) for
spinal tumor. In the present study, we evaluated the usefulness of PDD for spinal
ependymoma using 5-ALA. METHODS: Three patients with spinal ependymoma
received oral doses of 5-ALA (20 mg/kg body weight) 2 hours before anesthesia
induction. Intraoperatively, fluorescence was observed with a 420 nm sharp cut filter
after excitation with a violet semiconductor laser (405 nm) and was verified by
analysis of fluorescent spectra. Residual fluorescent samples taken from the tumor
cavity were examined histologically RESULTS: Fluorescence peaked at 636nm in
the removed tumors in all cases. Fluorescent tissue tended to exist at the cranial
and caudal portion in the tumor cavity or around the anterior median fissure. The
residual fluorescent tissue was not detected after removal of the tumor in case 1.
The residual fluorescent tissue was composed of tumor cells and ependymal lining
in case 2 or the infiltrated inflammatory cells and vascular endothelial cells in case
3. Postoperative magnetic resonance (MR) imaging showed no residual tumor in
any of the cases. CONCLUSION: The results of this study indicate the usefulness
of 5-ALA-induced tumor fluorescence in guiding resection of spinal ependymoma.
5-ALA-induced porphyrin fluorescence may label spinal ependymomas easily and
clearly enough to enhance the completeness of tumor removal.
Schlagwörter Adult; Aminolevulinic Acid; Ependymoma; Female; Fluorescence; Humans;
Intraoperative Period; Lighting; Magnetic Resonance Imaging; Male; Middle Aged;
Photosensitizing Agents; Porphyrins; Sensitivity and Specificity; Spinal Cord
Neoplasms

Atkinson, Arthur Dinham Stephen (1944): Fluorescent lighting. Dealing with the principles and practice of
fluorescent lighting, for electrical engineers, illuminating engineers and architects. London: Newnes.
Schlagwörter Fluorescent lighting.

Atkinson, Arthur Dinham Stephen (1946): Fluorescent lighting. Brooklyn N.Y.: Chemical publishing co. inc.
Schlagwörter Fluorescent lighting.
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Atkinson, Arthur Dinham Stephen (1951): Modern fluorescent lighting. Dealing with the principles and practice of
fluorescent lighting, for electrical engineers, illuminating engineers, and architects. London: Newnes.
Schlagwörter Fluorescent lighting.

Atkinson, Arthur Dinham Stephen (1955): Modern fluorescent lighting. Dealing with the principles and practice of
fluorescent lighting, for electrical engineers, illuminating engineers, and architects. 2d ed. London: Newnes.
Schlagwörter Fluorescent lighting.

Ben-Hur, E.; Elkind, M. M. (1972): Survival response of asynchronous and synchronous Chinese hamster cells
exposed to fluorescent light following 5-bromodeoxyuridine incorporation. In: Mutation research, Jg. 14, H. 2, S.
237–245.
Schlagwörter Animals; Bromodeoxyuridinemetabolismpharmacology; Cell Line; Cell Survivaldrug
effectsradiation effects; Cells, Culturedradiation effects; Cricetinae;
Cysteaminepharmacology; DNAradiation effects; DNA Replication; Fibroblastsdrug
effectsradiation effects; Fluorescence; Light; Mercaptoethylaminespharmacology;
Photic Stimulation; Radiation Dosage; Radiation Effects; Radiation-Protective
Agents; Radiation-Sensitizing Agents; Time Factors

Ben-Hur, E.; Elkind, M. M. (1972): Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese hamster
cells exposed to fluorescent light. In: Biophysical journal, Jg. 12, H. 6, S. 636–647. Online verfügbar unter
doi:10.1016/S0006-3495(72)86109-5.
Schlagwörter Animals; Bromodeoxyuridinemetabolism; Cell Line; Centrifugation, Density
Gradient; Cricetinae; Cysteaminepharmacology; DNAbiosynthesisradiation effects;
DNA Repair; Fibroblastsdrug effectsmetabolismradiation effects; Fluorescence;
Isotope Labeling; Kinetics; Light; Molecular Weight; Radiation Effects; Radiation-
Protective Agents; Thymidinemetabolism; Tritium

Ben-Hur, E.; Elkind, M. M. (1974): Letter: Damage and repair of DNA in 5-bromodeoxyuridine-labeled Chinese
hamster cells exposed to fluorescent light. In: Biophysical journal, Jg. 13, H. 12, S. 1342. Online verfügbar unter
doi:10.1016/S0006-3495(73)86067-9.
Schlagwörter Animals; Bromodeoxyuridine; Cell Line; Centrifugation, Density Gradient;
Cricetinae; DNA Repair; DNA, Single-Strandedbiosynthesis; Fluorescence;
Molecular Weight

Beral, V.; Evans, S.; Shaw, H.; Milton, G. (1982): Malignant melanoma and exposure to fluorescent lighting at
work. In: Lancet, Jg. 2, H. 8293, S. 290–293.
Abstract In a study of 274 women with malignant melanoma, aged 18--54 years, and 549
matched controls in New South Wales, Australia, reported exposure to fluorescent
light at work was associated with a doubling of melanoma risk (relative risk [RR] =
2.1; 95% confidence limits 1.32--3.32). The risk grew with increasing duration of
exposure to fluorescent light and was higher in women who had worked mainly in
offices (RR = 2.6) than in women whose main place of work was indoors but not in
offices (RR = 1.8). The findings could not be explained by the differences in
histories of sunlight exposure, in skin or hair colour, or in any other factor. There
was a relative excess of lesions on the trunk in the group exposed to fluorescent
light at work. 27 men with melanoma and 35 similarly aged controls were studied,
and a significant increase in risk was also found: the RB in those exposed for
greater than or equal to 10 years compared with those exposed for less than 10
years was 4.4 (95% confidence limits 1.1--17.5). Such an association has not been
reported before, but it is plausible and could explain many of the paradoxical
features of the epidemiology of melanoma. Until more data accumulate it must,
however, be viewed cautiously.
Schlagwörter Adolescent; Adult; Age Factors; Female; Fluorescence; Humans; Lightadverse
effects; Lighting; Melanomaetiology; Middle Aged; Occupational Diseasesetiology;
Risk; Sex Factors; Skin Neoplasmsetiology
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Boatright, Jeffrey H.; Moring, Anisha G.; McElroy, Clinton; Phillips, Michael J.; Do, Vi T.; Chang, Bo et al. (2007):
Tool from ancient pharmacopoeia prevents vision loss. In: Molecular vision, Jg. 12, S. 1706–1714.
Abstract PURPOSE: Bear bile has been used in Asia for over 3,000 years to treat visual
disorders, yet its therapeutic potential remains unexplored in Western vision
research. The purpose of this study was to test whether treatment of mice
undergoing retinal degeneration with tauroursodeoxycholic acid (TUDCA), a primary
constituent of bear bile, alters the course of degeneration. METHODS: Two retinal
degeneration models were tested: the rd10 mouse, which has a point mutation in
the gene encoding the beta subunit of rod phosphodiesterase, and light induced
retinal damage (LIRD). For LIRD studies, albino Balb/C adult mice were
subcutaneously injected with TUDCA (500 mg/kg body weight) or vehicle (0.15 M
NaHCO(3)). Sixteen h later, each mouse received repeat injections. Half of each
treatment group was then placed in bright light (10,000 lux) or dim light (200 lux) for
seven h. At the end of exposure, animals were transferred to their regular housing.
Electroretinograms (ERGs) were assessed 24 h later, mice sacrificed, eyes
embedded in paraffin and sectioned, and retina sections assayed for morphology
and apoptosis by TUNEL and anti-active caspase-3 immunoreactivity via
fluorescent confocal microscopy. A subset of mice were sacrificed 8 and 15 days
after exposure and retina sections analyzed for morphology and apoptosis. For rd10
studies, mice were injected subcutaneously with TUDCA or vehicle at postnatal (P)
days 6, 9, 12, and 15. At p18, ERGs were recorded, mice were euthanized and
eyes were harvested, fixed, and processed. Retinal sections were stained (toluidine
blue), and retinal cell layers morphometrically analyzed by light microscopy.
Consecutive sections were analyzed for apopotosis as above. RESULTS: By every
measure, TUDCA greatly slowed retinal degeneration in LIRD and rd10 mice. ERG
a-wave and b-wave amplitudes were greater in mice treated with TUDCA compared
to those treated with vehicle. Retinas of TUDCA-treated mice had thicker outer
nuclear layers, more photoreceptor cells, and more fully-developed photoreceptor
outer segments. Finally, TUDCA treatments dramatically suppressed signs of
apoptosis in both models. CONCLUSIONS: Systemic injection of TUDCA, a primary
constituent of bear bile, profoundly suppressed apoptosis and preserved function
and morphology of photoreceptor cells in two disparate mouse models of retinal
degeneration. It may be that bear bile has endured so long in Asian pharmacopeias
due to efficacy resulting from this anti-apoptotic and neuroprotective activity of
TUDCA. These results also indicate that a systematic, clinical assessment of
TUDCA may be warranted.
Schlagwörter Animals; Apoptosisdrug effects; Bilechemistry; Blindnessetiologyprevention &
control; Cyclic Nucleotide Phosphodiesterases, Type 6; Disease Models, Animal;
Electroretinography; Injections, Subcutaneous; Light; Medicine, East Asian
Traditional; Mice; Mice, Mutant Strains; Phosphoric Diester Hydrolasesgenetics;
Photoreceptor Cells, Vertebratedrug effectspathology; Retinal
Degenerationcomplicationsetiologygeneticsphysiopathology;
Taurochenodeoxycholic Acidadministration & dosagechemical
synthesispharmacology; Ursidae

Brondon, Philip; Stadler, Istvan; Lanzafame, Raymond J. (2005): A study of the effects of phototherapy dose
interval on photobiomodulation of cell cultures. In: Lasers in surgery and medicine, Jg. 36, H. 5, S. 409–413.
Online verfügbar unter doi:10.1002/lsm.20183.
Abstract BACKGROUND AND OBJECTIVES: Dosimetry and treatment frequency are
controversial phototherapy issues. Efficacy of dose fractionation on
photobiomodulation was evaluated in vitro. STUDY DESIGN/MATERIALS AND
METHODS: Human HEP-2 and murine L-929 cell lines were cultured in complete
DMEM media. Photoradiation (670 nm, 5 J/cm2/treatment, 50 J/cm2 total energy
delivery), was performed varying treatments per 24 hour period: Group I (Controls)-
0, Group II-1/d, Group III-2/d, Group IV-4/d. Cell proliferation was measured using
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Cyquant (fluorescent DNA content) and MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-
diphenyl tetrasolium bromide) assays for 240 hours post therapy. A proliferation
index: PI = (#Cells Experimental(t) / #Cells Control(t)) was computed. RESULTS:
MTT assay results demonstrated maximal response in Group III (P < 0.05, n = 3).
Cyquant maxima occurred in HEP-2 Groups II and III (P < 0.045) and L-929 Group
III (P < 0.091). CONCLUSIONS: Cellular response to dose frequency varies. More
frequent treatments (2/24 hours) increased metabolism and proliferation in both cell
lines. Further investigation of dose fractionation in phototherapy is warranted.
Schlagwörter Animals; Cell Line; Cell Proliferation; Coloring Agents; Connective Tissue Cells;
Dose Fractionation; Epithelial Cells; Humans; Mice; Phototherapy; Tetrazolium
Salts; Thiazoles; Time Factors

Bulina, Maria E.; Lukyanov, Konstantin A.; Britanova, Olga V.; Onichtchouk, Daria; Lukyanov, Sergey;
Chudakov, Dmitriy M. (2006): Chromophore-assisted light inactivation (CALI) using the phototoxic fluorescent
protein KillerRed. In: Nature protocols, Jg. 1, H. 2, S. 947–953. Online verfügbar unter
doi:10.1038/nprot.2006.89.
Abstract The phototoxic red fluorescent GFP-like protein KillerRed has recently been
described. The phototoxicity of KillerRed exceeds that of EGFP by at least 1,000-
fold, making it the first fully genetically encoded photosensitizer. KillerRed opens up
new possibilities for precise light-induced cell killing and target protein inactivation.
Because KillerRed is encoded by a gene, it can be expressed in a spatially and
temporally regulated manner, under a chosen promoter, and fused with the desired
protein of interest or localization signal. Here we provide a protocol for target protein
inactivation in cell culture using KillerRed. As KillerRed is a new tool, the protocol
focuses on aspects that will allow users to maximize the potential of this protein,
guiding the design of chimeric constructs, recommended control experiments and
preferred illumination parameters. The protocol, which describes target protein
visualization and subsequent inactivation, is a 2- or 3-d procedure.
Schlagwörter Bacteria; Epithelial Cells; Gene Expression Regulation; Green Fluorescent Proteins;
Hela Cells; Humans; Light; Luminescent Agents; Protein Binding

Chaloupka, R.; Sureau, F.; Kocisova, E.; Petrich, J. W. (1998): Hypocrellin A photosensitization involves an
intracellular pH decrease in 3T3 cells. In: Photochemistry and photobiology, Jg. 68, H. 1, S. 44–50.
Abstract The fluorescent pH probe carboxy-seminaphtorhodafluor-1 (C-Snarf-1) has been
used for laser microspectro-fluorometric assays of intracellular pH in 3T3 mouse
fibroblasts treated with hypocrellin A. These results are compared to those
previously obtained with the structurally related hydroxylated polycyclic quinone,
hypericin (Sureau et al., J. Am. Chem. Soc. 118, 9484-9487, 1996). A mean local
intracellular pH drop of 0.6 units has been observed in the presence of 1 microM
hypocrellin A after 90 s of exposure to 0.1 microW of laser irradiation at 514.5 nm.
The time evolution of the cytoplasm acidification for hypocrellin A-treated cells is
faster than that for cells treated by hypericin. Thus, release of protons from an
excited state of hypocrellin A appears to be more efficient than that from hypericin.
In addition, the pH dependence of the quenching of C-Snarf-1 fluorescence in 3T3
cells under continuous irradiation has been observed. It is shown here that under
continuous illumination, a pH decrease is able to induce a modification of the
intracellular binding equilibrium of C-Snarf-1 that results in an increase of C-Snarf-1
fluorescence intensity. This latter observation suggests that the protons generated
upon the photoexcitation of hypericin or its analogs may be involved in the
production of other photoreactive species. Finally, we suggest that, just as for
hypericin, this pH drop may be involved in the antiviral and antitumor activity of
hypocrellin A.
Schlagwörter 3T3 Cells; Animals; Benzopyrans; Fluorescent Dyes; Hydrogen-Ion Concentration;
Intracellular Fluid; Lasers; Mice; Naphthols; Perylene; Photobiology;
Photosensitizing Agents; Quinones; Rhodamines
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Duncan, T. E.; O'Steen, W. K. (1986): The diurnal susceptibility of rat retinal photoreceptors to light-induced
damage. In: Experimental eye research, Jg. 41, H. 4, S. 497–507.
Abstract Exposure of albino rats to high intensity light results in rapid, graded loss of
photoreceptors. The hormonal status and age of an animal at the time of exposure
affect the severity of light-induced retinal damage. The adrenal axis and pituitary
hormones (prolactin) have been demonstrated previously to affect the degree of cell
death in the retina. Because circadian rhythms for adrenal and pituitary secretion
have been demonstrated in the rat, a series of experiments was undertaken to
determine if a diurnal pattern of retinal susceptibility to light damage exists which
might be related to endogenous endocrine rhythms. Male Sprague-Dawley rats
were exposed to 4 hr of high intensity fluorescent light for 8 consecutive days during
different phases of the 14:10 hr light: dark animal room light cycle. Morphometric
analysis performed at the light microscopic level 2 weeks after exposure
demonstrated a differential susceptibility to light-induced cell death depending upon
the period during the light-dark cycle when animals received their daily light
exposure. Neuronal cell death was confined to the outer nuclear layer as previously
described. The retinas of animals exposed during the middle of the dark period or
during the first 5 hr of the light period were significantly more damaged than the
retinas of animals exposed during the last 9 hr of the light period. Control groups for
the relative amounts of dark-adaptation between groups suggested that the diurnal
susceptibility to light damage was not solely dependent upon the degree of dark
adaptation. These results demonstrate a diurnal susceptibility of photoreceptors to
light-induced cell death.
Schlagwörter Animals; Cell Survivalradiation effects; Circadian Rhythm; Dark Adaptation; Light;
Male; Photometry; Photoreceptor Cellsradiation effects; Rats; Rats, Inbred Strains;
Time Factors

Elenbaas, W. (1959): Fluorescent lamps and lighting. New York: Macmillan (Phillips' technical library).
Schlagwörter Fluorescent lighting.; Fluorescent lamps.

Elenbaas, W. (1971): Fluorescent lamps. 2nd ed. London: Macmillan (Philips technical library).
Schlagwörter Fluorescent lighting.; Fluorescent lamps.

Federal Construction Council; Task Group T-58 (1968): High-frequency lighting. United States. (Hg.).
Washington: National Academy of Sciences (National Academy of Sciences. Publication 1610., no. 53).
Schlagwörter Fluorescent lighting.

Forsythe, William Elmer; Adams, Elliot Quincy (1948): Fluorescent and other gaseous discharge lamps. New
York: Technical Division Murray Hill Books.
Schlagwörter Fluorescent lighting.; Electric discharge lighting.

Gaillard, E. R.; Atherton, S. J.; Eldred, G.; Dillon, J. (1995): Photophysical studies on human retinal lipofuscin.
In: Photochemistry and photobiology, Jg. 61, H. 5, S. 448–453.
Abstract Fluorescent material generated in the human retina accumulates within lipofuscin
granules of the retinal pigment epithelium (RPE) during aging. Its presence has
been suggested to contributed to various diseases including age-related macular
degeneration. Because this material absorbs light at wave lengths as long as 550
nm, photophysical studies were performed to determine whether lipofuscin could
contribute to light damage and to determine if its composition is similar to a
synthetically prepared lipofuscin. Time-resolved experiments were performed to
monitor (1) fluorescence decay, (2) the UV-visible absorption of longer-lived excited
states and (3) the formation and decay of singlet oxygen at 1270 nm. Steady-state
and time-resolved fluorescence studies indicate that human and synthetic lipofuscin
have fluorophores in common. Time-resolved absorption experiments on human
retinal lipofuscin and synthetic lipofuscin showed the presence of at least two
transient species, one absorbing at 430 nm (lifetime ca 7 microseconds) and a
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second absorbing at 580 nm, which decays via second order kinetics. In addition,
there is a third absorbing species stable to several hundred milliseconds. The
transient species at 430 nm is quenched by oxygen, suggesting that it is a triplet
state. Subsequent studies showed the formation of singlet oxygen, which was
monitored by its phosphorescence decay at 1270 nm. These studies demonstrate
that lipofuscin can act as a sensitizer for the generation of reactive oxygen species
that may contribute to the age-related decline of RPE function and blue light
damage.
Schlagwörter Adult; Humans; Kinetics; Lipofuscinchemistryisolation & purification;
Photochemistry; Photolysis; Pigment Epithelium of Eyemetabolism; Protein
Conformation; Quantum Theory; Spectrometry, Fluorescence; Spectrophotometry

Gantt, R.; Parshad, R.; Ewig, R. A.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Kohn, K. W. (1978): Fluorescent
light-induced DNA crosslinkage and chromatid breaks in mouse cells in culture. In: Proceedings of the National
Academy of Sciences of the United States of America, Jg. 75, H. 8, S. 3809–3812.
Abstract A single 20-hr exposure of mouse cells derived from embryonic or lung tissue to
cool-white fluorescent light (4.6 W/m2) causes both DNA damage and chromosome
aberrations including chromatid breaks, exchanges, and minutes. In Kohn's alkaline
elution technique, the DNA from exposed cells elutes more slowly than that from
shielded cells. Because larger molecular weight DNA elutes slower than smaller, we
interpret these results to mean that the DNA in cells exposed to light is crosslinked.
The estimated frequency of crosslinks is sufficient to account for the number of
chromatid breaks observed. The types of chromosome aberrations produced by
light indicate that the primary lesion results in chromatid rather than chromosome
breaks, and the results suggest an influence of cell density in that cells in densely
populated cultures showed few or no chromatid breaks after irradiation. The present
results, together with observations from the literature, suggest that the DNA
crosslinkage and the chromosome aberrations produced by light may be related.
Schlagwörter Cells, Cultured; Chromatidsradiation effects; Chromosome Aberrations;
DNAradiation effects; Fluorescence; Lightadverse effects; Time Factors

Gordon, William C.; Casey, Douglas M.; Lukiw, Walter J.; Bazan, Nicolas G. (2002): DNA damage and repair in
light-induced photoreceptor degeneration. In: Investigative ophthalmology & visual science, Jg. 43, H. 11, S.
3511–3521.
Abstract PURPOSE: Intense light causes photoreceptor death that is greatest in the superior
central retina. Short-duration treatment in a light-damage model results in TUNEL-
positive photoreceptor nuclei within this region. However, cells lost 10 days after
light treatment are fewer than the TUNEL-labeled cells observed earlier. Therefore,
this study was undertaken to monitor DNA fragmentation and cell death to explain
the discrepancy. METHODS: Eyes of dark-adapted rats were light damaged for 4 or
5 hours. DNA fragmentation was measured by TUNEL, laddering, and highly
repetitive short interspersed nuclear element (SINE) analysis in dark-adapted,
nondamaged control (dark-control) retinas and in retinas collected at 6-hour
intervals after light treatment. TUNEL-positive photoreceptor nuclei were counted in
these samples along a superior-to-inferior meridian and compared with control and
damaged 10-day retinas. Monocytes and DNA polymerase beta were monitored by
immunohistochemistry. RESULTS: TUNEL-positive staining of photoreceptors was
centered around the superior central retina. At 10 days, photoreceptor loss had
occurred in this region. In graphs of 6-hour-interval data, two DNA-fragmentation
peaks, 24 hours apart, were evident. Monocytes appeared after nuclear damage.
Total TUNEL-positive cells under both peaks exceeded the number of
photoreceptors lost. The DNA-repair enzyme, polymerase beta, was induced in the
superior central retina, within photoreceptor inner segments, 24 hours after light
treatment, but declined thereafter. CONCLUSIONS: One population of damaged
cells may mend DNA until the repair mechanism is exceeded and then revert to
apoptosis, or, alternatively, two populations may undergo DNA fragmentation 24
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hours apart. Either DNA fragmentation is masked at midpoint by temporary repair,
or two waves of damage occur, but repair rescues the first set, not the second.
Photoreceptors lost are fewer than TUNEL-positive cells. Thus, both possibilities
suggest photoreceptor DNA repair. The transient appearance of DNA polymerase
beta in photoreceptors under these experimental conditions further suggests
nuclear repair. Thus, maintenance of in-house DNA-repair mechanisms may
provide an alternate approach for the rescue of photoreceptors, as well as other
neurons with stress-induced damage. These events may provide useful drug
targets to promote photoreceptor survival in various forms of retinal degeneration.
Schlagwörter Animals; Blotting, Western; DNAanalysis; DNA Damageradiation effects; DNA
Fragmentation; DNA Polymerase betametabolism; DNA Repair; Fluorescent
Antibody Technique, Indirect; In Situ Nick-End Labeling; Light; Male; Photoreceptor
Cells, Vertebratepathologyradiation effects; Proliferating Cell Nuclear
Antigenmetabolism; Radiation Injuries, Experimentalgeneticsmetabolismpathology;
Rats; Rats, Sprague-Dawley; Retinal Degenerationgeneticsmetabolismpathology;
Time Factors; Up-Regulation

Heeke, D. S.; White, M. P.; Mele, G. D.; Hanifin, J. P.; Brainard, G. C.; Rollag, M. D. et al. (1999): Light-emitting
diodes and cool white fluorescent light similarly suppress pineal gland melatonin and maintain retinal function
and morphology in the rat. In: Laboratory animal science, Jg. 49, H. 3, S. 297–304.
Abstract BACKGROUND AND PURPOSE: A novel light-emitting diode (LED) light source for
use in animal-habitat lighting was evaluated. METHODS: The LED was evaluated
by comparing its effectiveness with that of cool white fluorescent light (CWF) in
suppressing pineal gland melatonin content and maintaining normal retinal
physiology, as evaluated by use of electroretinography (ERG), and morphology.
RESULTS: Pineal melatonin concentration was equally suppressed by LED and
CWF light at five light illuminances (100, 40, 10, 1, and 0.1 lux). There were no
significant differences in melatonin suppression between LED and CWF light,
compared with values for unexposed controls. There were no differences in ERG a-
wave implicit times and amplitudes or b-wave implicit times and amplitudes
between 100-lux LED-exposed rats and 100-lux CWF-exposed rats. Results of
retinal histologic examination indicated no differences in retinal thickness, rod outer
segment length, and number of rod nuclei between rats exposed to 100-lux LED
and 100-lux CWF for 14 days. Furthermore, in all eyes, the retinal pigmented
epithelium was intact and not vacuolated, whereas rod outer segments were of
normal thickness. CONCLUSION: LED light does not cause retinal damage and can
suppress pineal melatonin content at intensities similar to CWF light intensities.
Schlagwörter Animals; Electroretinographyradiation effects; Lightadverse effects; Male;
Melatoninmetabolism; Pineal Glandmetabolismradiation effects;
Radioimmunoassay; Rats; Rats, Sprague-Dawley; Retinaphysiologyradiation
effects

Kasperowski, Walther (195?): Mehr Licht durch Leuchtstofflampen. Technik und Anwendung der
Fluoreszenzbeleuchtung. Wien: A. Göschl.
Schlagwörter Fluorescent lighting.

Katz, M. L.; Eldred, G. E. (1989): Retinal light damage reduces autofluorescent pigment deposition in the retinal
pigment epithelium. In: Investigative ophthalmology & visual science, Jg. 30, H. 1, S. 37–43.
Abstract Lipofuscin in the retinal pigment epithelium (RPE) is thought to be derived from
phagocytosed photoreceptor outer segment disc membranes. Based on this
hypothesis, one would predict that the rate of lipofuscin deposition in the RPE would
be proportional to the density of photoreceptor cells in the retina. In previous studies
it was demonstrated that specific loss of photoreceptor cells due to a genetic defect
resulted in a substantial decrease in the rate of age-related lipofuscin accumulation
in the RPE. In order to confirm that this decreased RPE lipofuscin deposition was
directly related to reduced photoreceptor cell density, experiments were conducted
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to determine whether light-induced photoreceptor cell destruction affected RPE
lipofuscin content. The effects of retinal light damage on RPE autofluorescent
pigment accumulation resulting from both normal aging and vitamin E deficiency
were examined. Starting immediately after weaning, albino Fisher 344 rats were fed
diets either containing or lacking vitamin E. All animals were maintained on a 12
hr/12 hr light/dark cycle. During the light phases of the cycles, the cage illuminance
for one-half the animals in each dietary group was 750 lux, while the remaining rats
were exposed to a light level of 15 lux. Illumination was provided by 40 watt cool-
white fluorescent lamps. After 17 weeks, rats in both dietary groups that were
maintained under the higher light intensity had substantially reduced photoreceptor
cell densities relative to animals in the same dietary group maintained under dim
light conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Schlagwörter Agingmetabolism; Animals; Chromatography, Thin Layer; Fluorescence;
Lightadverse effects; Lipofuscinmetabolism; Male; Pigment Epithelium of
Eyemetabolism; Rats; Rats, Inbred F344; Retinainjuries; Retinal
Pigmentsmetabolism; Vitamin E Deficiencymetabolism

Kehat, Rinat; Zemel, Esther; Cuenca, Nicolas; Evron, Tama; Toiber, Debra; Loewenstein, Anat et al. (2007): A
novel isoform of acetylcholinesterase exacerbates photoreceptors death after photic stress. In: Investigative
ophthalmology & visual science, Jg. 48, H. 3, S. 1290–1297. Online verfügbar unter doi:10.1167/iovs.06-0847.
Abstract PURPOSE: To study the involvement of stress-induced acetylcholinesterase
(AChE) expression in light-induced retinal damage in albino rats. METHODS: Adult
albino rats were exposed for 24 hours to bright, damaging light. AChE expression
was monitored by in situ hybridization, by histochemistry for AChE activity, and by
immunocytochemistry. An orphan antisense agent (Monarsen; Ester
Neurosciences, Ltd., Herzlia Pituach, Israel) was administered intraperitoneally to
minimize light-induced AChE expression. The electroretinogram (ERG) was
recorded to assess retinal function. RESULTS: Twenty-four-hour exposure to bright
light caused severe reduction in the ERG responses and augmented expression of
mRNA for the "read-through" variant of AChE (AChE-R) in photoreceptor inner
segments (IS), bipolar cells, and ganglion cells. AChE activity increased in IS. The
expressed AChE protein was a novel variant, characterized by an extended N
terminus (N-AChE). Systemic administration of the orphan antisense agent,
Monarsen, reduced the photic induction of mRNA for AChE-R, and of the N-AChE
protein. Rats exposed to bright, damaging light and treated daily with Monarsen
exhibited larger ERG responses, relatively thicker outer nuclear layer (ONL), and
more ONL nuclei than did rats exposed to the same damaging light but treated daily
with saline. CONCLUSIONS: The findings indicate that the photic-induced novel
variant of AChE (N-AChE-R) may be causally involved with retinal light damage and
suggest the use of RNA targeting for limiting such damage.
Schlagwörter Acetylcholinesterasegeneticsmetabolism; Animals; Cell Death; DNA,
Antisensepharmacology; Electroretinographyradiation effects; Fluorescent Antibody
Technique, Indirect; Gene Expression Regulation, Enzymologicphysiology; In Situ
Hybridization; Isoenzymesmetabolism; Light; Male; Microscopy, Confocal;
Photoreceptor Cells, Vertebratepathology; RNA, Messengermetabolism; Radiation
Injuries, Experimentalenzymology; Rats; Rats, Sprague-Dawley; Retinaradiation
effects; Retinal Degenerationenzymologypathology

Kennedy, A. R.; Ritter, M. A.; Little, J. B. (1980): Fluorescent light induces malignant transformation in mouse
embryo cell cultures. In: Science (New York, N.Y.), Jg. 207, H. 4436, S. 1209–1211.
Abstract Fluorescent light induced a dose-dependent malignant transformation in mouse
C3H10T1/2 cells. A plateau in the dose-response curve for transformation was
correlated with that observed with ultraviolet light exposure. The similarity in the two
dose-response patterns suggests that similar molecular processes may be involved
in the induction of malignant transformation by the two types of radiation.
Schlagwörter Animals; Cell Survivalradiation effects; Cell Transformation, Neoplasticradiation
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effects; Cells, Cultured; DNAradiation effects; Dose-Response Relationship,
Radiation; Embryo, Mammalianradiation effects; Fluorescence; Light; Mice;
Pyrimidine Dimersradiation effects; Ultraviolet Rays

Koide, R.; Ueda, T. N.; Dawson, W. W.; Hope, G. M.; Ellis, A.; Somuelson, D. et al. (2001): [Retinal hazard from
blue light emitting diode]. In: Nippon Ganka Gakkai zasshi, Jg. 105, H. 10, S. 687–695.
Abstract PURPOSE: To compare the effect of exposure time from a blue(460 nm) light
emitting diode(LED) on the morphology of the outer retina and determine conditions
where damage occurs. MATERIALS AND METHODS: Young adult rhesus
monkeys were anesthetized, and received blue LED exposure from a modified slit-
lamp. A 3 mm beam of 0.85 mW was imaged onto the retina through a lens
positioned before the cornea and exposure damage was determined at time
intervals for 12 to 90 min. Fundus photography, fluorescein angiography(FAG),
retinal tomography(HRT), and s-cone electororetinogram(S-ERG) were recorded at
baseline, 2, and 30 days. RESULTS: Two days after 40 min exposure, there was a
grey, discolored region, which was over-fluorescent in FAG, and an incresse in HRT
and S-ERG corresponding to the site which was exposed to LED light. In
histological examination at 30 days, the LED had caused produced a marked
disruption of the disks of photoreceptor cells, damaged retinal pigment
epithelium(RPE) apical villi, and a loss of RPE melanin after 90 min exposure.
CONCLUSION: A threshold level was found around 40 min. This morphological
damage may impair function and continuous exposure to blue light is potentially
dangerous to vision.
Schlagwörter Animals; Lightadverse effects; Macaca mulatta; Male; Pigment Epithelium of
Eyeradiation effectsultrastructure; Radiation Injuries, Experimentalpathology;
Retinapathologyradiation effects

Laabich, Aicha; Vissvesvaran, Ganesh P.; Lieu, Kuo L.; Murata, Kyoko; McGinn, Tim E.; Manmoto, Corinne C.
et al. (2006): Protective effect of crocin against blue light- and white light-mediated photoreceptor cell death in
bovine and primate retinal primary cell culture. In: Investigative ophthalmology & visual science, Jg. 47, H. 7, S.
3156–3163. Online verfügbar unter doi:10.1167/iovs.05-1621.
Abstract PURPOSE: The present study was performed to investigate the effect of crocin on
blue light- and white light-induced rod and cone death in primary retinal cell
cultures. METHODS: Primary retinal cell cultures were prepared from primate and
bovine retinas. Fifteen-day-old cultures were exposed to blue actinic light or to white
fluorescent light for 24 hours. Cultures were treated by the addition of different
concentrations of crocin for 24 hours before light exposure or for 8 hours after light
exposure. Cultures kept in the dark were used as controls. Green nucleic acid stain
assay was used to evaluate cell death. Rods and cones were immunolabeled with
specific antibodies and counted. TUNEL labeling was used to detect fragmented
DNA in fixed cells after light exposure. RESULTS: Primary retinal cell cultures
contained a mixture of retinal cells enriched in photoreceptors, bipolar cells, and
Müller cells. Twenty-four-hour exposure to blue and white light induced death in
70% to 80% of the photoreceptors in bovine and primate retinal cell cultures. Crocin
protected the photoreceptors against blue light- or white light-mediated damage in a
concentration-dependent manner with an EC50 of approximately 30 microM.
TUNEL assays confirmed that crocin protected photoreceptors from light damage.
CONCLUSIONS: These results show that blue and white light selectively induce rod
and cone cell death in an in vitro model. Crocin protects retinal photoreceptors
against light-induced cell death.
Schlagwörter Animals; Carotenoidspharmacology; Cattle; Cell Count; Cell Culture Techniques;
Cell Deathdrug effectsradiation effects; Crocus; Dose-Response Relationship,
Drug; Flowers; Fluorescent Antibody Technique, Indirect; In Situ Nick-End Labeling;
Lightadverse effects; Macaca fascicularis; Photoreceptor Cells, Vertebratedrug
effectsradiation effects; Plant Extractspharmacology; Radiation Injuries,
Experimentaletiologyprevention & control; Retinal Degenerationetiologyprevention
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& control

Lam, R. W.; Buchanan, A.; Clark, C. M.; Remick, R. A. (1991): Ultraviolet versus non-ultraviolet light therapy for
seasonal affective disorder. In: The Journal of clinical psychiatry, Jg. 52, H. 5, S. 213–216.
Abstract Although light therapy has been shown to be effective in the treatment of seasonal
affective disorder (SAD), little research has been done to determine which light
wavelengths affect treatment outcome. In this triple crossover study the authors
compared 1 week of light therapy in which bright (2500 lux), full-spectrum
fluorescent light, with and without blockade of the ultraviolet (UV) spectrum, was
used with a dim (500 lux) light control in 11 SAD patients. The dim light condition
had no significant antidepressant effects as measured by the Hamilton Rating Scale
for Depression (HAM-D), the Beck Depression Inventory (BDI), and an atypical
depressive symptom (ATYP) score. The UV-light condition significantly reduced
HAM-D, BDI, and ATYP scores, whereas the UV-blocked condition significantly
reduced only the ATYP score. These results suggest that the UV-spectrum in light
therapy may have a differential effect on typical and atypical symptoms in SAD.
Schlagwörter Depressive Disorderpsychologytherapy; Evaluation Studies as Topic; Female;
Humans; Light; Male; Personality Inventory; Phototherapymethods; Psychiatric
Status Rating Scales; Research Design; Seasons; Ultraviolet Rays; Ultraviolet
Therapy

Lee, F. L.; Yu, D. Y.; Tso, M. O. (1990): Effect of continuous versus multiple intermittent light exposures on rat
retina. In: Current eye research, Jg. 9, H. 1, S. 11–21.
Abstract The damaging effects of continuous light exposure to the albino rat retina have
been well documented. However, the cumulative effects of multiple light exposures
are not well defined. We therefore compared the retinal injury induced by a single
24 hour light exposure with that caused by three intermittent exposures of 8 hours
each. Eight dark-adapted albino Lewis rats were exposed for 24 hours to green
fluorescent light (490-580 nm) at an illuminance level of 175 foot-candles. A second
group of 8 rats was exposed under similar conditions in three split doses of 8 hours
each at intervals of 7 days between each exposure. Recovery was allowed in total
darkness, and the animals were sacrificed 2 weeks following the last exposure.
Retinal damage was assessed by morphometry and light and electron microscopy.
Mild cumulative retinal injury, mostly in photoreceptor cells with relative sparing of
the retinal pigment epithelium, was seen in the split dose group, while extensive
damage involving photoreceptor cells and retinal pigment epithelium was noted in
the group exposed continuously for 24 hours.
Schlagwörter Animals; Lightadverse effects; Male; Periodicity; Photoreceptor Cellsradiation
effectsultrastructure; Pigment Epithelium of Eyeradiation effectsultrastructure; Rats;
Rats, Inbred Lew; Retinaradiation effectsultrastructure

McColl, S. L.; Veitch, J. A. (2001): Full-spectrum fluorescent lighting: a review of its effects on physiology and
health. In: Psychological medicine, Jg. 31, H. 6, S. 949–964.
Abstract BACKGROUND: Full-spectrum fluorescent lighting (FSFL) has been credited with
causing dramatic beneficial effects on a wide variety of behaviours, mental health
outcomes and physical health effects, as compared to other fluorescent lamp types.
These effects are hypothesized to occur because of similarity between FSFL
emissions and daylight, which is said to have evolutionary superiority over other
light sources. METHOD: This review, covering the period 1941-1999, critically
considers the evidence for direct effects of FSFL through skin absorption as well as
indirect effects on hormonal and neural processes. CONCLUSIONS: Overall, the
evidence does not show dramatic effects of fluorescent lamp type on behaviour or
health, neither does it support the evolutionary hypothesis.
Schlagwörter Arousalphysiology; Brainphysiology; Calciummetabolism; Evolution; Female;
Fluorescence; Health Status; Humans; Hydrocortisoneurine;
Hyperbilirubinemiatherapy; Light; Male; Melatoninurine; Phototherapy; Psychomotor
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Performancephysiology; Seasonal Affective Disordertherapy; Skinradiation effects;
Stress, Psychologicalmetabolism; Sympathetic Nervous Systemphysiology; Vitamin
Dmetabolism

Miller, Henry Arthur (1947): Luminous tube lighting. Including high voltage fluorescent lighting. 2d ed. London:
Newnes.
Schlagwörter Electric discharge lighting.

Miller, Henry Arthur (1949): Cold cathode fluorescent lighting. London: Technical Press.
Schlagwörter Fluorescent lighting.

Nell, Walter (1952): Beleuchtungstechnik mit Leuchtstofflampen und Leuchtröhren. Leipzig: Fachbuchverlag.
Schlagwörter Fluorescent lighting.

Noell, W. K.; Albrecht, R. (1971): Irreversible effects on visible light on the retina: role of vitamin A. In: Science
(New York, N.Y.), Jg. 172, H. 978, S. 76–79.
Abstract Diffuse retinal irradiation by visible light produces in the rat the death of visual cells
and pigment epithelium. Typically, cage illumination of 1500 lux from fluorescent
light through a green filter leads to severe damage when continued for 40 hours.
Vitamin A deficiency protects against this damage but experiments show that retinol
released by light from rhodopsin is probably not the toxic agent. Protection against
light damage depends on a long-range state of cell adaptation to light itself. The
normal diurnal cycle of light and dark seems to be the essential factor in controlling
visual cell viability and susceptibility.
Schlagwörter Animals; Electrocardiography; Eye Diseasesetiology; Lightadverse effects; Rats;
Retina; Retinal Pigmentsmetabolism; Time Factors; Vitamin
Ametabolismphysiology; Vitamin A Deficiencymetabolism

Okuno, Tsutomu; Saito, Hiroyuki; Ojima, Jun (2002): Evaluation of blue-light hazards from various light sources.
In: Developments in ophthalmology, Jg. 35, S. 104–112.
Abstract Visible light of short wavelength (blue light) may cause a photochemical injury to the
retina, called photoretinitis or blue-light hazard. In this study, various light sources
were evaluated for blue-light hazard. These sources include the sun, the arc
associated with arc welding and plasma cutting, molten steel, iron and glass, the
interior of furnaces, the arc or envelope of discharge lamps, the filament or
envelope of incandescent lamps, the envelope of fluorescent lamps and light-
emitting diodes. The spectral radiance of each light source was measured, and
blue-light effective radiance and the corresponding permissible exposure time per
day were calculated in accordance with the ACGIH (American Conference of
Governmental Industrial Hygienists) standard. The sun, arc welding, plasma cutting
and the arc of discharge lamps were found to have extremely high effective
radiances with corresponding permissible exposure times of only 0.6-40 s,
suggesting that viewing these light sources is very hazardous to the retina. Other
light sources were found to have low effective radiances under the study conditions
and would pose no hazard, at least for short exposure times.
Schlagwörter Dose-Response Relationship, Radiation; Humans; Light; Maximum Allowable
Concentration; Radiation Injuries; Radiation Monitoring; Radiometry; Retina;
Retinitis

Paddock, S. W.; Albrecht-Buehler, G. (1988): Rigidity of the nucleus during nuclear rotation in 3T3 cells. In:
Experimental cell research, Jg. 175, H. 2, S. 409–413.
Abstract Using near infrared microscopy and ultraviolet fluorescence microscopy of living
3T3 cells stained with the fluorochrome Hoechst 33342, we have demonstrated that
the nucleoli and Hoechst 33342-stained chromocenters in the nucleus maintain a
fixed pattern during nuclear rotation. We conclude that the term "nuclear rotation"
refers to rotation of the entire nucleus in the cytoplasm of interphase cells, and that
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nuclear rotation is not an expression of karyoplasmic streaming. In conjunction with
earlier results on nuclear rotation the data imply that the interface of nuclear rotation
is located either between the two nuclear membranes or in the adjacent cytoplasm.
Schlagwörter Benzimidazoles; Cell Nucleus; Fluorescent Dyes; Interphase; Microscopy,
Fluorescence; Microscopy, Ultraviolet; Rotation; Video Recording

Parshad, R.; Sanford, K. K.; Jones, G. M. (1985): Chromatid damage induced by fluorescent light during G2
phase in normal and Gardner syndrome fibroblasts. Interpretation in terms of deficient DNA repair. In: Mutation
research, Jg. 151, H. 1, S. 57–63.
Abstract Skin fibroblasts from Gardner syndrome (GS) compared with those from normal
donors showed a significantly higher incidence of chromatid gaps and breaks
following exposure to low-intensity, cool-white fluorescent light during G2 phase of
the cell cycle. Considerable evidence supports the concept that chromatid gaps and
breaks seen directly after exposure to DNA-damaging agents represent unrepaired
DNA single- and double-strand breaks respectively. The changes in incidence of
chromatid aberrations with time after light exposure are consistent with the
sequence of events known to follow DNA damage and repair. Initially, the incidence
of light-induced chromatid gaps was equivalent in GS and normal fibroblasts. In the
normal cells, the chromatid gaps disappeared by 1 h post-exposure, presumably as
a result of efficient repair of DNA single-strand breaks. In contrast, the incidence of
gaps increased in GS cells by 0.5 h followed by a decrease at 1 h and concomitant
increase in chromatid breaks. It appears from these findings that the increased
incidence of chromatid damage in GS fibroblasts results from deficient repair of
DNA single-strand breaks which arise from incomplete nucleotide excision of DNA
damage during G2 phase.
Schlagwörter Cells, Cultured; Chromatidsradiation effects; DNA Repair; Dose-Response
Relationship, Radiation; Gardner Syndromegenetics; Humans; Interphase; Light

Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E. (1978): Fluorescent light-induced chromosome damage
and its prevention in mouse cells in culture. In: Proceedings of the National Academy of Sciences of the United
States of America, Jg. 75, H. 4, S. 1830–1833.
Abstract Twenty-hour-exposure to fluorescent light produces chromatid breaks in a line of
adult mouse lung cells grown in Dulbecco-Vogt medium supplemented with fetal
bovine serum. The light-induced damage appears to be enhanced by increasing the
concentration of oxygen in the gas phase of the culture. The effective wavelength(s)
of light is in the visible range between 400 and 450 nm andis probably the mercury
emission peak at 405 or 436 nm. Addition of catalase or glutathione with ascorbic
acid to the culture medium reduced the number of chromatid breaks to a level not
significantly different from that in the shielded cultures. It thus appears that the
production of H2O2 in the culture medium or in the cell is responsible for the
chromatid breaks. Most of the chromosomal abnormalities observed in long-term
culture of mouse cells may result from exposure of cells or medium to fluorescent
room lights in the presence of atmospheric oxygen. These genetic abnormalities
can be minimized by shielding cells and medium from light, lowering the PO2 of the
medium, and including reducing agents such as glutathione and ascorbic acid in the
medium formulation.
Schlagwörter Ascorbic Acidpharmacology; Catalasemetabolism; Cells, Cultureddrug
effectsradiation effects; Chromosome Aberrations; Culture Media;
Glutathionepharmacology; Hydrogen Peroxide; Light; Oxygen; Spectrum Analysis;
Superoxide Dismutasemetabolism

Parshad, R.; Sanford, K. K.; Jones, G. M.; Tarone, R. E.; Hoffman, H. A.; Grier, A. H. (1981): Susceptibility to
fluorescent light-induced chromatid breaks associated with DNA repair deficiency and malignant transformation
in culture. In: Cancer research, Jg. 40, H. 12, S. 4415–4419.
Abstract The increased susceptibility of mouse cells to fluorescent light-induced chromatid
damage following their spontaneous malignant transformation in culture could result
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from loss or inactivation of catalase that decomposes the photoproduct H2O2 or
from impaired capacities to repair DNA damage. No consistent change in catalase
activity with respect to neoplastic state could be established. To interpret the
cytogenetic damage in terms of DNA strand breaks, we determined the incidence of
chromatid breaks induced by light exposure during the G1 and late S-G2 phases of
the cell cycle in normal and malignant derivatives of a C3H mouse cell line.
Chromatid breaks at metaphase following light exposure during G1 would result
from DNA strand breaks, cross-links, or base damage, whereas breaks following
exposure during late S-G2 would result from single-or double-strand breaks. Both
G1 and late S-G2 were susceptible in malignant cells but only G1 in normal. Since
caffeine inhibits DNA repair, we compared its effects on light-induced chromatid
damage in the normal and malignant cells to assess their DNA repair capacities.
Treatment of normal cells with caffeine (50 microgram/ml) directly following five hr
of light exposure in G1 increased the chromatid damage to that in malignant cells
exposed with or without caffeine. Similarly, treatment of normal cells with caffeine
during late S-G2 exposure increased chromatid damage to a level not significantly
different from that in malignant cells exposed without caffeine. Caffeine had little
influence on chromatid damage in malignant cells. The increased susceptibility of
malignant mouse cells to fluorescent light-induced chromatid breaks thus appears
to result from impaired capacities to repair DNA damage.
Schlagwörter Animals; Caffeinepharmacology; Catalasemetabolism; Cell Cycle; Cell Line; Cell
Transformation, Neoplasticmetabolism; Chromatidsradiation effects; Chromosome
Aberrations; DNA Repair; Interphase; Light; Mice

Parshad, R.; Sanford, K. K.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1979): Increased susceptibility of mouse
cells to fluorescent light-induced chromosome damage after long-term culture and malignant transformation. In:
Cancer research, Jg. 39, H. 3, S. 929–933.
Abstract Exposure of mouse cells in culture to fluorescent light has been shown to produce
chromatid breaks and exchanges. Hydrogen peroxide formed in the cell during
illumination has been implicated as the causative agent. The present results
indicate that susceptibility to light-induced chromosome damage increases with time
in culture and seems to be associated with or requisite for the spontaneous
malignant transformation of mouse cells. All three cell lines followed during long-
term culture that either became tumorigenic or showed cytological evidence of
neoplastic transformation developed a concomitant increase in susceptibility. In
three additional cell lines, susceptibility to light-induced chromatid damage was
significantly increased in the spontaneously transformed malignant cells as
compared with their nonneoplastic precursors. The increased susceptibility is not
simply the result of long-term culture, since three other nonneoplastic cell lines after
prolonged culture were significantly less susceptible than their malignant
counterparts. Increased susceptibility to light-induced chromatid damage could
result from impaired DNA repair or from the loss of defense mechanisms for
destroying H2O2 or scavenging free radicals.
Schlagwörter Animals; Cell Line; Cell Transformation, Neoplastic; Chromosome Aberrations;
Crossing Over, Geneticradiation effects; DNAmetabolism; Hydrogen
Peroxidemetabolism; Lightadverse effects; Mice; Time Factors

Parshad, R.; Sanford, K. K.; Taylor, W. G.; Tarone, R. E.; Jones, G. M.; Baeck, A. E. (1980): Effect of intensity
and wavelength of fluorescent light on chromosome damage in cultured mouse cells. In: Photochemistry and
photobiology, Jg. 29, H. 5, S. 971–975.
Schlagwörter Animals; Catalasemetabolism; Cell Line; Chromatidsmetabolism;
Chromosomesradiation effects; Fluorescence; Hydrogen Peroxidemetabolism;
Light; Mice

Pitts, D. G.; Bergmanson, J. P.; Chu, L. W. (1984): Rabbit eye exposure to broad-spectrum fluorescent light. In:
Acta ophthalmologica. Supplementum, Jg. 159, S. 1–54.
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Abstract Two F40CW fluorescent lamps mounted in an EYS-2404 fixture and 300 nm, 5 nm
waveband UV radiation were used to expose pigmented rabbit eyes. The results of
the exposures to the eye were evaluated with the biomicroscope, ophthalmoscope,
light microscope and electron microscope. The following conclusions were reached:
The adverse ocular responses to fluorescent radiation exposure were due to long-
duration, broadband radiation. These reactions were more generalized for
fluorescent exposures when the cornea and lens are compared to UV exposures.
The differences between the levels of threshold exposure needed to cause damage
for the fluorescent source and UV radiation were attributed to exposure duration
and the rate of delivery of the radiation. Corneal and lenticular damage was mild
when compared with UV 300 nm exposures, and the threshold occurred after 8 h to
12 h of exposure. The effect of the radiation was to interfere with the normal
functions of the cell while changes to the inert materials in the tissues was
secondary to injury to the cell. The damage was mild in the corneal epithelium,
somewhat more severe in the corneal endothelium, but minimal in the corneal
stroma. Early retinal changes were found after 8 h of exposure to the fluorescent
source. These induced changes were evident in the neural retina as spaces and
were assumed to represent oedema. The retinal oedema was initially found only in
the receptor cell, outer nuclear and nerve fibre layers. Many vacuoles or spaces
were located in the junctional area between the ganglion cell and nerve fibre layers
while smaller spacing occurred also within the nerve fibre layer. Twelve h of
exposure to the fluorescent source produced a further increase in the oedema in
the retina. The outer segments of the receptor cells appear to disintegrate and
significant open spaces are evident among the inner and outer segments of the
receptors. The inner plexiform layer shows an increased number of spaces within
and among the neural elements, and the mitochondria appeared to be undergoing
changes. The 20-h and longer exposure induced severe changes affecting all layers
of the retina. These changes include massive retinal oedema with degenerative
signs in all retinal neurons. A sympathetic reaction of the unexposed, contralateral
eye occurred as the result of the damage to the exposed eye. Minimal sympathetic
responses to the cornea and the lens began at exposure durations at or above 12
h, while the retina showed the sympathetic reaction beginning at 8 h.(ABSTRACT
TRUNCATED AT 400 WORDS)
Schlagwörter Animals; Cornearadiation effectsultrastructure; Eyeradiation effectsultrastructure;
Fluorescence; Lens, Crystallineradiation effectsultrastructure; Lightadverse effects;
Rabbits; Radiation Dosage; Time Factors; Ultraviolet Raysadverse effects

Reese, C. T.; Ntam, C.; Martin, T. V.; Carrington, S.; Leotaub, J.; Cox, L. et al. (2007): Internalization of near-
infrared fluorescent dyes within isolated macrophage populations. In: Cellular and molecular biology (Noisy-le-
Grand, France), Jg. 53, H. 3, S. 27–33.
Abstract The development and application of microsensor technology has enhanced the
ability of scientists to further understand various biological activities, such as
changes in the intracellular environment after injury or toxic exposure. NIR
microsensor technology may be useful in detecting the cellular injuries or adverse
changes during the early onset period, allowing for the administration of therapies to
initiate recovery. The development and use of Infrared (IR) and near infrared (NIR)
dyes as biological micro-sensors due to their advanced spectral characteristics may
be helpful. Three of the more useful NIR dye characteristics include the ability to
minimize background interference by extraneous biological matrices, the ability to
exhibit optimal molar absorptivity and quantum yields, and the ability to maintain
normal cellular activity. Thus, the current study was designed to investigate the
ability of selected NIR micro-sensor dyes to undergo cellular internalization,
demonstrate intracellular NIR fluorescent signaling, and maintain normal cellular
activity. The results demonstrate that the selected NIR micro-sensor dyes undergo
cellular internalization. The presence of the dyes within the cells did not affect cell
viability. In addition, these dyes demonstrate changes in absorbance and
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fluorescence after the immune cells were challenged with a stimulant. Moreover,
critical cellular functions, such as tumor necrosis factor release and superoxide
production were not compromised by the internalization of the fluorescent dyes.
These data suggest that selected NIR micro-sensor dyes can undergo intracellular
internalization within isolated macrophages without adversely affecting various
parameters of normal cellular activity.
Schlagwörter Analysis of Variance; Biological Transport; Biosensing Techniques; Chemotaxis;
Fluorescent Dyes; Fluorometry; Infrared Rays; Macrophages; Spectrometry,
Fluorescence; Superoxides; Tumor Necrosis Factor-alpha

Reinhardt, Harris (1942): The fluorescent lighting handbook. A practical guide to the performance,
characteristics and applications of fluorescent lighting. Hygrade Sylvania corporation. (Hg.). Salem Mass.:
Hygrade Sylvania Corporation.
Schlagwörter Fluorescent lighting.

Reszka, K.; Eldred, G. E.; Wang, R. H.; Chignell, C.; Dillon, J. (1996): The photochemistry of human retinal
lipofuscin as studied by EPR. In: Photochemistry and photobiology, Jg. 62, H. 6, S. 1005–1008.
Abstract Fluorescent material generated in the human retina accumulates within lipofuscin
(HLF) granules of the retinal pigment epithelium (RPE) during aging. We have been
investigating the possible light-induced contribution of these fluorophores to various
diseases including age-related macular degeneration. Our studies have shown that
some of the fluorescent components of HLF are products of the reaction of
retinaldehyde with ethanolamine and that synthetic mixtures of this reaction can
serve as a useful model for photophysical studies. Previous research by us has
demonstrated that irradiation of either natural or synthetic lipofuscin resulted in the
formation of a triplet state and possibly a free radical. Here EPR studies were
performed to verify the formation of that radical. The UV irradiation of either
synthetic or natural human retinal lipofuscin extracts in oxygen-free methanol led to
the formation of a 5,5-dimethylpyrroline-N-oxide (DMPO) spin-trapped carbon-
centered radical resulting from either hydrogen atom or electron abstraction from
solvent molecules. In the presence of oxygen superoxide was formed, which was
observed as a DMPO adduct. It is concluded that certain components of the
chloroform-soluble fluorophores of human RPE lipofuscin granules and the
fluorescent reaction products of retinaldehyde and ethanolamine are
photophysically similar but not the same. Electron or hydrogen abstraction from a
substrate by these fluorophores in vivo and the resulting radical products may
contribute to the age-related decline of RPE function and blue light damage in the
retina.
Schlagwörter Adult; Electron Spin Resonance Spectroscopy; Humans;
Lipofuscinchemistryisolation & purification; Photochemistry; Pigment Epithelium of
Eyechemistrymetabolism

Saltarelli, C. G.; Coppola, C. P. (1979): Influence of visible light on organ weights of mice. In: Laboratory animal
science, Jg. 29, H. 3, S. 319–322.
Abstract Hau:ICR mice separated by sex, were reared for 30 days under various fluorescent
lamps: pink, blue, black UV, cool white and full spectrum. Body weights and
absolute organ weights were compared. After light exposure, female body weights
were not significantly different between any groups; however, a difference in male
body weights was observed. Light affected the weights of the pituitary, adrenals,
kidneys and prostate in male mice and the adrenals, thyroid and pineal glands in
females. The weight of adrenal glands of both males and females were most
sensitive to changes in lighting.
Schlagwörter Adrenal Glandsradiation effects; Animals; Body Weightradiation effects; Female;
Light; Male; Micegrowth & development; Organ Sizeradiation effects; Pineal
Glandradiation effects; Pituitary Glandradiation effects; Sex Factors
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Sanford, K. K.; Parshad, R.; Jones, G.; Handleman, S.; Garrison, C.; Price, F. (1980): Role of photosensitization
and oxygen in chromosome stability and "spontaneous" malignant transformation in culture. In: Journal of the
National Cancer Institute, Jg. 63, H. 5, S. 1245–1255.
Abstract Visible light and oxygen enhanced both chromosome instability and malignant
transformation of mouse cells in culture. Nine cell lines were initiated from 8 pools
of 10- to 13-day C3H embryos. Each cell line was divided into sublines, which were
either maintained shielded from light or were exposed for 3 or 24 hours to
fluorescent light (approximately 150 foot-candles) two or three times weekly.
Cultures of the sublines were also maintained with either a gaseous phase of 0-1%
oxygen or atmospheric (18%) oxygen. Each line was monitored for cytologic
manifestations of malignant neoplastic transformation, and 8 lines were monitored
for chromosome alterations. Seven lines were assayed for tumorigenicity by
intraocular implantation into syngeneic hosts. Repeated light exposure and/or high
oxygen increased the frequency of minute chromosomes, which result from
chromatid breaks, and also increased the rate of shift from diploid to heteroploid
state. Four cell lines showed no cytologic changes indicative of neoplastic change
during the test period. Two of these were assayed in vivo and failed to grow as
tumors. In the remaining 6 lines, cytologically neoplastic colonies appeared earlier
or more abundantly in the light-exposed cultures and/or those gassed with high
oxygen. In 3 of these lines, tumors developed only from the light-exposed cultures;
in the other 2, tumor latency periods were significantly shorter in the cultures
exposed to light or gassed with atmospheric oxygen.
Schlagwörter Animals; Cell Divisionradiation effects; Cell Line; Cell Survivalradiation effects; Cell
Transformation, Neoplastic; Chromosome Aberrations; Embryo, Mammalian;
Lightadverse effects; Mice; Mice, Inbred C3H; Neoplasm Transplantation;
Neoplasms, Experimentaletiology; Oxygen; Transplantation, Homologous

Schmidt, Tiffany M.; Taniguchi, Kenichiro; Kofuji, Paulo (2008): Intrinsic and extrinsic light responses in
melanopsin-expressing ganglion cells during mouse development. In: Journal of neurophysiology, Jg. 100, H. 1,
S. 371–384. Online verfügbar unter doi:10.1152/jn.00062.2008.
Abstract Melanopsin (Opn4) is a photopigment found in a subset of retinal ganglion cells
(RGCs) that project to various brain areas. These neurons are intrinsically
photosensitive (ipRGCs) and are implicated in nonimage-forming responses to
environmental light such as the pupillary light reflex and circadian entrainment.
Recent evidence indicates that ipRGCs respond to light at birth, but questions
remain as to whether and when they undergo significant functional changes. We
used bacterial artificial chromosome transgenesis to engineer a mouse line in which
enhanced green fluorescent protein (EGFP) is expressed under the control of the
melanopsin promoter. Double immunolabeling for EGFP and melanopsin
demonstrates their colocalization in ganglion cells of mutant mouse retinas.
Electrophysiological recordings of ipRGCs in neonatal mice (postnatal day 0 [P0] to
P7) demonstrated that these cells responded to light with small and sluggish
depolarization. However, starting at P11 we observed ipRGCs that responded to
light with a larger and faster onset (<1 s) and offset (<1 s) depolarization. These
faster, larger depolarizations were observed in most ipRGCs by early adult ages.
However, on application of a cocktail of synaptic blockers, we found that all cells
responded to light with slow onset (>2.5 s) and offset (>10 s) depolarization,
revealing the intrinsic, melanopsin-mediated light responses. The extrinsic,
cone/rod influence on ipRGCs correlates with their extensive dendritic stratification
in the inner plexiform layer. Collectively, these results demonstrate that ipRGCs
make use of melanopsin for phototransduction before eye opening and that these
cells further integrate signals derived from the outer retina as the retina matures.
Schlagwörter Action Potentialsphysiologyradiation effects; Age Factors; Animals; Animals,
Newborn; Chromosomes, Artificial, Bacterialphysiology; Dose-Response
Relationship, Radiation; Gene Expression Regulation,
Developmentalphysiologyradiation effects; Green Fluorescent
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Proteinsgeneticsmetabolism; Light; Mice; Mice, Transgenic; Patch-Clamp
Techniquesmethods; Photic Stimulationmethods; Reaction Time;
Retinacytologygrowth & development; Retinal Ganglion Cellsmetabolismradiation
effects; Rod Opsinsgeneticsmetabolism

Sheng, Hui; Lu, Yi; Qing, Feng-ling (2008): [Blue light-induced damage to human retinal pigmented epithelial
cells mediated by A2E]. In: [Zhonghua yan ke za zhi] Chinese journal of ophthalmology, Jg. 43, H. 11, S.
1017–1021.
Abstract OBJECTIVE: To observe the internalization of A2E by human retinal pigmented
epithelial (hRPE) cells and study whether the lipofuscin fluorophore A2E (N-
retinylidene-N-retinylethanolamine) participates in blue light-induced damage to
hRPE cells. METHODS: A mixture of all-trans-retinal and ethanolamine was used to
produce A2E in one step. A2E granules were delivered to medium of cultured hRPE
cells for internalization. Confluent cultures were subsequently exposed to 450 nm
(blue) light for 20 minutes with or without A2E (25, 50, 100 micromol/L). The light
intensity was 70 mW/mm(2). Phototoxicity was quantified at 12, 24, 36, and 48 h
after exposure by CCK-8 of viable cells. Apoptosis of cells was detected by Hoechst
33342 DNA staining and flow cytometry. RESULTS: The reaction of all-trans-retinal
(100 mg) and ethanolamine (9.5 mg) produced 53.8 mg A2E in one step. When
A2E was delivered to hRPE cells in culture, it accumulated intracellularly.
Internalized A2E presented as autofluorescent granules having a perinuclear
distribution. As shown by CCK-8 analysis, the A2E-fed hRPE cell viability reduced
with duration after 450 nm light exposure. Conversely, blue light-exposed hRPE
cells that did not contain A2E showed less loss of cell viability. The percentage of
hRPE cell apoptosis with 25 micromol/L A2E 12, 24, 36 and 48 h after blue light
exposure was (12.11 +/- 2.32)%, (31.21 +/- 3.72)%, (64.23 +/- 3.53)% and (58.71
+/- 3.48)% respectively. Conversely, the apoptosis was less than 5% in other hRPE
cells. CONCLUSIONS: A2E is essential to blue light-induced hRPE cell damage.
Only blue light exposure and without A2E lead to little cell injury. hRPE cells in old
people which contain much lipofuscin are sensitive to blue light injury.

Siopes, T. D. (1984): The effect of full-spectrum fluorescent lighting on reproductive traits of caged turkey hens.
In: Poultry science, Jg. 63, H. 6, S. 1122–1128.
Abstract Large White turkey breeder hens were exposed to either incandescent or full-
spectrum (FS) fluorescent lighting during two 20-week reproductive cycles in closed
confinement. Data were recorded for body weights, feed intake, and reproductive
traits. Body weights and feed intake were similar between treatments in both egg
laying cycles. In addition, there were no significant differences in egg production,
fertility, hatchability, or poult weight between the incandescent and FS fluorescent
light treatment in either the first or second year egg laying cycle. It was concluded
that exposure of breeder turkey hens to FS fluorescent light in closed confinement
results in reproductive performance similar to that obtained with incandescent
lighting.
Schlagwörter Animals; Body Weight; Eating; Female; Fluorescence; Housing, Animal; Light;
Oviposition; Reproduction; Turkeysphysiology

Society for Visual Education. (Hg.) (1970): "Cool" light from electricity (Filmstrip). n.p.: Society for Visual
Education.
Schlagwörter Electric currents.; Neon lamps.; Fluorescent lighting.

Spreadbury, F. G. (1946): Electric discharge lighting. London: Sir I. Pitman & sons ltd.
Schlagwörter Electric lighting, Mercury vapor.; Electric lighting, Sodium vapor.; Fluorescent
lighting.

Stark, W. S.; Carlson, S. D. (1985): Blue and ultraviolet light induced damage to the Drosophila retina:
ultrastructure. In: Current eye research, Jg. 3, H. 12, S. 1441–1454.
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Abstract Intense ultraviolet (UV) and blue stimulation photolyses rhodopsin through a
fluorescent metarhodopsin (M') in the predominant photoreceptor type, R1-6, of the
compound eye of white eyed Drosophila melanogaster. We investigated the
associated retinal degeneration using High Voltage Electron Microscopy (HVEM).
The threshold for UV induced damage was about 19 log quanta/cm2 while for blue,
the threshold was about 20. These intensities are toward the upper level of the
dynamic range for rhodopsin photolysis. Thus, there is a sensitization for near UV
induced degeneration as had been found for photolysis of the visual pigment.
Vitamin A deprivation protects against light elicited retinal degeneration, particularly
in the UV. Since vitamin A deprivation eliminates the blue absorbing rhodopsin and
a UV sensitizing pigment in R1-6, the degeneration is likely mediated through
quantal absorption through these photoexcitation pigments. Intense light converts
the microvilli of the rhabdomeres (the photopigment containing organelles) into
dense strands and the cytoplasm fills with a dense reticulum. Such damage is
elicited shortly after stimulation and is permanent. Under most conditions, the
second order interneurons are spared. These results are discussed in the context of
other animal models of intense light retinal degeneration.
Schlagwörter Animals; Dose-Response Relationship, Radiation; Drosophila melanogaster;
Interneuronsradiation effects; Microscopy, Electron; Neurogliaradiation effects;
Neuronsradiation effects; Photoreceptor Cellsradiation effects; Radiation Injuries,
Experimentaletiologypathology; Retinapathologyradiation effects; Retinal
Degenerationetiologypathology; Synapsesradiation effects; Ultraviolet Raysadverse
effects

Stark, W. S.; Walker, K. D.; Eidel, J. M. (1985): Ultraviolet and blue light induced damage to the Drosophila
retina: microspectrophotometry and electrophysiology. In: Current eye research, Jg. 4, H. 10, S. 1059–1075.
Abstract Intense ultraviolet (UV) and blue stimulation decreases visual pigment
concentration and increases long wavelength fluorescent emission in R1-6
photoreceptors in the white eyed fruit fly Drosophila melanogaster. We used
microspectrophotometry to show that the threshold for visual pigment decrease is
about 1 log unit lower for UV than for blue light (18.7 vs approximately 19.9 log
quanta/cm2 respectively). UV and blue stimuli about 0.2 log units brighter had been
shown to cause structural degeneration. Above the threshold for structural damage,
visual pigment is decreased permanently while below this level, a recovery of visual
pigment was achieved within several hours. Microspectrofluorometric data are
partially consistent with the hypothesis that the visual pigment is converted into a
fluorescent product which had been named M'. M' had been proposed to be a new
form of metarhodopsin which absorbs chiefly in the yellow and which has a
fluorescent emission in the red; long wavelength stimulation had been reported to
regenerate the native visual pigment from M'. Our data suggest that the situation is
significantly more complex than this simple model. For instance, we report that long
wavelength stimulation regenerates only a small fraction of the visual pigment which
had been decreased by UV or blue stimulation. Furthermore, several lines of
evidence suggest that other fluorescent products are also created by intense UV
and blue stimulation. We were particularly interested in the lower damage threshold
for UV light because of the hypothesis that UV visual sensitivity is mediated by a
sensitizing pigment which absorbs UV light and transfers its energy to the blue
absorbing rhodopsin. Our data suggest that the UV light decreases the rhodopsin
without preferentially decreasing the sensitizing pigment.
Schlagwörter Animals; Drosophila melanogasterradiation effects; Electrophysiology;
Electroretinography; Fluorometry; Lightadverse effects; Retinaradiation effects;
Retinal Pigmentsbiosynthesismetabolismradiation effects;
Spectrophotometrymethods; Time Factors; Ultraviolet Raysadverse effects

Stenkamp, Deborah L.; Satterfield, Rosanna; Muhunthan, Kalyani; Sherpa, Tshering; Vihtelic, Thomas S.;
Cameron, David A. (2008): Age-related cone abnormalities in zebrafish with genetic lesions in sonic hedgehog.
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In: Investigative ophthalmology & visual science, Jg. 49, H. 10, S. 4631–4640. Online verfügbar unter
doi:10.1167/iovs.07-1224.
Abstract PURPOSE: Sonic hedgehog (Shh) signaling is essential for photoreceptor
differentiation and retinal cell survival in embryonic zebrafish. The study was
conducted to determine whether adult heterozygous carriers of mutant alleles for
the shh gene display retinal abnormalities. METHODS: Retinal cryosections from
young, middle-aged, and senescent wild-type and sonic-you(+/-) (syu(+/-)) zebrafish
were probed with retinal cell type-specific markers. Contralateral retinal flatmounts
from these fish, and from adult albino zebrafish subjected to light-induced
photoreceptor damage followed by regeneration, were hybridized with blue cone
opsin cRNA for quantitative analysis of the blue cone pattern. Retinal expression of
shh mRNA was measured by quantitative RT-PCR. RESULTS: Regions of cone
loss and abnormal cone morphology were observed in the oldest syu(+/-) zebrafish,
although no other retinal cell type was affected. This phenotype was age-related
and genotype-specific. Cone distribution in the oldest syu(+/-) zebrafish was
predominantly random, as assessed by measuring the short-range pattern, whereas
that of wild-type fish and the younger syu(+/-) zebrafish was statistically regular. A
measure of long-range pattern revealed atypical cone aggregation in the oldest
syu(+/-) zebrafish. The light-treated albino zebrafish displayed random cone
patterns immediately after light toxicity, but showed cone aggregation on
regeneration. Retinas from the syu(+/-) fish showed reduced expression of shh
mRNA compared with those of wild-type siblings. CONCLUSIONS: The syu(+/-)
zebrafish presents a model for the study of hereditary age-related cone
abnormalities. The syu(+/-) retinas most likely experience progressive cone
photoreceptor loss, accompanied by cone regeneration. Shh signaling may be
required to maintain cone viability throughout life.
Schlagwörter Agingphysiology; Alleles; Animals; Cell Death; Cell Proliferation; Fluorescent
Antibody Technique, Indirect; Gene Expressionphysiology; Hedgehog
Proteinsgenetics; In Situ Hybridization; In Situ Nick-End Labeling; Light;
Microscopy, Fluorescence; Mutation; RNA, Messengermetabolism; Radiation
Injuries, Experimentaletiologygeneticspathology; Retinaradiation effects; Retinal
Cone Photoreceptor Cellsmetabolismpathology; Retinal
Degenerationetiologygeneticspathology; Reverse Transcriptase Polymerase Chain
Reaction; Rod Opsinsmetabolism; Zebrafishgenetics; Zebrafish Proteinsgenetics

Stoutemyer, Vernon Theodore; Close, Albert William (1945): Plant propagation under fluorescent light. United
States. (Hg.). Beltsville Md.
Schlagwörter Plant propagation.; Fluorescent lighting.

Strum, Carl Heinz (1952): Vorschaltgeräte und Schaltungen für Leuchtstofflampen. Brown, Boveri &. Cie A. -G
(Hg.). Mannheim: Brown Boveri & Cie.
Schlagwörter Fluorescent lighting.

Taniguchi, Yukinori; Ikehara, Tatsuya; Kamo, Naoki; Watanabe, Yasutaka; Yamasaki, Hiroshi; Toyoshima,
Yoshinori (2007): Application of fluorescence resonance energy transfer (FRET) to investigation of light-induced
conformational changes of the phoborhodopsin/transducer complex. In: Photochemistry and photobiology, Jg.
83, H. 2, S. 311–316. Online verfügbar unter doi:10.1562/2006-06-15-RA-922.
Abstract The photoreceptor phoborhodopsin (ppR; also called sensory rhodopsin II) forms a
complex with its cognate the Halobacterial transducer II (pHtrII) in the membrane,
through which changes in the environmental light conditions are transmitted to the
cytoplasm in Natronomonas pharaonis to evoke negative phototaxis. We have
applied a fluorescence resonance energy transfer (FRET)-based method for
investigation of the light-induced conformational changes of the ppR/pHtrII complex.
Several far-red dyes were examined as possible fluorescence donors or acceptors
because of the absence of the spectral overlap of these dyes with all the
photointermediates of ppR. The flash-induced changes of distances between the
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donor and an acceptor linked to cysteine residues which were genetically
introduced at given positions in pHtrII(1-159) and ppR were determined from FRET
efficiency changes. The dye-labeled complex was studied as solubilized in 0.1% n-
dodecyl-beta-D-maltoside (DDM). The FRET-derived changes in distances from
V78 and A79 in pHtrII to V185 in ppR were consistent with the crystal structure data
(Moukhametzianov, R. et al. [2006] Nature, 440, 115-119). The distance from D102
in pHtrII linker region to V185 in ppR increased by 0.33 angstroms upon the flash
excitation. These changes arose within 70 ms (the dead time of instrument) and
decayed with a rate of 1.1 +/- 0.2 s. Thus, sub-angstrom-scale distance changes in
the ppR/pHtrII complex were detected with this FRET-based method using far-red
fluorescent dyes; this method should be a valuable tool to investigate conformation
changes in the transducer, in particular its dynamics.
Schlagwörter Archaeal Proteins; Fluorescence Resonance Energy Transfer; Halobacteriaceae;
Halorhodopsins; Multiprotein Complexes; Photochemistry; Protein Conformation;
Recombinant Proteins; Sensory Rhodopsins

Tanito, Masaki; Kaidzu, Sachiko; Anderson, Robert E. (2006): Protective effects of soft acrylic yellow filter
against blue light-induced retinal damage in rats. In: Experimental eye research, Jg. 83, H. 6, S. 1493–1504.
Online verfügbar unter doi:10.1016/j.exer.2006.08.006.
Abstract Recently, a yellow intraocular lens (IOL) was developed for the purpose of reducing
potential blue light-induced retinal damage after cataract surgery. However, the
effect of yellow filters on retinal protection remains to be clarified. To test the
protective effects of yellow filters on blue light-induced retinal damage, a yellow and
a clear soft acrylic filter were attached to the right and left eyes, respectively, of
albino rats and exposed to 4.5 k lux blue fluorescent lights with peak wavelength at
420 nm (ranging 380-500 nm; short blue) or 446 nm (ranging 400-540 nm; long
blue) for 6h. To assess retinal damage, the electroretinogram (ERG) was recorded
at 7 days, outer nuclear layer (ONL) thickness and area were measured at 7 days,
apoptosis was analyzed by TUNEL staining at 24 h, and the level of lipid
peroxidation in retinas was assessed by Western dot blots using specific antibodies
against 4-hydroxynonenal (4-HNE)- and carboxyethylpyrrole (CEP)-modified
proteins immediately after light exposure. After short blue light exposure, a- and b-
wave ERG amplitudes and the ONL thickness at 1-2.5 mm inferior and 0.5-2.5 mm
superior to optic nerve head (ONH) were significantly reduced. TUNEL staining in
the ONL at 0-2 mm inferior and 1-2 mm superior to the ONH, and retinal levels of 4-
HNE- and CEP-modified proteins were significantly increased in the clear filter-
covered eyes compared to yellow filter-covered eyes. After long blue light exposure,
the only difference seen was a greater ONL thickness at 1.5 mm superior to the
ONH in yellow filter-covered eye. Transmission of light through the yellow filter was
58% for short blue and 89% for long blue compared to the clear filter. The ONL area
was not different between clear filter-covered and -uncovered eyes after exposure
to short or long blue light. Given the results, yellow IOL material protects the retina
against acute shorter wavelength blue light exposure more effectively than the clear
IOL material.
Schlagwörter Animals; Apoptosisradiation effects; Color; Electroretinography; Eye
Proteinsmetabolism; Filtrationinstrumentation; Lens, Crystallinephysiologyradiation
effects; Lightadverse effects; Lipid Peroxidation; Photoreceptor Cells,
Vertebrateradiation effects; Radiation Injuries, Experimentalprevention & control;
Rats; Rats, Sprague-Dawley; Retinametabolismphysiopathologyradiation effects;
Retinal Degenerationpathologyprevention & control; Scattering, Radiation;
Ultraviolet Rays

Veitch, J. A.; McColl, S. L. (2001): A critical examination of perceptual and cognitive effects attributed to full-
spectrum fluorescent lighting. In: Ergonomics, Jg. 44, H. 3, S. 255–279.
Abstract Full-spectrum fluorescent lighting (FSFL) has been credited with causing dramatic
improvements in vision, perception and cognitive performance as compared with
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other fluorescent lamp types. These effects are hypothesized to occur because of
similarity between FSFL emissions and daylight, which is said to have evolutionary
superiority over other light sources. This review, covering 1945-98, critically
considers the evidence for these claims. In general, poor-quality research has
resulted in an absence of simple deterministic effects that can be confidently
attributed to fluorescent lamp type. Promising avenues for lighting behaviour
research include investigations of cognitive mediators of lighting-behaviour
relationships, and flicker rates and colour rendering effects on visual processing,
appearance judgements and affect. Good lighting solutions are more complex than
lamp type specification.
Schlagwörter Cognition; Humans; Job Satisfaction; Lighting; Task Performance and Analysis;
Visual Perception; Workplace

Wyse, J. P. (1980): Renewal of rod outer segments following light-induced damage of the retina. In: Canadian
journal of ophthalmology. Journal canadien d'ophtalmologie, Jg. 15, H. 1, S. 15–19.
Abstract Fluorescent lighting was used to induce severe but reversible damage of the rod
outer segments of the retinas of albino rats. The animals were then kept in
continuous darkness for up to 12 days. Pairs of animals were killed after 1, 3, 5, 7, 9
and 12 days of continuous darkness. Light microscopic examination of the retinas
demonstrated a sharp demarcation between the light-damaged distal ends of the
rod outer segments and the newly formed proximal ends. Measurement of the
proximal ends demonstrated proximo-distal renewal of the rod outer segments
during the first 9 days of continuous darkness. Parametric statistical analysis of the
data revealed that the renewal occurred linearly, at an average rate of 2.66
micron/d, which is similar to the rate of renewal of the rod outer segments in the
undamaged retina of the rat.
Schlagwörter Animals; Dark Adaptation; Lightadverse effects; Photoreceptor
Cellsphysiologyradiation effects; Rats; Regeneration

Xu, Xiaoyang; Zhao, Xiufeng; Liu, Timon Cheng-Yi; Pan, Hongying (2008): Low-Intensity Laser Irradiation
Improves the Mitochondrial Dysfunction of C2C12 Induced by Electrical Stimulation. In: Photomedicine and laser
surgery. Online verfügbar unter doi:10.1089/pho.2007.2125.
Abstract Abstract Objective: We investigated the effects of electrical stimulation and low-
intensity laser (LIL) energy on the mitochondrial function of cultured C2C12
myotubes in order to find a dosage that could be used to improve the function of
mitochondria, and then rehabilitate exercise-induced damage and fatigue.
Background Data: Many other studies in the past demonstrated that LIL had a
cytoprotective effect, and a recent study also found that LIL could reduce muscular
fatigue during tetanic contractions in rats. Methods: Cultured C2C12 myotubes were
subjected to electrical stimulation or/and LIL irradiation at various intensities.
Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA)
and mitochondrial function was assessed with an MTT assay. Results: The results
showed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can induce
mitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulation-
induced mitochondrial dysfunction was improved, but degeneration occurred with
LIL at doses of 0.33-8.22 and 11.22-14.16 J/cm(2), respectively, and these changes
were markedly increased with LIL at 0.33 and 1.34 J/cm(2), respectively.
Conclusions: We conclude that treatment of myotubes with the proper dosage of
LIL irradiation significantly diminished production of ROS and restored
mitochondrial function, and this may provide a foundation for the use of
photobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletal
muscular fatigue.

Yu, Xiaoping; Chen, Ka; Wei, Na; Zhang, Qianyong; Liu, Jihuan; Mi, Mantian (2007): Dietary taurine reduces
retinal damage produced by photochemical stress via antioxidant and anti-apoptotic mechanisms in Sprague-
Dawley rats. In: The British journal of nutrition, Jg. 98, H. 4, S. 711–719. Online verfügbar unter
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doi:10.1017/S0007114507744409.
Abstract Taurine has been shown to be tissue protective in many models of oxidant-induced
injury. However, its protective role against retinal damage induced by
photochemical stress is less well known. The purpose of the present study was to
investigate whether dietary taurine reduced retinal photochemical damage in
Sprague-Dawley rats and to further explore the underlying molecular mechanisms
of this action. Twenty rats fed AIN-93 formulation and maintained in the dark for 48
h were used as controls (n 20). Another forty rats were randomly divided into two
groups and then treated with (n 20) or without 4 % taurine (n 20) for 15 d
respectively. After treatment, these two groups were exposed to fluorescent light
(3000 +/- 200 lux and 25 degrees C), and the protective effects of dietary taurine
were then evaluated. The present results showed that dietary taurine effectively
prevented retinal photochemical damage as assessed by changes of morphology.
Also, the supplementation caused an increase of taurine in the retina, a decrease of
malondialdehyde (P < 0.01), and elevation of superoxide dismutase (P < 0.01) and
glutathione peroxidase activities in the retina (P < 0.01). Moreover, dietary taurine
inhibited activator protein-1 (AP-1) (c-fos/c-jun subunits) expression (P < 0.05), up
regulated NF-kappaB (p65) expression (P < 0.05), and decreased caspase-1
expression (P < 0.05) so as to reduce the apoptosis of photoreceptors in the retina
(P < 0.05). These results suggest that dietary taurine reduced retinal damage
produced by photochemical stress via antioxidant and anti-AP-1-NF-kappaB-
caspase-1 apoptotic mechanisms in rats.
Schlagwörter Animals; Antioxidantsphysiology; Apoptosisdrug effects; Diet; Oxidants,
Photochemicalpharmacology; Random Allocation; Rats; Rats, Sprague-Dawley;
Retinal Diseaseschemically inducedprevention & control; Taurineadministration &
dosagepharmacology; Treatment Outcome

Zand, M. S.; Albrecht-Buehler, G. (1989): Long-term observation of cultured cells by interference-reflection

microscopy: near-infrared illumination and Y-contrast image processing. In: Cell motility and the cytoskeleton,
Jg. 13, H. 2, S. 94–103. Online verfügbar unter doi:10.1002/cm.970130204.
Abstract Interference-reflection microscopy (IRM) is the only method presently available with
which to visualize cell-substratum adhesions in living tissue culture cells
continuously for long periods of time without the use of fluorescent markers (Curtis:
J. Cell Biol. 20:199-215, 1964; Izzard and Lochner: J. Cell Sci. 21:129-159, 1976).
This method utilizes approximately 1% of the incident illumination to produce the
IRM image (Verschueren: J. Cell Sci. 75:279-301, 1985) and so far has required the
use of high-intensity light sources in the visible spectral range (400-800 nm).
Unfortunately, visible light of this intensity and spectral range induces marked
changes in the behavior and morphology of motile fibroblasts, including cessation of
locomotion. In contrast, the present paper reports that continuous observations of
live cells in IRM for periods of up to 8 hours are possible if the illuminating light is in
the red to near-infrared range (650-950 nm) and without any observable change in
normal cell morphology or behavior. In addition, we describe how the technique of
Y-contrast image processing can be applied to IRM images to create a three-
dimensional image of the ventral cell surface topography.
Schlagwörter Animals; Cell Line; Cell Movement; Cells, Cultured; Fibroblasts; Infrared Rays;
Mice; Microscopy, Interference

Zwikker, C. (1952): Fluorescent lighting. A review of the scientific and technical fundamentals and of the
applications of the fluorescent lamp and its accessories. London: distributors for United Kingdom; Cleaver Hume
Press; distributors for U.S.A.: Elsevier Press Houston (Philips technical library).
Schlagwörter Fluorescent lighting.