CONCENTRATIONS OF ASCORBIC ACID IN PLASMA AND

WHITE BLOOD CELLS OF PATIENTS WITH CANCER

AND NONCANCEROUS CHRONIC DISEASE
OSCAR

BODANSKY,
M.D., FELIXWROBLEWSKI,

M.D., AND

BLANCH
hdARKARDT, M.A.

tients with cancer than in normal persons. For

example, Spellberg and Keeton found that
after continued daiIy administration of 400
mg. of ascorbic acid, normal persons excreted
56 to 80 per cent of the intake, whereas patients
with cancer excreted only 34 to 48 per cent.
Bodansky studied two patients with cancer, one
of whom was on a daily intake of 91 mg. and
the other on a n intake of 257 mg. of ascorbic
acid as part of a controlled metabolic regimen.
T h e daily urinary excretion ranged from about
5 to 10 per cent of the intake. Data in the
literature indicate that normal persons excrete
about 30 to 50 per cent of a daily intake
of about 100 mg. ascorbic acid and higher
percentages at greater intakes.G,11, l 2 T h e decreased excretion of ascorbic acid intake in
patients with cancer has been considered to
reflect a higher utilization of ascorbic acid by
cancerous tissue. Minor and Ramirez reported
that, after saturation with high ascorbic acid
intakes, the difference between the intake and
the excretion averaged 125 mg. per day in five
patients with cancer, as contrasted with an
average difference of 67 mg. per day in seven
patients with chronic noncancerous disease.
In view of the paucity and conflicting nature
of the evidence that we have described, it was
thought that additional information concerning the relationship between ascorbic acid metabolism and the presence of cancer in inan
could be obtained by studying the concentrations of ascorbic acid in the plasma and white
blood cells. T h e concentration of ascorbic acid
in the plasma has been investigated in several
diseases,R, z2-z4>3o but relatively few determinations in patients with cancer are available.
T h e determination of ascorbic acid in the
white blood-cell-platelet layer is of particular importance, since it has been shown by
Lowry and his associates that the concentraFrom the Memorial Center for Cancer and Allied tion of this component in the white blood
Diseases, and the Research Biochemistry Seciion, Sloan- cells seems to be a valid index of the total
Kettering Institute for Cancer Research, New York,
ascorbic acid content of the body. Since there
New York.
This work has been supported in part by a grant from appear to be practically no substantial rethe New York City Cancer Committee, donated by the
ports in the literature on the ascorbic aciti
Raymond Loewy Associates.
content of the white cells in other chronic disReceived for publication, Februaiy 4, 1952.
678

of reports in the literature that suggest a relationship between the

presence of cancer and the metabolism of ascorbic acid. T h e indication for this relationship
rests upon two types of data: (1) the relative
concentrations of ascorbic acid in normal and
neoplastic tissue; (2) the utilization of ascorbic
acid by the cancerous organism, as determined
by the urinary excretion of ascorbic acid at
varying levels of intake.
T h e question whether the concentration of
ascorbic acid is altered in cancerous tissue has
been the subject of considerable controversy.
Early studies by Boyland2p showed that extracts of rat and mouse sarcomas had a high
reducing potency, though it was not clear
whether this was due to ascorbic acid, glutathione, or some other reducing material. Woodward found that actively growing rat sarcoma and carcinoma contained glutathione in
amounts comparable to that present in other
body tissues of the rat but that the concentration of ascorbic acid, as determined by the reduction of 2,6-dichlorophenol-indophenoI,
was
higher than in any other tissue studied except
the adrenal. Woodward also observed that the
concentration was decreased in necrotic tumors. I n a series of papers,5, 1% x Kennaway
and his associates reported that a number of
carcinogenic compounds were capable of increasing the ascorbic acid content of the liver
in rats and mice, but Meduski failed to observe
any such effect in rats with 1,2,5,6-dibenzanthracene. I n human cancerous tissue, Gbth and
Littman reported that the ascorbic acid content was higher than that of the comparable
surrounding material, whereas the reverse situation was found to hold by Piacentini.
Several studies in the literature show that the
urinary excretion of ascorbic acid is less in paHERE ARE A NUMBER

77

16v

No. 4

PLASMA
& WHITECELL
ASCORBIC
ACIDIN CANCER. Bodansky et al.

6'79

plements for several weeks prior to determination of the ascorbic acid concentrations. It was
difficult to ascertain whether the cancer patients had been taking vitamin supplements
before admission. Blood for the ascorbic acid
CLINICAL
MATERIAL
determinations was taken as soon as possible
Three groups of subjects were studied. T h e after the admission of the patient, usually withfirst group consisted of twenty-three presuma- in a day or two and prior to any administration
bly healthy persons, twenty-two of whom were of vitamins. I n a very few instances, when the
less than 40 years of age, and the other was a 65- patient had been in the hospital for several
year-old woman. T h e second group consisted days, it was found that one or t w o doses of
of forty-three noncancerous, but chronically ill, vitamins had been given. Since, in these few
individuals ranging in age from 41 to 92 years. instances, the blood levels of ascorbic acid
A few of these patients had presented them- were low as well as high, i t was decided to inselves at the Memorial Hospital Clinic for di- clude them with the results of the determinaagnosis, b u t the majority consisted of patients tions on the other cancer patients.
at a chronic disease hospital. (Samples of blood
for these determinations were obtained from
M EIHOI)S
the T h i r d (New York University) Surgical Service, Goldwater Memorial Hospital through the
Ascorbic acid was determined by the dinitrocourtesy of Dr. Benjamin G . P. Shafiroff.) T h e phenylhydrazine method of Roe and Keuprincipal disorders in this group were degen- ther.25 T h e white-cell-platelct layer was oberative vascular and articular diseases; one pa- tained by centrifugation of oxalated blood in
tient had acute cholecystitis and another acute a Butler-Cushman tube' under the conditions
hepatitis. T h e patients at the chronic-disease described by Wagner. T h e concentration of ashospital had received an adequate hospital diet corbic acid in this layer will be referred to
for periods ranging from four months to sev- more simply in the course of this paper as
eral years. Patients who were incapacitated to white-cell ascorbic acid. Occasionally a sample
the extent that they could not feed themselves of the centrifugated plasma or white cells was
were helped by hospital attendants.
lost. Hence the numbers of determinations
T h e cancer group consisted of seventy pa- listed in the various tables and figures are less
tients, ranging in age from 21/, to 74 years. T h e than the numbers of patient$ studied in the
diagnoses were made on a clinical basis but various groups.
were confirmed in almost all instances by histological study of biopsy, smear, or surgical
KESULTS
specimen. (When the tumors were found to be
T h e values for the concentration or plas~ua
benign, the results of the determinations were
transferred to the group of noncancerous dis- ascorbic acid in the twenty three healthy indiease. However, as the result of an oversight, viduals ranged from 0.10 to 1.62 ing. per 100
one patient with an osteochondroma was left in cc., and averaged 0.70 mg. per 100 cc., with ;I
the group of cancer patients. Her inclusion standard deviation of 20.42 mg. per 100 cc.
in the group of cancer patients had n o effect Calculations from the values obtained by Roc
on the main results, particularly since only and his associates who used the same method in
thr plasma determination was done on this a group of fifty healthy young males show essenpatient.) Almost all of the group consisted of tially the same average value, namely, 0.75 mg.
patients who were candidates for surgery; there per 100 cc. with a standard deviation of k0.10
were, however, three cases of lymphomatous mg28
disease and a few patients who had undergone
T h e concentration of ascorbic acid in the
operation for cancer several months or years white layer in determinations on twenty-two of
previously.
the healthy subjects ranged from 22.5 to 51.5
T h e blood samples were fasting specimens. mg. and averaged 36.1 mg. per 100 gm. of cells.
In those cancer patients who were candidates These values are also in agreement with those
for surgery, the blood specimen was taken pre- of Butler and Cushman who employed another
operatively in almost all instances. I t was method in a series of seven healthy individual\
known that none of the patients in the non- and obtained a range of 25 to 38 mg. and a n
cancerous disease group received vitamin sup- average of 32 mg. per 100 gni. of cells.
eases, it also seemed important to obtain data
regarding this aspect so as to supply a control
series for the present study.

I-.~ULE 1

AlEAX \'ALLES FOR CONCEKTKA'TIONS OF

.\SCORRIC A C I D I N I'lASM.4 ASD WHI'I'I<
CELLS OF NOlZAI.11, I'EIISOSS, OF l'-\'lIES'I'S
WITH NONCrlSCRIIOUS L)ISEASE, RKL)
PATIENTS \\'ITH C'2SCER
~

Concentration of ascorbic acid in

White cells

Plasma

Mean

Mean

Sorninls

2.3

n. 79

Sonrariwrous

43

O..W

<0.01

('mrrr

h9

0 4%

<O

'1

22
01

361

30

2.3 8

<0.01

04

27 0

<0.1)1

Significanrr of iliffereiire betwrrn normals and t)iitif*llts.

'1';tblc 1 shows that the iiieiin \ d u e s f o r the

concentrations of ascorbic acid in plasnia were
significaii tly lower i n the noncancerous cliseasc
and in the cancer groups than in the group ol
normal individuals. However, there was no sigiiificant difference between the iiiean values lor
the group 0 1 noncancerous disease and that for
the group 01 patients with cancer. Siniilarly,
the mean v;tlues for the concentration ol ascorbic acid in the white cells were significantly
lower in the cancer arid noncaiicerous disease
group than in the group ol heal thy individuals,
;end there w a s no significant difference between
the means o f patients with cancer and with
tion-neoplastic disease.
Figure 1 shows the distribution of plasina;iscorbic acid concentrations in the three groups
of subjects. A s was noted previously, the
mean value and the standard deviation in the
group of healthy subjects were respectively 0.79
antl -t0.12 mg. per 100 cc. If the concentration
of 0.2 mg. per 100 cc. is chosen as an arbitrary
differentiating point, then, since this value is
lower than the inean value t y allout &lie antl
a half stantlard deviations, about 7 per cent
of the normal values should fall below this
point. Actually, 4 per cent of tlie healthy persons had I'lasrna-ascorl,i(: acid concentrations
less than 0.2 irig. per I00 cc. In contrast, -12 per
cent o f the patients with noncancerous chronic
diseases ant1 35 per cent of the patients with
cancer had values less than this level.
Figure 2 shows tlie distribution of the tvhitec-ell-ascorbic: acid concentrations i n tlie three
groups of subjects. T h e inean value for the
concentration i n the healthy young adults w i s
36.1 mg. per 100 gm., with ;I stantlard tleviatioii
of 8.3 nig. per 100 gni. When a concentration,
21.5 nig. per 100 gin.. or al)otit one and a h;t11
\t:inhrd deviations less t k i n the riorni;il 1ne;in

value was choseii a s a differentiating point, i t

was h i n d that 9 per cent of the healthy persons, 39 pcr cent o f the patients with cancer,
;ind .iO per cent of the patients with noncancerous chronic disease fell below this point.
Further analysis showed that none of the
healthy persons, 20 per cent o f the patients
with cancer, aiid 40 per cent of the patients
with noncancerous chronic disease had whitecell-ascorbic acid concentrations below 19.5
iiig. per 100 gin., a value less than the normal
nicm value by two standard deviations.
T h e major types in the group of cancer patients were as follows: carcinoma of the uterus
;ind vagina, twenty-two cases; cancers of the
gastrointestinal and oral tract, nineteen cases;
carcinoma of the breast, nine cases. T h e average concentrations of plasma ascorbic acid iii
these three groups were 0.51, 0.48, antl 0.43 nig.
per 100 cc. respectively. There were no significant differences between any two o f these
groups. T h e white-celI-ascorl)ic acid concentrations were respectively 27.4, 24.6 antl 28.8
mg. per 100 gni. Again, there were no significant differences between any two of these three
types.
These data showcd no significant differences
in the incidence of low plasma- and whitecell-ascorbic acid concentrations between patients with cancer antl those with chronic, nonneoplastic disease. T h e possibility arises that
the increased incidence of low concentrations
of ascorbic acid is ascribable to the older age
composition of the groups of patients with
chronic disease or with cancer and is not associated with illness. T h e data listed in Table 2

f 6or--

Heallhy Ywng Adults

Older Adults

I 40t

23 cases

Miscellonccus Disease

Cancer Pofients
69 cases

04

oa

I?

16

20

No. 4

PLASMA
& WHITE-CELL
ASCORBIC
Aciu i~ CANCER . B o d a n s k y et nl.

68 1

TABLE
2
discount this possibility. I n sixteen cancer patients, 40 years of age or less, the mean values MEAN VALUES FOR CONCENTRATIONS O F
for plasma- and white-cell-ascorbic acid con- ASCORBIC ACID I N PLASMA AND WHITE
centrations were, respectively, 0.41 nig. per 100 CELLS OF NORMAL PERSONS AND PATIENTS
cc. and 29.6 mg. per 100 gin., significantly lower WITH CANCER UNDER THE AGE OF FORTY
than the mean values for the healthy persons
Concentration of ascorbic acid in
and essentially the same as for the group of
Plasma
White cells
cancer patients as a whole.
Mean
Mean
Of the total number of 136 subjects in this
value,
value,
No.
mg./
No.
mg./
study, 115 had simultaneous values for the plasGroup
cases 100 cc.
P*
cases 100gm.
P*
ma and white-cell concentrations of ascorbic
Normals
22
o 78
21
36.3
acid. These subjects were subdivided into four Cancer
16
0.41
<0.01
13
29.6
0.04
.groups: thirteen with plasma-ascorbic acid val* Significance of difference between normals and patients.
ues of 0 mg. per 100 cc., twenty-four with values
ranging from 0.01 to 0.20 mg. per 100 cc., corbic acid in the white cells is a measure 01 the
thirty-six with values from 0.21 to 0.60 ing. per total body content of this vitamin. They stud100 cc., and forty-two with values from 0.61 to ied three gioups of volunteers who had been
1.80 mg. per 100 cc. T h e plasma-ascorbic acid placed for eight months on carefully regulated
concentrations and the corresponding white- intaker ok 8, 23, and 78 mg. of ascorbic acid per
cell-ascorbic acid concentrations in each group day. At the end of this period the white-cell
were averaged. T h e mean values for the white- concentrations in these three groups were, recell-ascorbic acid concentrations in these four spectively, 11.9, 12.9 and 24.2 mg. per 100 gm.
groups were found to differ significantly from of white cells. Upon the administration of
each other and were plotted against the corre- large doses, namely, 500 to 2000 mg. of ascorbic
sponding mean values for the plasma ascorbic acid daily, the white-cell concentration rose
acid as shown in Fig. 3. T h e resultant curve to maximal values of about 30 to 34 mg. per 100
is strikingly similar to that obtained by Lowry cc. From these intakes and the urinary excreand his associates in their study on ascor- tions over a period of four days, it was possible
bic acid realimentation of nornial men. T h e to calculate the amount of ascorbic acid that
significance of this finding will be discussed was destroyed or retained in the body. I t was
jxesen tly.
further found that during the administration
of these large doses, the extent of the increase
in the ascorbic acid content of the white cells
paralleled the degree of retention. Since subLowry and his co-workers have presented evi- jects who had been on the low ascorbic acid
dence showing that the concentration of as- intake, 8 or 23 mg. per day, retained 1800 mg.
ot ascorbic acid and showed an increase in
1. 3
0
Heallhy Young Adults
7
-acid concentrations to
the white-cell-ascorbic
somewhat more than double the value before
administration, it was concluded that the total
ascorbic arid content of the body was about
3 gm.
I t was found in the present study that the
M~scellaneousDisease
concentration of ascorbic acid in the white cells
was decreased to less than 24.5 ing. per 100 gin.
in 39 per cent of the patients with cancer and
to less than 19.5 mg. per 100 gm. in 20 per cent.
Cancer Patients
These decreases may be considered, in view of
64 cases
Lowrys study, as indicating definite depletions
ok the total body stores of ascorbic acid. T h e
question arises whether this depletion may be
ascribed to an accelerated usage of ascorbic
0
5
10
I5
20
25
30 35
40 45 50
55
Mq / 100 qm
acid by neoplastic tissue. Elevated concentraFIG. 2. Distributions of ascorbic acid concentIations i i i
tions ol ascorbic acid in neoplastic tissue might
white cells of healthy young adults, patients with niiscel- be taken as an evidence ol ruth usage but, as
laneoirs chronic disease, and patients wtih cancer.

1:;

CANCER
July 1952

682

VOl. 5

average value of 0.34 mg. per 100 cc. in thirtyone patients with peptic ulceration and hematemesis and one of 0.42 mg. per 100 cc. in
twenty-five patients with peptic ulceration, as
compared with an average of 1.28 mg. per 100
cc. in twenty-six healthy controls.21 Getz and
Koerners data show that 108 of 157 patients,
or 69 per cent, attending the chest clinic of
the Henry Phipps Institute had plasma-ascor.bic acid concentrations less than 0.5 mg. per
a
8 l0100 cc. I n contrast, only 12.5 per cent of fifteen
t
healthy staff workers showed concentrations
I
I
I
I
I
below this level.
It is of importance in connection with the
findings just presented to know whether low
Mg. Ascorbic Acid /I00 C.C. plasma
FIG. 3. Relationship bel.ween concentrations of plasnia plasma- o r serum-ascorbic acid concentrations
and white-cell ascorbic acid in 115 normal and ill per- also indicate low tissue stores of ascorbic acid.
sons grouped according t o plasma-ascorbic acid range T h a t the serum-ascorbic acid concentration is
(see text for derails).
definitely related to the white-cell-ascorbic
we have seen, there is no unanimous agree- acid concentration and hence is an index of
ment concerning the presence of such an eleva- the total body stores was demonstrated by Lowtion. Minor antl Raniirez found that after sat- ry and his associates in realimentation experiuration with high ascorbic acid intakes, the ments of normal persons on previously low asaverage utilization (difference between intake corbic acid intakes. Thus, the concentrations
and excretion) was higher in five patients with of white-cell ascorbic acid were 12 to 20 mg.
metastatic cancer than the average in seven per 100 gm. at a serum concentration of 0.2
patients with chronic noncancerous disease.19 mg. per 100 cc.; 18 to 24 mg. per 100 gm. at a
However, examination of their clinical data serum concentration of 0.4 mg. per 100 cc.,
shows that their cancer patients had lost more and practically maximal, 30 to 34 mg. per 100
weight than the control sub.jects. T h e possi- gm. at serum concentrations of 0.8 mg. per
hility exists, therefore, that the utilization of 100 cc. o r greater.17 O u r data, plotted in Fig. 3,
ascorbic acid was related to the general severity are in agreement with the conclusion of Lowry
of illness rather than to the presence of cancer. and his associates that there is a definite relaOur findings that low white-cell-ascorbic acid tionship between plasma- antl whi te-cell-asvalues in the group of chronic, noncancerous corbic acid concentrations and that the former
patients occur as frequently as in the cancer may, therefore, also be used as a guide to the
patients lend further support to the thesis that total body stores of ascorbic acid.
T h e data that we have presented in this
tissue depletion of ascorbic acid is not specific
paper as well as those cited from other investifor cancer.
As we have previously noted, there are prac- gations indicate that an increased utilization
tically no data in the literature, other than that of ascorbic acid occurs in cancer as well as i n
which we have reported here, on the concen- noncancerous chronic illness. Although there
tration of ascorbic acid in the white cells may be a quantitative difference between the
of patients with chronic disease. Wilson and extent of utilization in these two groups o f
1,ubscliez observed that children with inter- diseases, the evidence available at present is
current illness or with acute rheumatic fever inadequate to support the concept of such :I
on low ascorbic acid intakes tended to have difference.
It is of interest to consider the possible niechlower concentration of white cell ascorbic acid
than normal children.gO However, the groups anisms underlying the increased utilization ol
of sick children on low intakes were quite ascorbic acid in illness. Samuels has shown that
small, and no statistically significant conclu- the feeding of a high protein diet to rats leads
to a decrease in the concentration of ascorbic
sions can be drawn.
However, there are several studies which acid in the plasma and in tissues that metaboshow that the PLAshiA concentration of ascorbic lize considerable amounts of amino acids, such
acid is decreased in patients with chronic dis- as the liver. kidneys, and muscle. On the other
ease. Thus, Portnoy antl Wilkinson f o t I n t 1 an hand, 1 1 0 s u c h changes occur in the brain,
I

No. 4

PLASMA& WHITE-CELL
ASCORBIC
ACIDIN CANCER. Bodansky et al.

which does not metabolize amino acids, or in

the adrenal gland, which is characterized by an
unusually high concentration and perhaps specific function of ascorbic acid. I t has been
pointed out repeatedly that cancer as well as
othei chronic diseases 01
infections are, in general, characterized by an excessive catabolism ot
protein.lO9 13, Zo I t is possible then that the depletion of tissue ascorbic acid in these conditions may be related to such a n excessive
< atabolism.

SUMMARY
1. T h e concentrations of ascorbic acid in
the plasma, in the white-cell-platelet layer, or
in both were determined in twenty-three normal persons, forty-three patients with niiscellaneous chronic but rioncaiicerous diseases,
and seventy patients with cancer.

683

2. A considerable proportion 01 the patients

with cancer or chronic noncancerous disease
had low values for the ascorbic acid concentration in the plasma and white cells, and the
mean values for these concentrations in these
two groups were significantly lower than the
corresponding mean values for Lhe group of
normal persons.
3. There were no significant differences between the mean values or the distributions in
the group of patients with cancer and those
with chronic noncancerous disease.
4. O n the basis of the present results, other
data i n the literature, and Lowrys demonstration that the concentration of white-cell ascorbic acid appears to reflect the body store of
this vitamin, it is suggested that the depletion
of tissue ascorbic acid in cancer and other
chronic diseases is associated with an excessive
catabolism of protein.

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1: 554-560, 1938.

CANCER
J u l y 1952

684

KLI~.:I
I I L R , (:. A,: llle deterniiiia25. ROE, J. H.,
tion of ascorbic acid in whole blood antl urine through
the 2.4-dinitrophenylhydrazine derivative of dchytlroascorbic acid. .I. I j i o l . Chetrt. 147: 399-407, 1943.

26. Roe, J. H.; KUETHER.C. A,, arid ZIMLEK,R. G.:

T h e distribution of ascorbic acid in the blood. J. Clip&.
Investigation 26: 355-358, 1947.
27. SAMIIILS.
L.T.:T h e relation of ascorbic acid metabolism in the rat to diets high in protein, carbohydrate
or fat. .I.hutrition 36: 205-213, 1948.

28. SIWLRICRC,
M. A,, and KFETON,R. W.: Excretion of
ascorbic acid in relation to saturation antl utilization,

Vol. 5

with sottie diagnostic implications. Arclr. I r i L . nfcd. 6 s :

109.5-1116, 1939.
glycogen ill whole
21). jyA(;Nlc~t,
I<.: ~ 1 estiinatioli
, ~
I)lootl antl white blood cells. Arch. Bioclrein. 11: 249-258,
30. WILSON,
M. G.,and LURSCHEZ,
I<.: Studies in ascorbic acid with special reference to white layer. 11. T h e
relation of intake to blood levels in normal children antl
the effect of acute and chronic illness. .I. Clirc. Z?ix~e.stigc~25: 428.436, 1946,
31. WOODWARD.
G. E.: Glutathione antl ascorhic acid
in tissues of normal and tumoitr-hcaring alhino rats.
Rioclieni. J. 29: 2405-9412, 1935.

CANCER PROGRAM FOR FISCAL YEAR 1953

Clt~~rriical
or niological Syntlrrsir iir t h e A [ ) / d i c m t , <
Lnhoratory. All the activity t o be used in the synthesiu
of a radioisotope-labeled compound will be distrihutrtl
at the reduced price provided:
1. T h e labeled compound is for cancer research, diagnosis, or therapy, within the applicants institution.
2. The synthesis is performed in the applicants laboratories.
Iiocrssing o r Synthesis by n Supplier. 1supplier, who
has delivered processed radioisotopes to a person holtling an authorization to receive radioisotopes at thr
reduced price for cancer, may suhmit an application
for replacement. at the reduced price, of the activity
dclivercd provided the oriqinal activity was obtained
From the AEC or an AEC distrihutor. (Distributors currently are (I) Oak Ridge National Laboratory, Oak
Ridge. Tennessee; (2) Brookhaven National Laboratory,
IJpton, Long Island. New York: antl (3) Argonne National Laboratory, Chicago. Illinois. Suppliers are any
other persons or firms who furnish radioisotopes on authorization of the Commission.) T h e application for
replacement must include:
1 . Reference to the suppliers original authorization
number
2. Name of custonier
3. Customers authorization nuniher
4. Quantitv delivered
5. Date delivered
6 . Evidence of price reduction to purchasers of mdioPrice per Milliczrrie after July I , 1952
isotopes for approved cancer research. diagnosis, and
therapy.
Application Pt-ocedure. In applying for an authorizaCancer Use Non-Cancer IJse
_ _ ~ tion to receive radioisotopes under the program outlined
Radioiodine 131
$0.15
$0.75
herein, the applicant is requested to:
Radiophosphorus 32 0.22
1.10
1. Complete an Application for Radioisotope ProcureRadiogold 198
0.05
0.24
ment, Form AEC-313, for each radioisotope I-eRadiocarbon 14
7.20
36.00
quested.
-..
2. In addition to the prescribed information include the
followinq in Item 1 1 , Statement o f IJse. or on an
APPLICATION PROCEDURE
attached sheet:
Cancer Research. All radioisotopes will he available
a. T h e statement This application is f o r a ratlio6 at the reduced price for this purpose. Cancer research
isotope to be procured a t a reduction of 80 per
is interpreted to mean the following:
cent from the AEC o r AEC distributed catalog
1. Investigations of the hasic aspects of normal and
price and to be used in cancer . . . (research. diabnormal cellular growth.
agnosis, therapy).
2. Development and evaluation of therapeutic and diagI,. T h e statement The work will (will not) be done
nostic procedures for cancer and allied diseases.
under a contract with the Atomic Energy ComCancer Diagnosis and Therapy. P32, 1131, and Aulos
mission. Give contract number, if any.
will be distributed a t the reduced price for use in roilT h e phrase reduction of 80 per cent from AEC cattine or nonexperimental diagnosis and treatment of
alog price means the authorized person may purchase
cancer and allied diseases. (Radioisotopes for treatment
radioisotopes. except synthesized labelet1 cnnipoiinds. at
of nonmalignant diseases-such as hyperthyroidism antl
20 per cent of the price listed in a catalog issued Iiy the
cardiac decompensation-are not included in this proCommission or a distributor. Each shipment from a
gram. Separate application forms should be submitted
Commission distributor will be subject to the regular
to obtain materials for noncancer uses.) Radioactive mahandling charge made to cover costs of packaging, monterial for fixed sources such as Coo0 and Cs137 are not
itoring, and accounting. Transportation charges will
included under this arrangement.
be paid by the purchaser.
T h e L. S. Atomic Energy Commission, in fiscal year
1953, is changing its previous policy of distributing radioisotopes for cancer research and therapy free of production costs. Instead, it will make a charge of 20 per
cent of production costs. This change in policy affects
only the price, and not the availability, of isotopes; productipn will continue to meet all demands.
1)istribution of radioisotopes free of production costs
for cancer studies has proved a n extremely helpful and
valuable program, as evidenced by the fact that it has
expanded rapidlv and is continuing to expand. T h e
program has fulfilled its objective of providing a strong
stimulus to the fullest possible exploration of the usefulness of radioisotopes in cancer studies. T h e field has
developed so rapidly that certain clinical applications
of radioisotopes now have become a matter of routine.
and research workers have become fully aware of the
usefulness of these atomic tools in cancer research. T h e
Commissions Advisory Committee for Biology and Medicine and Advisory C1ommittee on Isotopes Distribution
recently have advised that the stimulus of completely
free distribution no longer is necessary to encourage the
use of radioisotopes in the field of cancer. These committees have agreed with the view of the AEC that a
charge of 20 per cent of catalog prices will not hamper
advances in this field, and that it will help to indicate
the future demand for radioisotopes in relation to other
tools for cancer research and therapy.

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