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ISSN (Print) 0975-685X
J. Appl.
Appl. Biosci.,
Biosci., 41(1)
41(1): 54-56, June, 2015 ISSN (Online) 0975-864X


Department of Zoology, D.D.U. Gorakhpur University, Gorakhpur-273008, U.P., India

Monosodium glutamate is a flavor enhancer, commonly added to commercially produced food
products to make them tastier. 5 mg and 10 mg monosodium glutamate/g body weight was administered
orally to normal adult male mice for seven days and its effect was seen on 31 st day after the last dose
on lipid peroxidation and antioxidant enzymes; xanthine oxidase, superoxide dismutase and catalase
in skeletal muscles. A significant dose dependent increase in lipid peroxidation and xanthine oxidase
level was observed in both monosodium glutamate treated groups whereas the activity of free radical
scavenging enzymes such as superoxide dismutase and catalase decreased. Hence, monosodium
glutamate induces oxidative stress in muscles by affecting the activity of radical initiating enzyme
such as xanthine oxidase and scavenging enzymes like superoxide dismutase and catalase.

KEY WORDS: Oxidative stress, lipid peroxidation, xanthine oxidase, superoxide dismutase,

INTRODUCTION 2000; Kukreja & Hass, 1992). Therefore, this study deals
Monosodium glutamate (MSG) known as Aji-no-moto, with the effect of MSG on some antioxidant enzymes in
Sasa, Ve-tsin, Miwon and Weichaun etc. is sodium salt of the muscles (skeletal) of adult male mice.
glutamic acid. It contains 78% glutamic acid, 22% sodium
and water (Adrienne, 1999). Glutamate is the most common
amino acid in nature. It is synthesized in the body and Animals and treatment
plays a vital role in human metabolism. It is the main Normal adult male albino mice weighing 140-150 gm
component of many protein and peptides in tissue. MSG were procured from the local animal supplier of Gorakhpur.
is commonly used as flavour enhancer in various food These were divided into three groups with six mice in each
products. It is palatable and favourite flavour in almost all group (A, B, and C). MSG was given orally at dose level of
Chinese and South Asian dishes. As a food additive, it 5 mg/g and 10 mg/g body weight for seven continuous
stimulates the oro-sensory receptors and improves the days to group B and C, group A served as control. The
palatability of food. It influences the appetite positively animals were housed in polypropylene cages. They were
and induces weight gain (Moore, 1999). Though, it provided with ad libitum food and water, 12:12 L: D cycle
stimulates taste and enhances appetite, it is reported to be at 25± 2°C room temperature throughout the study. The
toxic to humans and experimental animals (Inuwa et al., protocol for the experiment was approved by the Ethical
2011). It is also known for its association with Chinese Committee of the D.D.U. Gorakhpur University, Gorakhpur,
restaurant syndrome (Kwok, 1968). MSG used as flavour U.P., India.
enhancer in all Chinese, Japanese and ready to serve foods
like 2 minute noodles, soups, sauces etc, induces oxidative Sample Preparation
stress (Ahluwalia et al., 1996; Ahluwalia & Kuldeep, 2002). Animals were fasted overnight and sacrificed on 31st
Increase in oxidative stress can bring changes in membrane day after the last oral treatment of MSG administration
lipids and proteins leading to many diseases like cancer, because obesity is known to establish after a month of
diabetes, coronary heart disease (CHD) etc., (Dhalla et al., MSG administration (Hamaoka & Kusunoki, 1986; Ochi et
*Corresponding author; email:

J. Appl. Biosci., 41(1)

al., 1991). The muscles were removed, washed with normal An increase in lipid peroxidation following MSG
saline and 10% homogenate was prepared in potassium administration in mice could be due to increase in the level
phosphate buffer (100mM, pH 7.5). Homogenate was of Glutamine. Glutamine is known to initiates change in
centrifuged at 1000 rpm for 15 minutes at 4°C and redox potential of cell and favour lipogenesis (Malik &
supernatant was used for various biochemical estimations. Ahluwalia, 1994). MSG is also reported to induce
hyperglycemia, which can result in peroxidation of
Biochemical assays membrane lipids via glucose oxidation, (Chaudhary et al.,
The lipid peroxidation level was estimated by 1996).
measuring the pink color chromophore formed by the Xanthine oxidase (XOD) is a superoxide generating
reaction of thiobarbituric acid with malondialdehyde enzyme and the activity of XOD significantly increased
(MDA) according to the method of Hochestein et al., by 3%-9% in treated group B and group C respectively
(1964). The activity of xanthine oxidase (XOD) was (Table 1).
measured by the method of Fried and Fried, (1974) using
XOD has ability to generate free radicals in the cell
nitroblue tetrazolium (NBT), which formed farmazan. The
and it exists as NAD dependent xanthine dehydrogenase
increment in color intensity with time was measured
(XDH) in wide variety of living organisms. It has no role in
spectrophotometrically at 540 nm for 10 minutes.
initiation of oxidative damage in cells. In many conditions
Superoxide dismutase (SOD) activity was analyzed where the cells are damaged, XDH is converted to XOD
by applying the method of Kono, (1978). The activity of that catalyses the oxidation of hypoxanthine/xanthine to
SOD was measured by monitoring the rate of inhibition of uric acid and generates superoxide radicals (O2-), (De Groot
NBT reduction. One unit is defined as the amount of & Littauer, 1988; Batteli et al., 1992). An increase in level
enzyme, which is causing half maximum inhibition of NBT of XOD after administration of MSG may produce free
reduction. radicals inducing oxidative stress leading to tissue injury.
Catalase (CAT) activity was estimated by the method An increase in oxidative stress was accompanied by
of Luck (1971) in which decomposition of H2O2 catalyzed decrease in the activity of Superoxide dismutase (SOD)
by the enzyme was measured by decrease in absorbance by 7%-14% in both treated groups respectively (Table 1).
at 240 nm, taking 0.0394 mM-1 cm-1 extinction coefficient SOD has an initiative effect against superoxide anion. The
and enzyme activity was express as K/mg protein. Here presence of SOD in cells enables cell to remove superoxide
“K” is the first order rate constant. Total protein content radical and protect cell from oxidative damage, (Fridovich,
was estimated by the method of Lowry et al. (1951). 1995; Mandund, 1984). Hence, a decrease in SOD after
administration of MSG further increases oxidative stress
in this study.
Oral administration of MSG at a dose level of 5 mg/g Catalase another antioxidant enzyme showed a
and 10mg/g body weight significantly increased the level decrease in its activity by 4%-10% after administration of
of malondialdehyde (representing lipid peroxidation) by
MSG in both groups (Table 1). Enzyme catalase provides
5%-12% (Table 1) in muscle tissue of both MSG treated
protection to cell from H2O2 by removing it to form H2O+O2
group (group B and group C) with respect to control group
or by using it as an oxidant like peroxidases (Roberford &
(group A).
Calderon, 1995). A decrease in catalase in the present

Table 1: Effect of oral administration of MSG for seven days on lipid peroxidation and xanthine oxidase, superoxide dismutase and
catalase level /activity in skeletal muscle tissue of adult male mice

Groups Lipid Peroxidation Xanthine Oxidase Superoxide dismutase Catalase (n mole

(n mol of MDA (Units/mg protein) (Units/mg protein) H2O2 decomposed/
formed/mg protein) min/mg protein)

Control A 4.650 0.0100 3.15 3.13

(0 mg MSG/g body wt.)
Experimental B 4.897 0.0103 2.93 2.99
(5 mg MSG/g body wt.) (+5.31%) (+3%) (-6.98%) (-4.47%)
Experimental C 5.245 0.0109 2.70 2.81
(10 mg MSG/g body wt.) (+12.79%) (+9%) (-14.28%) (-10.22%)

J. Appl. Biosci., 41(1)

activity further suggests that MSG favours lipogenesis Hamaoka, K. & Kusunoki, T. (1986). Morphological and cell
by increasing the level of glutamine. proliferative study on the growth of visceral organism
monosodium L-glutamate treated obese mice. J. Nutr. Sci.
CONCLUSION and Vitamol., 32: 395.
Present study indicates that administration of MSG Hochestein, P., Nordenbr, K. & Ernster, L. (1964). Evidence for
induces oxidative stress in the muscle tissue by altering the involvement of iron in the ADP-activated peroxidation
of lipids in microsomes and mitochondria. Biochem. Biophys.
the activity of antioxidant enzymes like XOD, SOD, and
Res. Commun., 14: 323-328.
Inuwa, H.M., Aina. V.O., Gabi, B., Aim ola, I. & Ja´afaru, L.
REFERENCES (2011). Determination of nephrotoxicity and hepatoxicity
of Monosodium Glutamate (MSG) consumption. British
Adrienne, S.(1999). The toxicity of MSG, a study in suppression J. Pharmacol. Toxicol., 2(3): 148-153.
of information. Accountability in Research, 6(4): 259-310.
Kono, Y. (1978). Generation of superoxide radical during
Ahluwalia, P. & Kuldip, S.(2002). Alteration in lipid peroxidation, autoxidation of hydroxylamine and an assay for superoxide
cytochrome P450, glutathione and its metabolizing enzymes dismutase. Arch Biochem. Biophys., 186: 189-195.
upon monosodium glutamate administration in hepatic tissue
of adult male mice. Ind. J. Toxicol., 9: 23-27. Kukreja, R.C. & Hass, M.L. (1992). The oxygen free radical
system: from equations through membrane protein
Ahluwalia, P., Tewari, K. & Chaudhary, P. (1996). Studies on interactions to cardiovascular injury and protection.
the effect of monosodium glutamate (MSG) on oxidative Cardiovasc. Res., 26: 641-655.
stress in erythrocytes of adult male mice. Toxicol. Lett., 84:
161-165. Kwok, R.H.M. (1968). Chinese restaurant syndrome. New Eng.
J. Med., 278: 796-799.
Batteli, M.G., Abbondanza, A. & Stripe, F. (1992). Effect of
hypoxia and ethanol on xanthine oxidase of isolated rat Lowry, O.H., Rosenbrough, J.N., Farr, A.L. & Randall, R.J.
hepatocytes: Conversion from D to O form and leakage (1951). Protein measurement with Folin phenol reagent. J.
from cells. Chem. Biol. Interact., 83: 73-77. Biol. Chem., 193: 265.
Chaudhary, P., Malik, V.B.T., Puri, S. & Ahluwalia, P. (1996). Luck, H. (1971). Catalase, methods of enzymatic analysis E.D
Studies on the effect of monosodium glutamate on hepatic Bergmeyer HO, Academic Press, New York, London, P.
microsomal lipid peroxidation, calcium, ascorbic acid and 855.
glutathione and its dependent enzymes in adult male mice. Malik, V.B.T. & Ahluwalia, P. (1994). Studies on the effect of
Toxicol. Lett., 89: 71-76. monosodium glutamate (MSG) on various fractions of lipids
De Groot, H. & Littauer, A. (1988). Reoxygenation injury in and certain carbohydrate metabolic enzymes in liver and
isolated rat hepatocytes: Cell death precedes the conversion blood of adult male mice. Toxicol. Lett., 74: 69-77.
of xanthine dehydrogenase to xanthine oxidase. Biochem. Mandund, S.L. (1984). Properties of extra cellular superoxide
Biophys. Res. Commun., 155: 278-282. dismutase from human lung. Biochem. J., 220: 269-272.
Dhalla, N.S., Temsah, R.M. & Netticadan, T. (2000). Role of Moore, K.L. (1999). Congenital malformations due to
oxidative stress in cardiovascular disease. J. Hypertension, environmental factors. 2nd Edn., Developing humans. W.B
18: 655-673. Saunders Co. Ltd. Philadelphia, 173-183.
Fridovich, I. (1995). Superoxide radical and superoxide dismutase. Ochi, M., Furukowa, H., Yoshioka, H., Sawada, T., Kusunoki,
Ann. Rev. Biochem., 64: 97-112. T. & Hattori, T. Adipocyte dynamics in hypothelmic obese
Fried, R. & Fried, L.W. (1974). Xanthine oxidase (Xanthine mice during food deprivation and refeeding. J. Nurt. Sci. &
dehydrogenase). Method of enzymatic analyses, Ed. Vitamol., 37: 497-491.
Bergmeyer H.U. Academic Press, New York, London, 2: Roberford, M.B. & Calderon, P.B. (1995). Free radicals and
644-649. oxidation phenomena in biological system. Marcel Decker
inc., 270 Madison Avenue, New York, pp 193-203.


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