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ORIGINAL ARTICLE
Year : 2012  |  Volume : 2  |  Issue : 3  |  Page : 217-222

Biochemical changes in cardiac tissue upon monosodium glutamate administration in hypercholestremic mice


1 Department of Biochemistry, Govt. Medical College- Amritsar, India
2 Department of Horticulture, Punjab Agricultural university-Ludhiana, India
3 Department of Biochemistry, Panjab University-Chandigarh, India

Date of Web Publication8-Aug-2012

Correspondence Address:
Kuldip Singh
House No. B-2, Govt. Medical College Campus, Amritsar, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.99473

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   Abstract 

Background: Monosodium glutamate, a flavour enhancer ubiquitously used all over the World as a flavour enhancer in a variety of foods like two minute noodles, soups, sauces etc. prepared at home or restaurants. Aim:Monosodium glutamate was administrated at dose levels of 4 and 8mg/g body weight to hypercholestremic adult male mice for 6 consecutive days and its effect was observed on 31 st day after the last injection for the genesis of atherosclerosis by evaluating the changes in plasma lipid peroxidation and certain antioxidant enzymes in cardiac tissue of hypercholestremic adult male mice. Materials and Methods: The animals were divided in four groups each comprising 6 mice. Group-I: Control, Group-II: Hypercholestremic animals, Group-III: 4mgMSG/g body weight + hypercholestremic animals and Group-IV: 8mgMSG/g body weight + hypercholestremic animals. Animals were fasted overnight and sacrificed by decapitation. The 10% homogenate was prepared in 100mMpotassium phosphate buffer (pH7.5). The homogenate was centrifuged at 1,000g and supernatant was used for the estimation of lipid peroxidation, xanthine oxidase, superoxide dismutase and catalase. Results:A significant increase was observed in lipid peroxidation and xanthine oxidase levels while a significant decrease was found in superoxide dismutase and catalase levels of all the studied groups. Conclusion: These observations suggested that administration of monosodium glutamate at dose levels of 4 mg/g body weight and above to hypercholestremic animals had no beneficial effect instead it further enhanced the lipid peroxidation and alter the status of free radical initiating (xanthine oxidase) and scavenging (superoxide dismutase and catalase) enzymes and thereby being responsible for the initiation of coronary heart disease/atherosclerosis.

Keywords: Monosodium glutamate, hypercholestremia, malondialdehyde, coronary heart disease and atherosclerosis


How to cite this article:
Singh K, Kaur AP, Ahluwalia P. Biochemical changes in cardiac tissue upon monosodium glutamate administration in hypercholestremic mice. Int J Nutr Pharmacol Neurol Dis 2012;2:217-22

How to cite this URL:
Singh K, Kaur AP, Ahluwalia P. Biochemical changes in cardiac tissue upon monosodium glutamate administration in hypercholestremic mice. Int J Nutr Pharmacol Neurol Dis [serial online] 2012 [cited 2019 Nov 12];2:217-22. Available from: http://www.ijnpnd.com/text.asp?2012/2/3/217/99473


   Introduction Top


Cardiovascular disease (CVD) remained one of the main causes of death in all over the World. Coronary artery disease (CAD) is the single most important disease entity, in terms of mortality and morbidity in the entire World population. Both men and women between the age group of 40-60 years of age are susceptible to CAD. [1],[2] Despite all round efforts, it remains a challenge to the healthy managers and scientists. It is predicted that by the years 2020, this disease would be persists as the major and the most common threat to human life. In developing countries like India, the incidences of CAD are increasing alarmingly. [3] The risk of CAD in Indian is three times higher than in the white Americans, six times higher than in the Chinese and twenty times higher than in the Japanese. At the threshold of this millennium, CAD is looming large as a new epidemic afflicting Indians at a relatively younger age. [3],[4] The underlining cause of CAD is atherosclerosis. Atherosclerosis is one of the major causes of death in developing and developed nations and is reported to be responsible for about 10% of deaths all over the World. This trend has increased about three fold in the last decade. [5] Atherosclerosis is a multifactorial disease and results from complex interactions among injurious stimuli and healing and reparative responses of the arterial wall occurring in a hyperlipidemia and dyslipoproteinemic environment. The increase in the scientific literature reflects the opinion that oxidative stress is likely to be involved in the pathogenesis of various diseases like atherosclerosis. [6]

Monosodium glutamate (MSG) [C 5 H 8 NO 4 NaH 2 O], a sodium salt non essential L-form of glutamic acid used as flavour enhancer in various Chinese, Japanese, fast food and ready to serve foods like 2 minute noodles, soups, sauces etc. The use of MSG is wide spreading due to increased craze for Chinese, Japanese, fast food and ready to serve foods like 2 minute noodles, soups, sauces etc. all containing MSG and plays a critical role as a part of socioeconomic development. Concomitantly, there is a tremendous increase in the incidences of CHD/atherosclerosis in developed and developing nations like India. From our own laboratory, we reported that MSG at dose levels of 4 mg/g body weight and 8 mg/g body weight for consecutive 6 days induced hyperlipidemia without altering the levels of total cholesterol and also initiated the oxidative stress in various tissues of normal adult male mice's, well known risk factors for atherosclerosis. [5],[6],[7],[8],[9],[10],[11],[12],[13] So, in the present work we studied the effect of MSG on hypercholestremic adult male mice to observe whether MSG has beneficiary effects or not in hypercholestremic adult animals.


   Materials and Methods Top


Animals

Normal adult male mice of LAKA strain (UK) weighing 25-30g in body weight was procured from the animal house of Panjab University, Chandigarh - India. Animals were maintained on standard pellet diet (Hindustan Lever Ltd., Mumbai) with free access to water.

Grouping

MSG was subcutaneously administered at dose levels of 4 and 8 mg/g body weight for consecutive 6days that is 31 st to 36 th day to 1% cholesterol fed animals and continuing the feeding of cholesterol (1%) for 67 days. These animals were divided into following four groups and each group containing 6 mice;

Group-I (Control):0 mg MSG/g body weight.

Group-II: 0 mg MSG/g body weight + 67days of 1%cholesterol fed animals

Group-III:4 mg MSG/g body weight + 67days of 1%cholesterol fed animals

Group-IV:8 mg MSG/g body weight + 67days of 1%cholesterol fed animals

This experimental design was approved by the animal experimental ethics committee of Panjab University, Chandigarh and experiments were conducted according to Indian National Science Academy Guidelines for the use and care of experimental animals.

Sample preparation

After the dose period, animals were fasted overnight and sacrificed by decapitation. The hearts were removed and washed with ice cold saline and 10% homogenate was prepared in potassium phosphate buffer (100mM, pH 7.5). The homogenate was centrifuged at 1000xg for 15 minute in a cold centrifuge (4°C). The supernatant was stored at 4°C and used for various biochemical assays.

Biochemical assays

Lipid peroxidation (LPO)


The LPO levels were assayed by measuring the pink color chromophore formed by the reaction of thiobarbituric acid with malondialdehyde (MDA) according to the method of Beuge and Aust, 1978. [14]

Xanthine Oxidase (EC 1.2.3.2)

The activity of XOD was measured by the method of Fried and Fried, 1974 [15] using nitro blue tetrazolium (NBT), which formed farmazan. The increase in the intensity of color with time was measured spectrophotometrically at 540 nm for 10 minutes.

Superoxide dismutase (EC 1.5.1.1):

The activity of SOD was assayed by applying the method of Kono, 1978. [16] The activity of SOD was measured by monitoring the rate of inhibition of NBT reduction. One unit is defined as the amount of enzyme, which caused half-maximal inhibition of NBT reduction.

Catalase (EC 1.11.1.6)

The CAT activity was estimated by the method of Luck 1971, [17] in which decomposition of H 2 O 2 catalyzed by thisenzyme was measured by decrease in absorbance at 240nm, taking 0.0394 mM-1 cm-1 extinction coefficient and enzyme activity was expressed as nmol of H 2 O 2 degraded/min/ mg protein.

Protein assay

The protein contents were estimated by Lowry et al, 1951 methods. [18]

Statistical analysis

Results of biochemical analyses are presented as mean value ± standard deviation (S.D.). The difference between control and test groups was analyzed by using Student "t" test (significant difference at p< 0.05 confidence level). Correlation between the investigated groups was performed using test one-way variance of analysis (ANOVA).


   Results Top


Effect of cholesterol on lipid peroxidation, xanthine oxidase, superoxide dismutase and catalase

The results of lipid peroxidation, xanthine oxidase, superoxide dismutase and catalase upon oral ingestion of cholesterol (1%) for 67 days to normal adult male mice are summarized in [Table 1], [Table 2], [Table 3] and [Table 4].Oral ingestion of cholesterol (1%) for 67 days to normal adult male mice (Group-II) significantly increased lipid peroxidation and xanthine oxidase levels by 46.04% (from 3.54 ± 0.102 n mol of TBARS/mg protein to 5.17± 0.140n mol of TBARS/mg protein) and by 36.00% (from 0.0100±0.0003 U/mg protein to 0.0136±0.0005 U/mg protein) respectively with respect to control (Group-I) animals while the levels of superoxide dismutase and catalase were significantly decreased by 19.45% (from 3.861 ± 0.0991 to 3.110 ±0.0858U/mg protein) and by 18.53% (from 3.830±0.0961 nmol of H 2 O 2 decomposed/min/mg protein to 3.120±0.0818 nmol of H 2 O 2 decomposed/min/mg protein) respectively as compared to control (Group-I) animals [Table 1],[Table 2],[Table 3] and [Table 4].

Effect of MSG (4 and 8 mg/g body weight) on lipid peroxidation, xanthine oxidase, superoxide dismutase and catalase in hypercholestremic animals

A highly significant increase by 58.75% (P<0.001) and 83.33% (P<0.001) in lipid peroxidation and 48.00% (P<0.001) and 55.00% (P<0.001) in xanthine oxidase levels was observed in group-III [4mg MSG/g b.wt. + Cholesterol (1% for 67days)] and group-IV [8mg MSG/g b.wt. + Cholesterol (1% for 67days)] animals respectively as compared to control (Group-I) animals whereas the levels of free radical scavenging enzymes i.e. superoxide dismutase and catalase was significantly decreased by 38.85% (P<0.001) and 48.19% (P<0.001) and 36.29% (P<0.001) and 42.81(P<0.001) in group-III [4mg MSG/g b.wt. + Cholesterol (1% for 67days)] and group-IV [8mg MSG/g b.wt.+ Cholesterol (1% for 67days)] respectively as compared to control (Group-I) animals. A similar trend of increased LPO and XOD and decreased SOD and CAT levels were also observed in cardiac tissue of group-III and Group-IV animals with respect to group-II animals [Table 1],[Table 2],[Table 3] and [Table 4].
Table 1: Effect of subcutaneous administration of MSG at dose levels of 0, 4 and 8mg/g body weight (for 6 consecutive days) on lipid peroxidation and xanthine oxidase, in cardiac tissue of hypercholestremic adult male mice's

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Table 2: Percentage change in lipid peroxidation and xanthine oxidase levels upon subcutaneous administration of MSG (for consecutive 6 days) to hypercholestremic adult male mice's

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Table 3: Effect of subcutaneous administration of MSG at dose levels of 0, 4 and 8mg/g body weight (for 6 consecutive days) on superoxide dismutase and catalase in cardiac tissue of hypercholestremic adult male mice's

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Table 4: Percentage change in superoxide dismutase and catalase levels upon subcutaneous administration of MSG (for consecutive 6 days) to hypercholestremic adult male mice's

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   Discussion Top


Malondialdehyde, representing LPO was found to be significantly increased in the cardiac tissue of hypercholestremic and MSG treated hypercholestremic (Group-III and Group-IV) animals. High cholesterol might lead to an increased production of oxygen free radicals, which in turn might lipid peroxidation, causing endothelial cell damage. High blood cholesterol may damage the endothelial cell in various ways. Hypercholestremia may increase the cholesterol content of platelets. Cholesterol-rich platelets have been shown to increase the release of arachidonic acid from the platelets and to enhance the production of thromoboxane A 2 . [19] Cholesterol enhances platelet function and cholesterol-rich platelets release histamine, ADP and serotonin. [20],[21] Histamine and ADP are known to increase phospholipase A2 activity. [22] Phospholipase A2 acts on phospholipids to form arachidonic acids. [23] Another possibility for an increase in the arachidonic acid in hypercholestremia may be an increase in the calcium influx in endothelialcells. Phospholipase A2 activity is calcium dependent. [23] Hence an increase in the intracellular calcium would increase phospholipase A2 activity. Cholesterol is known to increase membrane fluidity. [24] Increase in the membrane fluidity would increase the calcium influx. It has also been suggested that cholesterol can affect phospholipase A2 through alteration in lipid water interphase, [19] The increase in the arachidonic acid through these mechanisms would increase the formation of prostaglandins and leukotrienes. It is known that the intermediate steps in the biosynthesis of prostaglandins from arachidonic acid produce oxygen free radical. [25],[26] Leukocytes will produce leukotrienes through arachidonic acid metabolism. One of the leukotriene B4 (LTB4) has been found to be a potent inducer of leukocyte chemotaxis, aggregation and degranulation. Leukotriene B4 would activate polymorphonuclear leukocytes (PMN) to secrete oxygen free radicals. [27] Oxygen free radicals thus produced would induce endothelial cell damage by causing peroxidation of membrane phospholipids. The first step in lipid peroxidation is the initiation reaction, which begins by taking out hydrogen atom from polyunsaturated fatty acid (PUFA) by oxygen radical. The second step is the propagation and the final step is termination. [28],[29] The extent of lipid peroxidation has often been determined by the thiobarbituric acid (TBA) test, which has also been considered for the determination of malondialdehyde. A significant increase in lipid peroxidation levels in hypercholestremic (Group-II) and MSG treated hypercholestremic (Group-III and Group-IV) animals was observed in the present study might lead to susceptibility of the biomembrane, which ultimately leads to tissue injury/damage.

XOD, a superoxide initiating enzyme was found to be significantly increased by 36% in hypercholestremic animals (Group-II), 48% in 4mgMSG/g body weight treated hypercholestremic animals (Group-III) and 55%% in 8mgMSG/g body weight treated hypercholestremic animals (Group-IV) with respect to control animals and we also observed a significant increase by 8% (P

lt;0.05) and 9.15% (P<0.05) in group-III and Group-IV with respect to hypercholestremic animals not receiving MSG (Group-II). XOD, catalyses the oxidation of hypoxanthine/ xanthine to uric acid and generates superoxide radical (O2 .- ). Hydrogen peroxide (H 2 O 2 ) formed from O2 .- could be converted into highly reactive hydroxyl radical ( . OH) leading to oxidative stress as a result of oxidation of biological molecules. A significant increase in XOD activity in cardiac tissue of hypercholestremic and MSG treated hypercholestremic animals could produce a burst of free radicals. Once O2 .- radical produced then H 2 O 2 and . OH are continuously produced by Haber-Weiss reaction and / or Fenton type reaction. [30] Oxygen radicals might cause the lipid peroxidation of biomembrane through a chain reaction.

SOD levels were decreased cholesterol ingested animals (Group-II), and also in MSG treated groups (Group-III and Group-IV). SOD is considered the first line of defence against the deleterious effect of oxygen radicals in the cells and it scavenges reactive oxygen radical species by catalyzing the dismutation of O2 .- radical to H 2 O 2 and O 2 . In mammals, three isozyms of SOD that is CuZn-SOD, Mn-SOD and extra cellular-SOD are occur. [31] CuZn-SOD located primarily in the cytosol. CuZn-SOD consists of two protein sub units each has an active site containing one Cu ion and One Zn ion. Cu ion serves as active redox site and Zn ion maintain the protein structure. Mn-SOD, located in mitochondrial matrix. [32] It has four subunits each with Mn ion. EC-SOD is present in plasma, bound to heparin sulfate ion the surface of endothelial cells. EC-SOD is tetrameric glycoprotein, which contains Cu and Zn ion. The presences of SOD in various compartments of the our body enables it to dismutate O2 .- radicals immediately and protects the cells from oxidative damage. A significant inhibition of SOD activity in cardiac tissue of 4 and 8mg MSG/g body weight treated hypercholestremic animals (Group-III and Group-IV) may results in an increased flux of O2 .- radical and hence reflects the tissue damage/injury.

The activity of CAT, another potent antioxidant enzyme, especially against theO2 .- radicals and singlet oxygen, was also significantly decreased in cardiac tissue by 14.88% in group-II, 22.97% (P<0.01) in group-III and 45.69% (P<0.001) in group-IV respectively with respect to control animals [Table 2] and a similar trend in the activity of CAT was also observed in 4 and 8mg MSG/g body weight treated hypercholestremic mice (Group-III and Group-IV) as compared to chronic alcoholic (Group-II) animals [Table 2]. CAT, protects cells from the accumulation of H 2 O 2 by dismutating it to form H 2 O and O 2 or by using it as an oxidant, in which it works as a peroxidase. Therefore, the decrease in the activity of CAT observed in present work could be due to less availability of NADH as MSG favours lipogenesis [7] and hence administration of MSG to hypercholestremic animals had no beneficial effect on CAT activity to reduce lipogenesis/oxidative stress.

Inclusion, a aforementioned observations suggested that administration of MSG at dose levels of 4mg/g body weight and above along with cholesterol produced hyperlipidemia andenhanced the oxidative stress by further increasing the levels of lipid peroxidation thereby MSG along with cholesterol had additive effect. Hence could act as an additional factor for the initiation of atherosclerosis.

 
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]


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