Sub-Acute Study on the Cardiotoxic Effects of Monosodium Glutamate Ingestion in Albino Rat

Introduction

The white, crystalline powder known as monosodium glutamate is nearly odourless. This sodium salt is a form of glutamic acid, an amino acid that is present in meat, chicken, and other high-protein foods. In the majority of markets, it is sold as “white maggi” or “ajinomoto” and serves as an addition and food enhancer [1, 2]. It is produced by the action of Micrococcus glutamicus on a carbohydrate source, such as sugar beetroot molasses, or by the partial neutralisation and acid hydrolysis of vegetable proteins [3, 4].

Conversely, it has been widely documented that monosodium glutamate poses a risk to people and, consequently, laboratory animals, particularly when administered in larger quantities. There have been instances of hypersensitivity reactions, such as burning and tingling, caused by Chinese restaurant cooks’ over usage of glutamate. “Monosodium glutamate symptom complex” or “Chinese restaurant syndrome” are terms used to describe this illness [5].

Chinese restaurant syndrome is a collection of symptoms, including headaches, dizziness, palpitations, and numbness in the neck, arms, and back, that are thought to affect vulnerable people who eat food that is highly seasoned with monosodium glutamate, according to the Merriam-Webster dictionary. Large quantities of monosodium glutamate are utilised in South Asian, Chinese, and Japanese cooking. The precise origin of this condition is unknown, despite research demonstrating that monosodium glutamate has neurotoxic and neuro-excitatory effects in the hypothalamus region of the central nervous system [6, 7]. Monosodium glutamate at high concentration was also linked to an increased risk of the aforementioned symptoms. Two people had acute bronchial asthma after consuming monosodium glutamate [8].

Toxin buildup causes damage to the heart muscles, which is known as cardiotoxicity. Heart failure or heart dysfunction are other names for it. Myocardial infarction, angina, and acute arrhythmia are among the several kinds [9–11]. Toxicological level can be used to identify sub-acute cardiac damage. Damage to the heart causes changes in the way the heart pumps [12]. Dyspnea, heart palpitations, blood pressure fluctuations, chest pain, and malaise are the most typical signs of cardiotoxicity. Among its complications are congenital heart failure, cardiomyopathy, myocardial infarction, and sudden death [13].

A disruption in the heart tissue’s blood flow causes a heart attack, often referred to as an acute myocardial infarction [14]. When evaluating heart problems, biochemical indicators of the cardiac system might lower the morbidity or fatality rate linked to acute myocardial infarction. The most often utilised diagnostic markers are Lactate Dehydrogenase (LDH), its isoenzyme Creatine Kinase (CK), and Aspartate Amino Transferase (AST). These enzymes are found in kidney, liver, bones, skeletal muscle, brain erythrocytes, gastrointestinal system, uterus, prostate, tongue, and other tissues in addition to heart tissue [15].

Serum levels of cardiac enzymes are typically relatively low. Consequently, when the membrane disrupts these enzymes, they leak out into the plasma and multiply greatly, providing information on the degree of cardiac damage brought on by oxidative stress and lipid peroxidase [16]. AST and LDH are nonspecific and rise significantly in the later stages (24–72 hours) following the onset of symptoms.

The most effective cardiac indicators should be sensitive and specific, able to identify long-term storage problems and early infarctions. Analysis of a single biomarker is not advised because there is no perfect and particular biomarker; instead, enzymes with key characteristics of the ideal biomarker are used. However, it has been noted that the most optimal marker, CK-MB (CK-2), and the LDH1 and LDH2 ratio are more sensitive and specific to acute cardiac damage. Acute myocardial infarction causes an elevation in these enzymes. After myocardial damage, CK-MB peaks within 24 hours, rises 4–9 hours later, and then returns to normal within 48– 72 hours [15, 17]. Along with a number of dietary sweeteners, salt, and hydrogenated fats, monosodium glutamate is an excitatory neurotransmitter that can generate excite-toxicity, which increases safety concerns when used as a flavour enhancer. The purpose of the study is to examine how albino rats’ hearts respond to two oral low doses of monosodium glutamate, 0.5 ml.kg and 1 ml/kg.

Statistical Analysis

Data analysis was done using GraphPad prism version 7.0 (GraphPad, San Diego, CA, USA). The results of the biochemical assays were reported as mean±SEM (standard error of mean). The level of significance was tested using one-way analysis of variance (ANOVA), followed by the Tukey post hoc analysis. Probability levels less than 0.05 (p<0.05) was considered significant.

Results

Effects of monosodium glutamate (MSG) on body weight of rats following 21days of administration is represented in Figure 1. It was observed that rats in the High dose of MGS (1ml/kg) group gained significant weight when compared to normal control rats. The mean increase in body weight was highest in the High dose of MGS (1ml/kg) in comparison with other groups.

Click to enlarge

Discussion

In this study, it was observed that rats in the High dose of MGS (1ml/kg) group gained significant mean increase in weight when compared to normal control rats. This observation agrees with the findings of a study titled “Organ toxicity of monosodium glutamate in adult albino Wister rats.” [22], in their study a significant increase was observed in the Wister rats.

Further findings in this study showed a non-statistically significant decreased levels of CK-MB, a slightly increased levels of LDH and decreased levels of AST, were seen in the High dose of MGS (1ml/kg) group B when compared with group A (normal control). The observation in the low dose (0.5mg/kg) showed no significant alterations in the biochemical parameters measured. It is more common for both levels of LDH and AST to be increased in cardiotoxicity due to cardiac cell damage. This study did not establish cardiotoxicity at the doses used in the study and this is confirmed by the histopathological results. The possible explanation for the slight increase in LDH level may be due to the high presence of LDH in red blood cells as oppose to AST. The breakdown of red blood cells, known as haemolysis, is not directly caused by monosodium glutamate (MSG), but it can have an impact on the lifespan and function of red blood cells. Excessive doses of MSG can raise sodium levels, which may cause red blood cells to shrink and shorten their lifespan and other hematological factors, which could result in anaemia, thus slight increase in LDH level in the plasma [23, 24, 25].

However, the histopathological findings in this study showed normal myocardial fibres in all the study groups A-C. The cardiac fibres also showed a well-conserved morphology. The findings were in tandem with the biochemical results as we observed that monosodium glutamate (MSG) did not pose any serious observable danger to the heart at the doses studied. This finding didn’t agree with a previous study carried out by Okon, et al. [26], titled “Studies of the effect of monosodium glutamate on the cardiac muscle fibres of adult Albino Rats”. Here they found that the histological organisation of the cardiac m`uscles fibres can be significantly altered with continuous or increased use of Monosodium glutamate. However, this disparity can be attributed to the fact that their study was conducted on higher doses (4mg/kg and 8mg/kg) of MSG than this study (0.5ml/kg and 1.ml/kg).

Conclusion

From the investigation, it was observed that rats in the high dose of MGS (1mg/kg) group gained significant weight when compared to control rats. Asides this gain in weight at high dose, it was observed that monosodium glutamate (MSG) did not pose any serious observable danger to the heart at the doses studied. Cardiotoxicity by monosodium glutamate is dose-dependent, therefore it could pose a great risk to the heart if ingested in high amount.