Monosodium glutamate induces cardiac toxicity via oxidative stress, fibrosis, and P53 proapoptotic protein expression in rats

Monosodium glutamate (MSG) is widely used as food additive and flavor enhancer; however, consumption of high dose ofMSG
provokes oxidative stress in many organs and its safety and side effects on the body are still controversial. Therefore, it is crucial
to investigate the long-lasting effects of MSG on cardiac muscle functions and structure. Forty male Wister albino rats were
assigned into 3 groups. Control group was injected intraperitoneally with physiological saline for 7 days. Second group was
injected intraperitoneally with MSG at a dose of 4 mg/g b.w/day for 7 consecutive days and then kept without any treatment till
45th day of the experiment. Third group was injected intraperitoneally withMSG at a dose of 6 mg/g b.w/day for 7 consecutive
days and then kept without any treatment till 45th day of the experiment. Monosodium glutamate significantly reduced body
weight, force of cardiacmuscle contractility, serumlevel of high-density lipoprotein, and superoxide dismutase activity in cardiac
muscle, while it significantly elevated heart rate, serum levels of total cholesterol, low-density lipoprotein, triacylglycerides,
atherogenic index and troponin T, activities of serum lactate dehydrogenase and creatine kinase-MB, malondialdehyde concentration,
and P53 protein expression in cardiac muscle. In addition, it induced myocardial degeneration, cellular infiltration,
deposition of collagen in cardiac muscle, and periodic acid–Schiff staining reaction. This study indicated that MSG exerted
long-lasting functional and structural alterations in the heart of male albino rats through induction of oxidative stress, atherogenesis,
and apoptosis.