Effect of monosodium glutamate on lipid peroxidation and certain antioxidant enzymes in cardiac tissue of alcoholic adult male mice

Abstract

Background:Monosodium glutamate (MSG), a sodium salt of glutamic acid is commonly used as flavor enhancer in Chinese, Japanese and ready to serve foods all over the World, is the inducer of oxidative stress. In the present era, MSG and alcohol is becoming a part of daily food. Concomitantly, there is a tremendous increase in the incidences of cardiovascular diseases. So, the present study was designed to elucidate the effect of MSG by evaluating the changes in oxidative stress markers in cardiac tissue of normal and alcoholic adult male mice.Materials and Methods:Animals were divided into six groups of six mice each and MSG at dose levels of 0, 4, and 8 mg/g body weight was given orally for seven consecutive days (that is from 31st day to 37th day of alcohol ingestion) to chronic alcoholic (30% ethanol/100 g body weight) adult male mice. After the dose period (38th day), animals were fasted overnight, sacrificed by decapitation and hearts were removed for the estimation of lipid peroxidation (LPO), xanthine oxidase (XOD), superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) and its metabolizing enzymes like glutathione peroxidase (GPx) and glutathione reductase (GR).Results:A significant (P < 0.001) increase was observed in LPO and XOD levels while a significant decrease (P < 0.001) in the levels of SOD, CAT, GSH, GPx and GR was found in cardiac tissue of normal and alcoholic animals.Conclusion:These observations suggested that oral ingestion of MSG at dose levels of 4 mg/g body weight and above with and without alcohol increased the oxidative stress and thereby, could act as an additional factor for the initiation of atherosclerosis.

Etiology of alcoholic cardiomyopathy: Mitochondria, oxidative stress and apoptosis

“…Alcohol has been reported to downregulate both GPx and GSH (59, 60, 63, 71, 72) in all but one study (58). GPx may also be influenced by sex as no change was observed following acute or chronic alcohol intake in female rats (64, 72).…”

“…GPx may also be influenced by sex as no change was observed following acute or chronic alcohol intake in female rats (64, 72). The anti-oxidant GSH was also decreased by chronic alcohol in mice and rats after shorter periods of alcohol (10–30 days) (59, 61, 62, 71), while it was increased in response to alcohol consumption of longer duration (50 days) (58). In agreement, acute alcohol intoxication (1 dose (65) or 3 doses (64)) decreased (65) or did not change (64) GSH in myocardial tissue from female rats.…”

“…The effect of chronic alcohol on catalase may be duration-dependent as enzyme activity was increased after 7–8 wks of alcohol intake (58, 63) while a shorter duration of alcohol ingestion (15, 30 or 37 days) decreased catalase (59, 62, 71). The relative importance of sex hormones in regulating catalase activity has also been highlighted by data that showed that estrogen pretreatment increased catalase activity in male rats in a binge drinking model (54, 56) and after a single acute dose of alcohol (0.5, 1.0, 1.5 g/kg) (54).…”

Evaluation of Ginsenoside Rg1 as a Potential Antioxidant for Preventing or Ameliorating Progression of Atherosclerosis

“…SOD and GSH play a pivotal role in preventing ROS-induced cellular damage. Therefore, intracellular ROS can be effectively eliminated by the combined action of SOD and GSH, providing a repairing mechanism for oxidized membrane components [18]. In the present study, the activities of SOD and GSH in HUVECs significantly decreased after exposure to H 2 O 2 , indicating impairment of antioxidant defenses.…”

Vitamin C-E ve Monosodyum Glutamata Bağlı Ovaryan Toksisite

“…Previous studies show that oral ingestion of MSG at dose level 4 mg/g body weight and above increased the oxidative stress in cardiac tissue 23 . The administration of second and third dose of combined vitamin C and E significantly (P< 0.05) decreased the MDA levels compared to the MSGexposed groups, to reach level in control groups.…”