Effects of reduced glutathion and vitamin c on cisplatin-induced hepatotoxicity in rats

Cisplatin [CDDP] is a widely used anticancer drug, however it can produce undesirable side effects such as hepatotoxicity when used at high doses. The aim of the present work to evaluate the protective effect of reduced glutathione [GSH] and vitamin C on CDDP-induced hepatotoxicity. Eighty male Sprague-Dawley rats were divided into eight groups, 10 rats each. Group I, control group. Group II received Cisplatin [7.5 mg /kg, i.p] for 5 consecutive days. Group III received GSH [600 mg/kg /day, i.p]. Group IV received vitamin C [250 mg/kg/day, orally]. Group V received GSH for 15 days then CDDP for 5 days. Group VI administered vitamin C for 15 days then CDDP for 5 days. Group VII administered both GSH and CDDP for 5 days. The last Group [VIII] administered both vitamin C and CDDP for 5 days. Serum alanine aminotransferase [ALT] and aspartate aminotransferase [AST] activities [markers of hepatotoxicity], antioxidants [superoxide dismutase [SOD], glutathione peroxidase [GSHPx], catalase [CAT], glutathione reductase [GSHR] activities and gene expression, glutathione [GSH] content] and lipid peroxidation products [malondialdehyde, MDA] in rat liver tissue were measured. CDDP hepatotoxicity was manifested by an increase in serum ALT and AST, elevation of MDA as well as a decrease in GSH and the activities and gene expression of antioxidant enzymes [SOD, GSHPx, CAT, GSHR] in liver tissues. Serum ALT, AST and hepatic MDA decreased in the combination groups in comparison with the CDDP group. The activities and gene expression of SOD, GSHPx, CAT and GSHR and the GSH concentration increased in the combination groups as compared to the CDDP group. Reduced glutathione and vitamin C either taken before or concomitant with cisplatin attenuated the CDDP hepatotoxicity

Mechanism of food additive [monosodium glutamate]- induced obesity a molecular study

There is no question that there is an obesity epidemic in our country, as well as in some other countries. Obesity during pregnancy increases maternal and fetal morbidity and is a risk factor for gestational diabetes and hypertensive disorders of pregnancy. There are many causes of obesity from them the bad use of food additives, the monosodium glutamate is considered one of the most popular food additives. The results of previous studies on the role of monosodium glutamate in developing of obesity are controversial so the aim of this paper is to determine the role of MSG in developing obesity through studying its effect on Ob gene expression and leptin receptor-b gene expression and to determine its effect on some cardiac disease indicators as apo-A[1] and apo-B. We used in this study 60 pregnant female rats which were divided into 2 groups, control group and group supplemented with monosodium glutamate. In all rats, determination of biochemical parameters as serum glucose, insulin, leptin, total lipids, cholesterol HDL, LDL, VLDL, apo A1, apo B, as well as determination of Ob and leptin receptor-b gene expression were done. Our results indicated that the administration of monosodium glutamate is accompanied with increase of Ob gene expression, leptin, insulin, lipoprotein B, lipogram, glucose and decrease of brain leptin receptor-b gene expression, lipoprotein lipase activity and HDL concentrations. It can be concluded that the administration of MSG may be considered as one of the main causes of obesity by increasing of leptin and insulin resistance and so developing of hyperphagia. Also it is accompanied by increasing the risk of atherosclerosis through development of diabetes mellitus type II and increasing total cholesterol and LDL. Moreover, maternal obesity is a serious condition that significantly impacts health of mothers and their children