The protective effect of selenium on the neurotoxicity of vanadium in different brain regions of rats was investigated. The lipid peroxidation was significantly accentuated after intraperitoneal (i.p.) administration of vanadium (1.5 mg kg71 b.wt) for a period of 12 consecutive days to rats. The increase in lipid peroxidation was inhibited by selenium treatment (0.02 mg kg71 b.wt., i.p.) for 12 consecutive days. Vanadium exposure produced a decrease in nonprotein sulfhydryl group. Selenium treatment prevented the depression in nonprotein sulfhydryl group in all the brain regions of the vanadium exposed rats. The concentration of ascorbic acid was decreased after co-administration of selenium and vanadium. These results suggest that selenium protects neuronal cells against neurotoxic effects of vanadium by maintaining the availability of antioxidant nonprotein sulfhydryl groups. The decrease in ascorbic acid levels may have been due to its consumption in forming complexes with vanadium.

Obesity is a chronic disease of multifactorial origin and resulted in perturbations of whole body metabolism in this study. It is thus likely that this imbalance was associated with an inhibition in protective antioxidants and occurrence of oxidative stress. The staging concept of sleeve gastrectomy is a safe and effective approach with remarkable efficacy in sustaining weight loss and bringing back normal metabolism of variables in tissues over a 1-year follow-up period.

Adult male rats were treated intraperitoneally with chloroquine (5 mg/kg/day) for 9 days. A reduction in the fasting plasma glucose level by 17.6% and ascorbic acid by 45% were discernable. The treatment caused significant increase in liver lactate dehydrogenase and glucose-6-phosphate dehydrogenase activities and reduced the activity of succinate dehydrogenase enzyme. Chloroquine also caused significant reductions in the contents of reduced glutathione and ascorbic acid in the brain and erythrocytes with a significant increase in lipid peroxidation.

: Guinea pigs were exposed to exhaust pollutant sulfur dioxide (10 ppm) one hour daily for 30 days and the effect was studied on the lipid profiles of the liver, heart, lung and kidney.The liver exhibited depletion of phospholipids, cholesterol and C/P ratio, but ganglioside contents diminished. Elevated levels of cholesterol, C/P ratio, total lipids and phospholipids were discernible in the heart, and interestingly ganglioside concentration decreased.On the other hand, the lung showed increased concentration of cholesterol, total lipids, C/P ratio, and gangliosides, however, phospholipid values decreased. Moreover, in the kidney, contents of all the lipid investigated were diminished.The rate of malonaldialdehyde formation enhanced significantly in the lung and the heart. However, the liver and kidney exhibited decreased lipid peroxidation.Results revealed SO2-intoxication enhanced lipid peroxidation in the heart and the lung by modification of lipids, however, in the liver and the kidney endogeneous lipid peroxidation was diminished.Other lipid fractions exhibited correlative findings.