This study aims to investigate the role of oxidants in cisplatin-induced nephrotoxicity. Cisplatin was administered intraperitoneally (i.p.) in a single dose (5 mg/kg) and guinea pigs were killed either after 24 h or 7 days. The same experiment was performed using animals treated with vitamins C and E combination and a natural antioxidant extract (SARMEX). The kidneys were then removed to be used in the analyses. Blood samples were also obtained from the animals to be used in routine biochemical assays. Twenty-four hours after treatment there was a significant decrease in the renal activities of total superoxide scavenger activity (TSSA), superoxide dismutase (SOD) and catalase (CAT) accompanied by a rise in malondialdehyde (MDA) levels. After 7 days, the fall in kidney enzymatic activities was far greater, while the increase in blood urea (BUN) and creatinine (CRE) was marked. Treatment with antioxidants causes significant increases in renal TSSA (7 day), non-enzymatic superoxide scavenger activity (NSSA) (24 h and 7 day) and SOD (7 day) activities, does not change glutathione peroxidase (GSH-Px) activity and decreases renal MDA (24 h and 7 day), blood BUN (7 day) and CRE (7 day) levels. Our results suggest that cisplatin treatment impairs both enzymatic and non-enzymatic antioxidant systems and causes peroxidation in the renal tissue, which leads to kidney failure. Antioxidant supplementation strengthens the renal antioxidant system, eliminates oxidation reactions, and prevents cisplatin-induced kidney failure.

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In this study, the effects of cigarettes with differing tar content on erythrocyte oxidant/antioxidant status was investigated. Malondialdehyde (MDA) as an indicator of oxidant status and superoxide radical scavenger activity (SSA) as an indicator of antioxidant status were measured in erythrocytes from 20 smokers and 10 non-smoker controls. Ten of the 20 smoking subjects smoked five cigarettes with full flavour low tar (FFLT with 12 mg tar) and the others smoked five cigarettes with full flavour high tar (FF with 23 mg tar) over 1 hour. Initial blood samples from both groups at fasting, followed by further samples from smokers at 1.5 hours and 3 hours after smoking. Initial erythrocyte MDA level and SSA activity were found to be higher in the smoking groups compared to non-smokers. Furthermore, both parameters were significantly higher at the 1.5-hour and 3-hour erythrocyte samples when compared to initial values in the FFLT group. However, there were no statistically significant differences between SSA values established at different times in FF group. Results suggest that smoking causes oxidant load in the erythrocytes. Although a compensatory mechanism (i.e. increased SSA activities) develops in the FFLT group after smoking, this cannot prevent peroxidation reactions (i.e. increased MDA levels) in the erythrocytes. As to the types of cigarettes, both seem to have oxidant potential, but oxidation degree in the FFLT group is higher than that of FF group. These results suggest that antioxidant supplementation to smokers might be beneficial to decrease cellular oxidation damages.

Activities of adenosine deaminase (ADA), 5'nucleotidase (5'NT), xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) and levels of thiobarbituric acid reagent substances (TBARS) were measured in 10 cancerous and 10 noncancerous human prostate tissues. Decreased activities of DNA turnover enzymes (ADA and 5'NT), increased activities of GSH-Px and CAT, and unchanged activities of SOD and XO were observed in cancerous prostate tissues compared with those of noncancerous ones. TBARS levels were found to be higher in cancerous tissues than noncancerous ones. In correlation analysis, mostly positive correlations were established between enzyme activities of the cancerous tissues, whereas no meaningful correlations were found between enzyme activities of the noncancerous tissues except for a positive correlation between XO and SOD. The results indicate that the activities of DNA turnover enzymes were reduced, which was possibly an attempt to lower the rate of purine catabolism, and the activities of GSH-Px and CAT enzymes were increased, probably in response to increased free radical stress occurring in cancerous prostate tissues. Increased concentrations of TBARS suggested oxidant stress and thus accelerated peroxidative reactions in the cancerous tissues, even though antioxidant defense mechanisms were activated. These findings suggest that enzymatic antioxidant systems of cancerous prostate tissues cannot sufficiently eliminate oxidant factors and prevent cellular peroxidative reactions occurring during the carcinogenic process.

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