Investigation of oxidan/antioxidant status treated with CCl4 in rat kidney tissues

To investigate the free radical metabolysing enzyme activities such as SOD, CAT, GSH-Px and GST and as known index of lipid peroxidation, thiobarbituric acid rective substances (TBARS) and free radical scavenger properties of stobadine were studied treated by CCl4 in rat kidney tissues.Forty male Wistar-Albino rats weighing approximately 250-300 grams were used in the study. The rats were randomly divided into equal 4 groups such as Control (K), Stobadine (S), Carbon tetrachloride (C) and Stobodine+ CCl4(C+S)CCl4 was given intraperitionealy in sequentially increasing doses 0.3, 0.7 and 1.0mL/kg body weight for 8 weeks period. Stobadine treatment was applied orally at 3 dose/week 24.7 mg/kg/day for 8 week priods. The animals were sacrificed after 8 week of treatment and kidney tissues were removed.The level of TBARS as a lipid peroxidation index was measured in kidney homogenates. Also, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione-S-transferase (GST) in kidney tissues were determined.In CCl4-treated group, the level of TBARS was significantly increased (p<0.05) compared to controls. The enzyme activities of SOD, CAT and GSH-Px in kidney were significantly decreased (p<0.001, p<0.01 and p<0.01 respectively), but GST activities were significantly elevated (p<0.025) in comparison with controls.While SOD activities were significantly decreased (p<0.025) GST activities and TBARS levels were significantly elevated (p<0.01 and p<0.05 respectively) in stobadine group versus controls. However no meaningfull differences were found CAT and GSH-Px activities.In CCl4+Stobadine -treated group, the changes in the levels of TBARS and GST activities were significantly increased (p<0.05, p<0.05 and p<0.001 respectively) compared to controls, but SOD and GSH-Px activities were significantly lowered (p<0.001and p<0.005). No meaningfull differences were found CAT activities.Oxidative stress may be a major mechanism for the toxicity of CCl4. Stobadine served a protective effect against CCl4 toxicity by histopathologically, in contrast increased the lipid peroxidation. These results suggest that the protective effects of stobadine against CCl4 toxicity in kidneys is due at least partly to its antioxidant properties, scavenging CCl4 associated free radicals. Additional kinetic research may be necessary to determine effects of the stobadine on the antioxidant enzymes activities via carbon tetrachloride exposure.