and the activities of antioxidant enzymes in rat kidneys

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group 11, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and superoxide dismutase (SOD) levels were found to be significantly decreased (P 0.05). In the desferrioxamine (P 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine

Effect of amifostine pre-treatment against adriamycin-induced lipid peroxidation in rat heart

To investigate the effect of amifostine (AMI, WR-2721) against lipid peroxidation caused by adriamycin in rat heart tissue, male Wistar rats, weighing 190-220 g, were divided into three groups and treated as follows: 1) vehicle (saline) control (n = 6); 2) Adriamycin (10 mg/kg, intraperitoneally) (n = 6); 3) Adriamycin plus amifostine (200 mg/kg) (n = 6). Amifostine was applicated to rats 30 minutes previously from Adriamycin application. Rats were sacrificed on third day after drug application and hearts were removed. The hearts were washed with cold saline solution and were stored at -20°C until analysed. The tissues were thawed and homogenised with an Ultra Turrax. Lipid peroxidation was assayed as the malondialdehyde (MDA) levels reacting with thiobarbituric acid, according to the method of Ohkawa. Tissue MDA levels were significantly increased by adriamycin (p<0.05). MDA levels were 168±15 nmol/g wt in the control group. Adriamycin increased the MDA levels to 212±34 nmol/g wt. In the adriamycin plus AMI group, the heart tissue MDA levels were not different from the control levels (156±31 nmol/g wt). This study showed that the MDA levels were not increased if AMI were given previously Adriamycin in rats. AMI can reduce adriamycin induced cardiotoxicity and may be protective for adriamycin induced free radical damage in the heart tissues. So we suggest that the protective effect of AMI pretreatment on ADR heart toxicity should be evaluated extensively