Protective effect of captopril against cisplatin induced nephrotoxicity in rats

This study has been initiated to determine whether captopril, an angiotensin-converting enzyme [ACE] inhibitor containing sulfhydryl [-SH] group can protect against cisplatin-induced nephrotoxicity in rats. A single dose of cisplatin [7.5mg/kg bwt] injected i.p. caused a significant increase in blood urea nitrogen [BUN] and creatinine levels amounting to 402% and 573%, respectively with a marked elevation in lipid peroxides measured as malondialdehyde [MDA] content [54%], accompanied by a significant decrease in reduced glutathione [GSH] content [27%] of kidney tissue as compared to control group. In addition, there were marked increases in kidney tissue content of nitric oxide [NO] [43%] and plasma endothelin-1[ET-1] [37%]. On the other hand, administration of captopril [60mg/kg bwt, i.p.] 1 h before cisplatin protected the kidney as indicated by restoration of BUN, creatinine, MDA, GSH, NO and ET-1. These results indicate that captopril, an ACEI, has a protective effect against cisplatin-induced damage to kidney. This reflects the beneficial role of captopril in treatment of renovascular hypertention and congestive heart failure; an effect that may be related to its free radicals scavenging and antioxidant effects which are sulfhydryl dependent

Hesperidin, an antioxidant flavonoid, prevents acrylonitrile-induced oxidative stress in rat brain

Acrylonitrile [ACN] is a volatile, toxic liquid used as a monomer in the manufacture of synthetic rubber, styrene plastics, acrylic fiber and adhesives. ACN is a potent neurotoxin. A role for free radical-mediated lipid peroxidation in the toxicity of ACN has been suggested. We examined the ability of hesperidin, an antioxidant flavonoid, to attenuate ACN-induced alterations in lipid peroxidation in rat brains. The daily oral administration of ACN to male albino rats in a dose of 50 mg/kg bwt for a period of 28 days produced a significant elevation in brain lipid peroxides measured as malondialdehyde [MDA] amounting to 107%, accompanied by a marked decrease in brain reduced glutathione [GSH] content reaching 63%. In addition, ACN administration resulted in significant reductions in the enzymatic antioxidant parameters of brain; superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GSH-Px] and glutathione-S-transferase [GST] recording 43%, 64%, 52% and 43%, respectively. On the other hand, pretreatment with hesperidin and its co-administration with ACN once daily in a dose of 200 mg/kg bwt, i.p. for 28 days ameliorated ACN-induced alterations in brain lipid peroxidation. These results suggest that hesperidin may have a beneficial role against ACN-induced oxidative stress in brain; an effect that is mainly attributed to the antioxidant property of hesperidin