@entity2493 prevents @entity1499 -induced hepatorenal oxidative injury in XXXX .

@entity137 @entity26 @entity2041 @entity2493 @entity2197 @entity1234 @entity1500 @entity35 @entity1589 @entity1499 @entity1865
Regarding the mechanisms of @entity1499 ( @entity1500 ) hepatotoxicity and nephrotoxicity, several hypotheses have been put forward, among which oxidative stress (including depletion of @entity2041 ) is likely. This investigation elucidates the role of free radicals in @entity1500 -induced @entity137 and the protection by @entity2493 . @entity35 albino @entity35 were injected with @entity1500 intraperitoneally. Following a single dose of @entity1500 (20 mg/kg), either saline ( @entity1500 group) or @entity2493 (10 mg/kg, @entity1500 + Mel group) was administered for 5 days. In other @entity35 , physiologic saline (control group) or @entity2493 (10 mg/kg, Mel group) was injected for 5 days, following a single injection of saline. On the sixth day, @entity35 were killed to obtain blood, liver, and kidney tissue samples. @entity1234 ( @entity1865 ), an end product of lipid peroxidation, and @entity2041 ( @entity2197 ), a key antioxidant, levels were evaluated in blood and tissue homogenates. Reactive @entity26 metabolite-induced inflammatory changes in kidney and liver tissues were evaluated by measuring @entity1589 ( @entity1589 ) activity, an index of neutrophil infiltration. @entity1500 administration resulted in increased @entity1865 levels and @entity1589 activity and decreased @entity2197 levels in the blood, liver, and kidney whereas @entity2493 reversed these effects. When @entity2493 was administered alone, no significant changes in biochemical parameters were noted. In conclusion, the present study suggests that @entity2493 may be of therapeutic benefit when used with @entity1500 .
