[The role of NO-dependent mechanisms in melatonin antioxidant activity during hepatic ischemia-reperfusion in rats].

The antioxidant effect of melatonin on the blood oxygen transport and prooxidant-antioxidant balance during with hepatic ischemia-reperfusion (HIR) with inhibited NO synthase function has been studied in male Wistar rats. The animals were divided into 4 groups: (1) control; (2) hepatic ischemia (Pringle m., 30 min) and reperfusion for 120 min (HIR, n = 9); (9) HIR with melatonin (10 mg/kg, i.p., 10 min before HIR, n = 9); and (4) same with NO inhibitor (L-NAME, 10 mg/kg) added 5 min before melatonin administration. The indices of blood oxygen transport (p50act, pCO2, pH, pO2, etc.) and prooxidant-antioxidant balance (Schiff bases, conjugated dienes, catalase, retinol, alpha-tocopherol) were measured in blood and liver. HIR in group 1 resulted in higher p50act in mixed venous blood and sever oxidative disturbances: rise of CD and SB, decrease of alpha-T, Ret, and Cat. Melatonin in group 3 significantly improved these changes in p50act and prooxidant-antioxidant balance during HIR, but L-NAME in group 4 partly eliminated this effect. It is concluded that the antioxidant effect of melatonin during HIR is partly associated with NO-depended mechanisms, which can modify blood hemoglobin affinity to oxygen, thus limiting oxygen binding in free-radical processes.