Effect of melatonin on changes in hepatic antioxidant enzyme activities inrats treated with alpha-naphthylisothiocyanate

We have reported that melatonin protects against alpha -naphthylisothiocyan ate (ANIT)-induced acute liver injury in rats by preventing enhanced lipid peroxidation. Herein, we examine the effect of melatonin on hepatic antioxi dant enzyme activities in rats with a single i.p. injection of ANIT (75 mg/ kg body weight) in order to clarify the protective mechanism of the indolea mine against ANIT-induced acute liver injury. Rats received a single oral a dministration of melatonin (10 or 100 mg/kg body weight) at 12 hr after ANI T treatment. Hepatic Cu,Zn-superoxide dismutase (Cu,Zn-SOD), Mn-superoxide dismutase (Mn-SOD), catalase (CAT), Se-glutathione peroxidase (Se-GSH-Px), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6- PDH) activities and reduced glutathione (GSH) concentration were determined 12 and 24 hr after ANIT treatment. ANIT-treated rats showed decreases in h epatic Cu,Zn-SOD and GSSG-R activities at 24 hr after treatment. transient increases in hepatic CAT and Se-GSH-Px activities at 12 hr, and no changes in hepatic Mn-SOD and G-6-PDH activities at 12 or 24 hr. Only the high dose of melatonin attenuated the decrease in hepatic Cu,Zn-SOD activity, while both doses of the indoleamine almost completely attenuated the decrease in hepatic GSSG-R activity. Neither dose of melatonin affected hepatic CAT, Se -GSH-Px, and G-6-PDH activities. ANIT-treated rats showed an increase in he patic GSH concentration at 24 hr after treatment. Neither dose of melatonin affected the increase in hepatic GSH concentration. These results indicate that orally administered melatonin prevents decreases in Cu,Zn-SOD and GSS G-R activities in the liver of ANIT-treated rats. and suggest that the indo leamine may protect against ANIT-induced acute liver injury by attenuating the disruption of hepatic antioxidant defense systems.