Protective Effects of Melatonin on CCl4-induced Acute Liver Damage and Testicular Toxicity in Rats

Effects of melatonin against carbon tetrachloride-induced acute liver and testicular toxicity in rats as well as the possible mechanisms were investigated in the present study. Rats were acclimatized and the serum levels of alanine aminotransferase, aspartate aminotransferase and reduced glutathione were measured. The malondialdehyde, superoxide dismutase, and reduced glutathione concentrations in the hepatic homogenate, and histopathological changes in rat liver and testes were also determined. Membrane potential was analysed with flow cytometry. The expression level of telomerase and caspase-3 were determined by reverse transcriptase polymerase chain reaction. Melatonin increased the content of serum reduced glutathione in rats with acute liver injury induced by carbon tetrachloride. The extent of malondialdehyde formation was reduced; superoxide dismutase activity and the reduced glutathione contents were increased in the hepatic homogenate in melatonin groups. Histopathological examination of rat liver and testicular sections confirmed the biochemical observations. Melatonin significantly restored the plasma membrane potential and decreased mRNA level of telomerase and caspase-3. These results indicated that melatonin exerted a significant protective effect against acute hepatotoxicity induced by carbon tetrachloride in rats, which might be due to free radical scavenging, inhibition of lipid peroxidation, increasing antioxidant activity as well as restoration plasma membrane potential. The expression of telomerase and caspase-3 might partially contribute to the protective effects on carbon tetrachloride-induced acute liver damage. Reduced glutathione content might also partially contribute to the protective effects of melatonin on the oxidative damage caused by carbon tetrachloride in rat testis.