POSSIBLE ROLE OF OXIDATIVE STRESS IN ACUTE CADMIUM HEPATOTOXICITY IN RATS

It is known that cadmium induces a variety of functional disorders, especially liver and kidney dysfunction. The main mechanism involved in cadmium hepatotoxicity is its binding to sulfhydryl groups and initiation of inflammation. Additionally, oxidative stress, due to a decrease in antioxidative capacity, plays a role in chronic cadmium hepatotoxicity. The role of oxidative stress in acute cadmium intoxication is still not clear. The aim of our study was to investigate the role of reactive oxygen species and efficiency of antioxidant protection in rat liver in acute cadmium intoxication. Male Wistar rats (n=16) were divided into the following groups: 1. control group (n=7), treated with saline, 2. cadmium-treated (n=9) with a single dose of 2.5 mg/kg intraperitoneally. After administration (24 hours), blood samples from the right side of the heart and liver samples were collected for the determination of oxidative stress parameters. In our study malondialdehyde concentration was elevated both in plasma and liver after cadmium administration (p<0.01). Moreover, superoxide dismutase activity was increased in the cadmium-treated group, mainly due to increasean in copper/zinc superoxide dismutase activity (p<0.01). Reduced glutathione level in liver and plasma and concentration of sulfhydryl groups were not significantly changed by cadmium. The present study suggests that lipid peroxidation plays an important role in acute cadmium-induced liver injury. Antioxidant capacity of hepatocytes is partly increased due to an adaptive increase of superoxide dismutase activity.