Cadmium induced hepatotoxicity in chickens (Gallus domesticus) and ameliorative effect by selenium

•Cd induced significant reduction in chicken hepatic function and histopathological changes.•The level of Cd accumulated in chicken liver could been reduced by dietary Se.•Cd induced oxidative stress and increased the LPO and NO production in chicken liver.•Cd increased significantly the numbers of apoptotic cells in chicken liver.•Se may have ameliorative effects on these disturbances caused by Cd.

Cadmium (Cd) is one of the most toxic metal compounds released into the environment. It was well known that Cd induced hepatotoxicity in animal models. However, little is known about the negative effects of Cd toxicity in the liver of birds. To investigate the Cd hepatotoxicity in birds and the protective effects of selenium (Se) against subchronic exposure to dietary Cd, 100-day-old cocks received either Se (as 10 mg Na2SeO3 per kg of diet), Cd (as 150 mg CdCl2 per kg of diet) or Cd+Se in their diets for 60 days. Histological and ultrastructural changes in the liver, the concentrations of Cd and Se, the lipid peroxidation (LPO) and nitric oxide (NO) production, the activities of the antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx), nitric oxide synthase (NOS) activities and apoptosis were determined. Exposure to Cd significantly reduced SOD and GPx activity, Se content in the liver tissue. It increased the LPO and NO production, the numbers of apoptotic cells and Cd concentration and caused obvious histopathological changes in the liver. Concurrent treatment with Se reduced the Cd-induced liver histopathological changes, oxidative stress, overexpression of NO and apoptosis, suggesting that the toxic effects of Cd on the liver is partly ameliorated by inorganic Se. Se supplementation also modified the distribution of Cd in the liver.