Cadmium and nickel co‐exposure exacerbates genotoxicity and not oxido‐inflammatory stress in liver and kidney of rats: Protective role of omega‐3 fatty acid.

The present study examined the influence of co‐exposure to cadmium (Cd) and nickel (Ni) on hepatorenal function as well as the protective role of omega‐3 polyunsaturated fatty acids (ω‐3FA) in rats. The animals were exposed to Cd (5 mg/kg) and Ni (150 μg/L in drinking water) singly or co‐exposed to both metals and ω‐3FA at 20 mg/kg for 14 consecutive days. Results showed that hepatorenal injury resulting from individual exposure to Cd or Ni was not aggravated in the co‐exposure group. Moreover, ω‐3FA markedly abrogated the reduction in the antioxidant enzyme activities, the increase in reactive oxygen and nitrogen species, and lipid peroxidation induced by Cd and Ni co‐exposure. Additionally, ω‐3FA administration markedly suppressed the increase in hepatic and renal myeloperoxidase activity, nitric oxide, tumor necrosis factor alpha, and interleukin‐1 β levels in the co‐exposure group. Genotoxicity resulting from individual exposure to Cd or Ni was intensified in the co‐exposure group. However, ω‐3FA administration markedly ameliorated the genotoxicity and histological lesions in the co‐exposure group. Taken together, co‐exposure to Cd and Ni aggravated genotoxicity and not oxido‐inflammatory stress in the liver and kidney of rats. ω‐3FA abated hepatorenal injury and genotoxicity induced by Cd and Ni co‐exposure in rats. [ABSTRACT FROM AUTHOR]