Major distinctions in the antioxidant responses in liver and kidney of Cd(2+)-treated common carp (Cyprinus carpio).

This study is related to the accumulation of Cd(2+), its effects on oxidative stress biomarkers and its role in macromolecule damage in liver and kidney of common carp. We present evidence of an increased ratio of reduced to oxidized glutathione (GSH/GSSG) in both organs after 10 mg/L Cd(2+) exposure, with different underlying biological mechanisms and consequences. In the liver, the expressions and/or activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase increased to cope with the Cd(2+)-generated toxic effects during the first 48 h of treatment. In contrast, none of these selected antioxidant markers was significantly altered in the kidney, whereas the expression of glutathione synthetase was upregulated. These results suggest that the major defense mechanism provoked by Cd(2+) exposure involves the regeneration of GSH in the liver, while its de novo synthesis predominates in the kidney. High levels of accumulation of Cd(2+) and peroxynitrite anion (ONOO(-)) were detected in the kidney; the major consequences of ONOO(-) toxicity were enhanced lipid peroxidation and GSH depletion. The accumulation of ONOO(-) in the kidney suggests intensive production of NO and the development of nitrosative stress. In the liver the level of hydrogen peroxide was elevated.