Tissue lipid peroxidative responses in Atlantic salmon (Salmo salar L.) parr fed high levels of dietary copper and cadmium

Atlantic salmon (Salmo salar L.) parr were fed for one month on fish meal b ased diets supplemented with Cd (0, 0.7, or 204 mg Cd kg(-1) DW) or Cu (0, 34, or 691 mg Cu kg(-1) DW) to assess the effects of non-essential (Cd) and essential (Cu) dietary metals on lipid peroxidation and the oxidative defe nce system. Cadmium accumulated significantly in the liver, intestine, and kidney of 204 mg Cd kg(-1) exposed fish compared to controls. Copper accumu lated significantly in the intestine, kidney, and liver of fish exposed to 691 mg Cu kg(-1), and in the intestine of 34 mg Cu kg(-1) exposed fish. Tis sue Cu accumulation significantly increased intestinal and hepatic lipid pe roxidation (as seen from thiobarbituric acid reactive substances, TBARS, le vels) and subsequently decreased intestinal alpha -tocopherol levels and in creased intestinal and hepatic selenium dependent glutathione peroxidase (S eGSH-Px) activity. Dietary Cd significantly reduced SeGSH-Px activity in th e intestine and liver of 204 mg Cd kg(-1) exposed fish compared to controls . No significant increase in tissue TBARS or reduction of alpha -tocopherol levels was observed in the intestine of fish exposed to dietary Cd, with e xception of the highest exposure group (204 mg Cd kg(-1)). Dietary Cu cause d depletion of tissue Se and glutathione levels, however the reduced availa bility of GSH and Se did not seem to explain the differences in SeGSH-Px ac tivity. Dietary Cu had a direct effect on lipid peroxidation at a relativel y low concentration (34 mg Cu kg(-1)). Cadmium indirectly affected tissue l ipid peroxidation by damaging the oxidative defence system at the highest d ietary concentration (204 mg Cd kg(-1)).