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

Abstract

Atlantic salmon (Salmo salar L.) parr were fed for one month on fish meal based 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 defence system. Cadmium accumulated significantly in the liver, intestine, and kidney of 204 mg Cd kg−1exposed fish compared to controls. Copper accumulated 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. Tissue Cu accumulation significantly increased intestinal and hepatic lipid peroxidation (as seen from thiobarbituric acid reactive substances, TBARS, levels) and subsequently decreased intestinal α-tocopherol levels and increased intestinal and hepatic selenium dependent glutathione peroxidase (SeGSH-Px) activity. Dietary Cd significantly reduced SeGSH-Px activity in the intestine and liver of 204 mg Cd kg−1 exposed fish compared to controls. No significant increase in tissue TBARS or reduction of α-tocopherol levels was observed in the intestine of fish exposed to dietary Cd, with exception of the highest exposure group (204 mg Cd kg−1). Dietary Cu caused depletion of tissue Se and glutathione levels, however the reduced availability of GSH and Se did not seem to explain the differences in SeGSH-Px activity. Dietary Cu had a direct effect on lipid peroxidation at a relatively low concentration (34 mg Cu kg−1). Cadmium indirectly affected tissue lipid peroxidation by damaging the oxidative defence system at the highest dietary concentration (204 mg Cd kg−1).