Cobalt-induced oxidative stress in brain, liver and kidney of goldfish Carassius auratus

Abstract

Cobalt is an essential element, but at high concentrations it is toxic. In addition to its well-known function as an integral part of cobalamin (vitamin B 12), cobalt has recently been shown to be a mimetic of hypoxia and a stimulator of the production of reactive oxygen species. The present study investigated the responses of goldfish, Carassius auratus, to 96 h exposure to 50, 100 or 150 mg L −1 Co 2+ in aquarium water (administered as CoCl 2). The concentrations of cobalt in aquaria did not change during fish exposure. Exposure to cobalt resulted in increased levels of lipid peroxides in brain (a 111% increase after exposure to 150 mg L −1 Co 2+) and liver (30–66% increases after exposure to 50–150 mg L −1 Co 2+), whereas the content of protein carbonyls rose only in kidney (by 112%) after exposure to 150 mg L −1 cobalt. Low molecular mass thiols were depleted by 24–41% in brain in response to cobalt treatment. The activities of primary antioxidant enzymes, superoxide dismutase (SOD) and catalase, were substantially suppressed in brain and liver as a result of Co 2+ exposure, whereas in kidney catalase activity was unchanged and SOD activity increased. The activities of glutathione-related enzymes, glutathione peroxidase and glutathione-S-transferase, did not change as a result of cobalt exposure, but glutathione reductase activity increased by ∼40% and ∼70% in brain and kidney, respectively. Taken together, these data show that exposure of fish to Co 2+ ions results in the development of oxidative stress and the activation of defense systems in different goldfish tissues.