title: 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 B₁₂), 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 Co²⁺ in aquarium water (administered as CoCl₂). 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 Co²⁺) and liver (30-66% increases after exposure to 50-150 mg L⁻¹ Co²⁺), 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 Co²⁺ 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 Co²⁺ ions results in the development of oxidative stress and the activation of defense systems in different goldfish tissues.
authors.affiliation: Department of Biochemistry and Biotechnology, Precarpathian National University named after Vassyl Stefanyk, Ivano-Frankivsk 76025, Ukraine.
authors.forename: Olha I
authors.initials: OI
authors.lastname: Kubrak
authors.forename: Viktor V
authors.initials: VV
authors.lastname: Husak
authors.forename: Bohdana M
authors.initials: BM
authors.lastname: Rovenko
authors.forename: Janet M
authors.initials: JM
authors.lastname: Storey
authors.forename: Kenneth B
authors.initials: KB
authors.lastname: Storey
authors.forename: Volodymyr I
authors.initials: VI
authors.lastname: Lushchak
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D003035:Cobalt / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D054750:Ecotoxicology / Q000379:methods*; D004785:Environmental Pollutants / Q000633:toxicity*; D006054:Goldfish / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D009928:Organ Specificity / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation / Q000187:drug effects; D013438:Sulfhydryl Compounds / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D004785:Environmental Pollutants; D013438:Sulfhydryl Compounds; D003035:Cobalt