Cobalt ions can enhance the generation of reactive oxygen species (ROS), which may be the reason for cobalt toxicity. This study aimed to determine whether Co 2+ toxicity in goldfish is related to induced oxidative stress in gills, heart and spleen, and to assess responses of antioxidant systems. Exposure of goldfish to 50, 100 and 150 mg L -1 of Co 2+ for 96 h elevated total hemoglobin in blood by 23, 44 and 78%, respectively. In gills, cobalt exposure enhanced lipid peroxide levels and activities of primary antioxidant enzymes; superoxide dismutase (SOD) rose by 125% and glutathione peroxidase (GPx) increased by 53-296%. Glutathione-S- transferase (GST) activity also increased by 117-157% and glucose-6-phosphate dehydrogenase (G6PDH) enhanced by 46-96%. Heart showed limited effects of fish exposure to 50 or 100 mg L -1 of Co 2+, but the exposure to 150 mg L -1 of Co 2+ elevated concentrations of lipid peroxides by 123% and activities of GPx by 98% and SOD by 208%. The most substantial effects of goldfish exposure to Co 2+ were observed in spleen: a decrease in total protein concentration by 44-60% and high molecular mass thiols by 59-82%, reduced activities of catalase by 24-58% and GR by 25-68%, whereas the level of low molecular mass thiols increased by 153-279% and activities of GPx, GST, G6PDH were enhanced by 114-120%, 192-769%, and 256-581%, respectively. The data show that fish exposure to 50-150 mg L -1 of Co 2+ elevates blood hemoglobin level, mimicking effects of hypoxia, and causes the activation of defense systems against ROS.

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Keywords Antioxidant enzymes, Cobalt, Goldfish, Hemoglobin, Lipid peroxides, Reactive oxygen species, Toxicity
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Journal Comparative Biochemistry and Physiology - C Toxicology and Pharmacology
Kubrak, O.I. (Olga I.), Rovenko, B.M. (Bohdana M.), Husak, V.V. (Viktor V.), Vasylkiv, O.Y. (Olena Yu.), Storey, K, Storey, J, & Lushchak, V.I. (Volodymyr I.). (2012). Goldfish exposure to cobalt enhances hemoglobin level and triggers tissue-specific elevation of antioxidant defenses in gills, heart and spleen. Comparative Biochemistry and Physiology - C Toxicology and Pharmacology, 155(2), 325–332. doi:10.1016/j.cbpc.2011.09.012