Nickel induces hyperglycemia and glycogenolysis and affects the antioxidant system in liver and white muscle of goldfish Carassius auratus L

• Published in: Ecotoxicology and environmental safety 2012-06, Vol.80, p.231-237
• Main Authors: Kubrak, Olga I., Rovenko, Bohdana M., Husak, Viktor V., Storey, Janet M., Storey, Kenneth B., Lushchak, Volodymyr I.
• Format: Article
• Language: English
• Subjects: Animal and plant ecology; Animal, plant and microbial ecology; Animals; Antioxidant enzymes; antioxidants; Applied ecology; Biological and medical sciences; blood glucose; Carassius auratus; Catalase; Catalase - metabolism; Ecotoxicology, biological effects of pollution; enzyme activity; Fish; Fish Diseases - chemically induced; Fish Diseases - metabolism; Fresh water ecosystems; Fundamental and applied biological sciences. Psychology; General aspects; glucose-6-phosphate 1-dehydrogenase; Glucosephosphate Dehydrogenase - metabolism; Glutathione; glutathione peroxidase; Glutathione Peroxidase - metabolism; Glutathione Reductase - metabolism; glutathione-disulfide reductase; Glycogenolysis; Glycogenolysis - drug effects; Goldfish; Hyperglycemia; Hyperglycemia - chemically induced; Hyperglycemia - metabolism; Hyperglycemia - veterinary; Kidney - drug effects; Kidney - enzymology; Kidney - metabolism; Lipid Peroxides - metabolism; Lipids; Liver; Liver - drug effects; Liver - enzymology; Liver - metabolism; mammals; Muscles; Muscles - drug effects; Muscles - enzymology; Muscles - metabolism; NADP (coenzyme); Nickel; Nickel - toxicity; Oxidative Stress - physiology; peroxides; proteins; superoxide dismutase; Superoxide Dismutase - metabolism; Synecology; Water Pollutants, Chemical - toxicity
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2012.03.006

The toxicity of nickel to mammals is well studied, whereas information on nickel effects on fish is scant. Goldfish exposure to 10–50mgL−1 of waterborne Ni2+ for 96h showed reduced glycogen levels by 27–33% and 37–40% in liver and white muscle, respectively, accompanied by substantial increases in blood glucose levels (by 15–99%). However, indices of oxidative damage to proteins (carbonyl proteins) and lipids (lipid peroxides) were largely unaffected by nickel exposure. In liver, the activities of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPx), were not affected by Ni2+ treatment, while catalase activity was elevated by 26%. In white muscle, however, substantial increases in SOD (by 38–147%) and GPx (by 2.5–5.5-fold) activities appeared to compensate for decreased catalase activity (by 59–69%) in order to resist Ni-induced oxidative perturbations. Both hepatic and muscular glutathione reductase activities were suppressed by 10–30% and 12–21%, respectively, after goldfish exposure to all Ni2+ concentrations used. However, the activity of glucose-6-phosphate dehydrogenase was remarkably enhanced (by 1.6–5.4-fold) in white muscle of Ni-exposed fish, indicating a strong potential increase in NADPH production under Ni exposure. Thus, the exposure of goldfish to 10–50mgL−1 of Ni2+ for 96h induces glycogenolysis and hyperglycemia, showing some similarities with a hypoxia response, and leads to a substantial activation of defense systems against reactive oxygen species in liver and white muscle in tissue-specific and concentration-dependent manner. Goldfish exposure to 10–50mgL−1 of Ni2+ for 96h induces glycogenolysis and hyperglycemia, showing some similarities with hypoxia response, and leads to a substantial activation of defense systems against reactive oxygen species liver and white muscle in tissue-specific and concentration-dependent manner. [Display omitted] ► Data are presented as means±S.E.M, n=5–6. ⁎Significantly different from the control group with P