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Tissue specificity in nickel uptake and induction of oxidative stress in kidney and spleen of goldfish Carassius auratus, exposed to waterborne nickel

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Kubrak, O. I. , Husak, V. V. , Rovenko, B. M. , Poigner, H. , Mazepa, M. A. , Kriews, M. , Abele, D. and Lushchak, V. I. (2012): Tissue specificity in nickel uptake and induction of oxidative stress in kidney and spleen of goldfish Carassius auratus, exposed to waterborne nickel , Aquatic Toxicology, 118-11 , pp. 88-96 .
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Abstract:

Toxic and carcinogenic effects of nickel compounds are suggested to result from nickel-mediated oxidative damage to macromolecules and/or inhibition of cellular antioxidant defenses. We investigated the effects of waterborne Ni2+ (10, 25 and 50 mg/L) on the blood and blood-producing tissues (kidney and spleen) of goldfish to identify relationships between Ni accumulation and oxidative stress. Whereas the main hematological parameters (total hemoglobin and hematocrit) were unaffected, Ni2+ exposure had substantial influence on goldfish immune system, causing lymphopenia. Ni accumulation increased renal iron content (by 49-78%) and resulted in elevated lipid peroxide (by 29%) and protein carbonyl content (by 274-278%), accompanied by suppression of the activities of superoxide dismutase (by 50-53%), glutathione peroxidase (15-45%), glutathione reductase (31-37%) and glucose-6-phosphate dehydrogenase (20-44%), indicating development of oxidative stress in kidney. In contrast to kidney, in spleen the activation of glutathione peroxidase (by 34-118%), glutathione-S-transferase (by 41-216%) and glutathione reductase (by 47%), as well as constant levels of low molecular mass thiols and metals together with enhanced activity of glucose-6-phosphate dehydrogenase (by 41-94%) speaks for a powerful antioxidant potential that counteracts Ni-induced ROS production. Further, as Ni accumulation in this organ was negligible, Ni-toxicity in spleen may be minimized by efficient exclusion of this otherwise toxic heavy metal.

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