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

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 metal.

► The effect of goldfish exposure for 96 h to 10, 25 and 50 mg/L of Ni2+ was studied. ► Nickel affects blood and blood-producing organs of Carassius auratus. ► Ni accumulation in kidney increases renal iron content and leads to oxidative stress. ► Ni2+ exposure resulted in antioxidant system activation in goldfish spleen.