Oxidative stress in gill, erythrocytes, liver and kidney of Nile tilapia (Oreochromis niloticus) from a polluted site

Abstract

A comparison between some pro- and antioxidant parameters in erythrocyte, gill, liver and kidney of Nile tilapia, O. niloticus from a fish farm (Control group) and from a polluted site in the Billings Reservoir (Reservoir group) was done. No hematological alterations were observed in blood of Billings fish. The erythrocyte oxidative stress was characterized by increased oxygen uptake and decreased induction time (induced by t-butyl hydroperoxide, t-BHP) evidencing a higher susceptibility to oxidative damage. Moreover, beside the augmented erythrocyte superoxide dismutase (SOD), glucose-6-phosphate dehydrogenase (G6PDH) and glutathione peroxidase activities, a decrease in both catalase (CAT) activity and total glutathione content (GSH), in erythrocytes of Reservoir fish was observed. The higher cytochrome b5 levels observed in the gill microsomal fraction is likely to be the cause of the enhanced oxyradical production. This fact, associated with the diminished CAT and G6PDH activities, accounts for a gill oxidative stress of Reservoir fish. Except for the NADPH-cytochrome P-450 (c) reductase activity, the other liver pro-oxidant parameters were greatly increased in the Reservoir fish. These results together with the increase in SOD activity and decrease in CAT, glutathione reductase (GR) and G6PDH activities indicated a liver oxidative stress status. The observed increases in kidney NADH cytochrome c reductase and in both cytochromes P-450 and b5 contents were not reflected in enhanced oxyradical production, suggesting a well coupled P-450 catalytic cycle in this tissue. However, the antioxidant enzymes had a similar pattern in liver. The decrease in GSH observed in kidney is probably associated with conjugation reactions for subsequent excretion. All these results furnish useful data for future investigations of polluted aquatic sites in order to provide a data base relating the presence of pollutants to biological effects at a molecular level.