Oxidative stress biomarkers, biochemical responses and Na+ -K+ -ATPase activities in Nile tilapia, Oreochromis niloticus exposed to diclofenac.

The residues and metabolites from pharmaceuticals have been noted to cause adverse effects to both target and non-target aquatic organisms. The sublethal effects of diclofenac at 0.17, 0.34 and 0.68 mg L-1 on oxidative stress biomarkers, biochemical responses and Na+ -K+ -ATPase activities in the gill tissue of Nile tilapia, Oreochromis niloticus were investigated for 60 days. Elevated levels of some serum biochemical parameters including protein, glutamic oxalacetic transaminase, glucose, glutamic pyruvic transaminase, lactate dehydrogenase, alkaline phosphatase and also some catalysts of gluconeogenic enzymes such as glucose-6-phosphatase, fructose 1, 6 bisphosphatase in the fish liver, increase as the concentration of the diclofenac increased. The reactions of glutathione-S-transferase, catalase, lipid peroxidation, superoxide dismutase, glutathione peroxidase, carbonyl protein and reduced glutathione were elevated (p < 0.05) while the activities of Na+ -K+ -ATPase was significantly reduced (p < 0.05) in fish gill, indicating an adaptive response strategies to mitigate the impact of the drug on the exposed fish. Chronic exposure to sublethal diclofenac can induce oxidative stress and modulates serum biochemical indexes of O. niloticus, suggesting the need for close monitoring of the drug and their metabolites in aquatic environment considering the possible potential adverse effects it may cause even to non-target organisms.