Sublethal diclofenac induced oxidative stress, neurotoxicity, molecular responses and alters energy metabolism proteins in Nile tilapia, Oreochromis niloticus.

Abstract

Reports have shown that residues of pharmaceuticals and their metabolites can pose toxicological threats to organisms living in aquatic ecosystem. Nile tilapia, Oreochromis niloticus, was exposed at 0.17, 0.34, and 0.68 mg L-1 of diclofenac up to 60 days in a renewal static bioassay system. Antioxidant enzymes reactions, molecular responses, activities of energy metabolism proteins, and the neurotoxic potentials of the drug in the brain and fish muscle were evaluated. Antioxidant enzyme activities such as superoxide dismutase, glutathione-S-transferase, and also fructose 1, 6 bisphosphatase and glucose-6-phosphate dehydrogenase as well as the levels of lipid peroxidation and protein carbonyl were elevated, while glutathione peroxidase, total reduced glutathione, and acetylcholinesterase in the brain and muscles of the treated groups were significantly inhibited in a dose-dependent association. Expression of superoxide dismutase (sod), catalase (cat), and heat shock proteins (hsp 70) genes in brain and muscle tissues was up-regulated. Continuous treatment with sublethal diclofenac for a long time can induce oxidative imbalance, cause neurotoxicity, and alter the expression of genes related to stress in Nile tilapia, suggesting the use of these biomarkers in monitoring the adverse effects the pharmaceuticals could cause to organisms in aquatic ecosystem for possible mitigation.