Diclofenac and caffeine inhibit hepatic antioxidant enzymes in the freshwater fish Astyanax altiparanae (Teleostei: Characiformes)

Although concentrations of pharmaceutical compounds in aquatic ecosystems are low, they can cause toxic effects on organisms. The aim this study was to evaluate the diclofenac (DCF), a non-steroidal anti-inflammatory drug, and caffeine (CAF), central nervous system stimulant, both alone or combined, Astyanax altiparanae males under acute exposure (96 h), measuring neurotoxicity biomarkers, antioxidant response damage at biochemical cellular levels. DCF concentration water, separated 3.08 mg L ?1 that CAF 9.59 . To assess neurotoxicity, brain muscle acetylcholinesterase (AChE) activities were measured. oxidative stress, enzymatic superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) S-transferase (GST), as well lipoperoxidation (LPO), analyzed liver gills. Activity hepatic cyclooxygenase (COX) also evaluated. Genotoxicity assessed blood using comet assay micronucleus test, nuclear abnormalities. CAF, had neither effect AChE activity, nor activity SOD, CAT, GPx GST In liver, inhibited SOD CAT mixture activity; although only fish exposed showed increased LPO. Under these experimental conditions, no COX observed, cytotoxic genotoxic damage. most pronounced caused by drugs separately, since altered enzymes, but triggered LPO, showing more harmful effects. • Diclofenac enzymes A. Caffeine promoted did not genotoxicity gills defenses