The ability of diphenyl diselenide [(PhSe)2] to attenuate oxidative damage was evaluated in the liver, gills, brain, and muscle of carp (Cyprinus carpio) and silver catfish (Rhamdia quelen) experimentally exposed to fipronil (FPN). Initially, the fish were fed a diet without (PhSe)2 or a diet containing 3.0 mg/kg of (PhSe)2 for 60 days. After the 60-day period, the fish were exposed to 0.65 µg/L of FPN for 192 h. The results showed that carp exposed to FPN and not fed with (PhSe)2 exhibited acetylcholinesterase (AChE) inhibition in brain and muscle, and increased thiobarbituric acid-reactive substance (TBARS) in liver, gills, and brain. Furthermore, FPN decreased nonprotein thiols (NPSH) and δ-aminolevulinate dehydratase (δ-ALA-D) in carp liver and gills, and increased plasma glucose and protein levels. In silver catfish, FPN inhibited AChE and increased TBARS levels in muscle. In addition, glutathione S-transferase (GST) decreased in liver and muscle, and plasma glucose was increased. (PhSe)2 reversed some of these effects. It prevented the increase in TBARS levels in liver, gills, and brain in carp and in silver catfish muscle, and reversed the increase in plasma glucose levels in both species. Additionally, (PhSe)2 increased the NPSH levels in carp and silver catfish that had decreased in response to FPN exposure. However, (PhSe)2 was not effective in reversing the AChE inhibition in brain and muscle or the δ-ALA-D decrease in carp liver. Thus, (PhSe)2 protects tissues of both species of fish, mainly by preventing or counteracting the effects of FPN, on TBARS levels, antioxidants, and present anti-hyperglycemic property.
Keywords: Antioxidant; Fish; Oxidative stress; Pesticide; Selenium.