Fenpropathrin Induces Oxidative Stress, Inhibits Cholinesterase, and Causes Genotoxicity in <i>Pethia conchonius</i> (Hamilton, 1822)

Abstract

Pesticide contamination in water bodies is a serious threat to aquatic organisms. Among the new generation pesticides, synthetic pyrethroids enter the aquatic environment from agricultural runoff and are more persistent in aquatic environment. In this study, we investigated the effect of fenpropathrin, a type II pyrethroid, on Pethia conchonius. The median lethal concentration for commercial formulation of fenpropathrin (Danitol®) was determined to be 2.43 μg/L. Based on the median lethal concentration, the fish were exposed to 1/5th (0.486 μg/L) and 1/10th (0.243 μg/L) of median lethal concentrations for 30 days. After the exposure period, antioxidant enzymes status (superoxide dismutase and catalase), oxidative stress parameters (lipid peroxidation and reduced glutathione) in brain, liver, and kidney, cholinesterase enzyme activity in brain and muscles, and incidences of micronucleus were evaluated. In the treatment groups, alteration in antioxidant enzyme levels were observed in brain, liver, and kidney. Lipid peroxidation, which is indicative of oxidative stress, was observed but did not show much variation. Reduced glutathione was also altered. Cholinesterase activity was significantly different in the brain tissues between control and treatment groups; however, no significant difference was observed between the cholinesterase activities of muscles in control and treatment groups. Micronucleus incidence in treatment groups was higher than that in the control. Our study indicates that fenpropathrin altered the antioxidative enzyme status, inhibited cholinesterase activity in brain, and exhibited potential genotoxic effects in the fish Pethia conchonius.