Dimethoate-induced oxidative stress and DNA damage in Oncorhynchus mykiss.

The present study was conducted in order to investigate pro-oxidant activity of dimethoate in liver and brain tissues following sublethal pesticide exposure for 5, 15 and 30 d by using SOD, GPx, CAT enzyme activities and lipid peroxidation as biomarkers as well as DNA damaging potential via detecting% Tail DNA, Tail moment and Olive tail moment as endpoints in erythrocytes of Oncorhynchus mykiss in an in vitro experiment. Antioxidant enzyme activities were found to elicit two staged response which was an initial induction followed by a sharp inhibition in liver tissue while a sustained increase in GPx activity and slight stimulation in SOD activity were detected in brain tissue. Lipid peroxidation showed an ascending pattern throughout the exposure period in both tissues and a decreasing trend was determined in tissue protein levels which was proved to be positively correlated with duration. Similar findings were obtained from outcomes preferred to quantify DNA damage and TM was decided to reflect the extent of damage more sensitively because of determined positive correlation with concentrations applied. Considering these results, it can be concluded that oxidative stress condition evoked by dimethoate could not be responded effectively and genotoxic nature of pesticide was proven by determined clastogenic effect possibly via being an alkylation agent or stimulating the production of reactive species.