Investigation of cytotoxic effects of di(2-ethylhexyl) phtalate on primary hepatocytes of rainbow trout (Oncorhyncus mykiss)

Di(2-ethylhexyl) phtalate (DEHP) is a widely used plasticizer. In the present study, primary cultured hepatocytes of rainbow trout (Oncorhyncus mykiss) were exposed to DEHP (0, 25, 50, 100 and 200 µM) for 24 hours and cytotoxic effects were investigated using lactate dehydrogenase (LDH) release and antioxidant defense system biomarkers. According to the results, DEHP caused significant LDH release at concentrations of 50, 100 and 200 µM. Superoxide dismutase (SOD) activity increased significantly at 25 µM DEHP concentration whereas its activity was significantly decreased at 100 µM DEHP concentration. Activity of catalase (CAT) was significantly increased in all concentrations of DEHP while a simultaneous decrease in CAT activity with SOD activity was observed at 100 µM concentration of DEHP. Glutathione peroxidase activity was determined to be increased in all concentrations of DEHP. Levels of reduced glutathione elevated at 50 and 200 µM of DEHP concentrations. Glutathione-S-transferase (GST) activity remained unchanged at 25, 50 and 100 µM concentrations, whereas a significant increase in GST activity was observed at 200 µM treated hepatocytes. The results suggest that DEHP cytotoxicity is involved in antioxidant responses in hepatocytes. The study will offer insight into the mechanism of DEHP-induced cytotoxicity.