Hepatotoxic evaluation in di-ethyl phthalate (DEP)-exposed goldfish

The extensive use of di-ethyl phthalate (DEP) as a plasticizer in plastic products, is a major threat to organisms as it leaches out easily from the plastic matrix into the environment. In this study, we evaluated the hepatotoxicity in goldfish (Carassius auratus) upon treatment with DEP. The 96 hr acute DEP LC50 value was determined as > 4 mg/L, using probit analysis. Three sub-lethal concentrations, 1/5th, 1/10th & 1/20th of DEP LC50 were used for 7 and 14 days. Blood and liver samples were taken out, following liver perfusion with saline, homogenates were made. In this study, the content of lipid peroxidation (LPO/MDA) as a marker for membrane disorders, content of carbonylated proteins (CP), and the levels of ALT and AST (as hepatic necrosis markers) were increased in the liver of DEP-treated fish. Meanwhile, the total antioxidant capacity (TAC) was found to be lowered in liver homogentes. In brief, DEP caused hepatotoxicity in fish through induction of oxidative stress followed by cell membrane instability.