Anti-oxidative status and hepatic enzymes following acute administration of diethyl phthalate in olive flounder Paralichthys olivaceus, a marine culture fish.

Although diethyl phthalate (DEP) is one of the most frequently used phthalates in solvents and fixatives for numerous industrial products, almost no research has been done on its biochemical toxicity in aquatic animals. Olive flounder (Paralichthys olivaceus), an important culture fish in far eastern Asian countries, were treated with intraperitoneal DEP at 0, 100, 300 or 900 mg/kg for three consecutive days and biochemical effects were assessed in the liver, kidney and serum 24 h after the final dosing. Measured parameters were mostly restricted to oxidative status and toxicity of the organs. In the hepatic tissue, there were significant increases in lipid peroxide (LPO) at 100mg/kg and above. Other hepatic parameters, which were examined, changed only after 900 mg/kg: reduced glutathione content (GSH), glutathione reductase activity (GR), glutathione peroxidase (GPx) activity increased; catalase (CAT) activity decreased. DEP also induced elevation in LPO levels at above 100 mg/kg in renal tissues; however, there was only a decrease in GR and glutathione S-transferase (GST) activities with DEP 900 mg/kg in contrast to the liver. Enzyme activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in hepatic tissues decreased in a dose-dependent manner in response to DEP at above 300 mg/kg. DEP at 300-900 mg/kg, although not uniform among parameters, caused increases in serum alkaline phosphatase (ALP), lactate dehydrogenase (LDH), AST, ALT activities and osmolality value, suggesting that DEP at these doses induced hepatic cell damage. The results indicate that 100-900 mg/kg DEP induced oxidative stress and the fish seemed to activate compensatory anti-oxidant systems to cope with the imposed substance on the liver. Such compensatory activation was not evident in the kidney. Overall, DEP was only weakly toxic to olive flounder in terms of oxidative and hepatic damage. Copyright (c) 2010 Elsevier Inc. All rights reserved.