Effects of acute di-n-butyl phthalate administration on oxidative stress parameters

Di-n-butyl phthalate (DBP) is used extensively in the plastic industry and has been known as an environmental hormone (endocrine disruptor). Present study was undertaken to examine whether DBP can induce oxidative stress in mice. In this study, oxidative stress was measured in terms of the modification of lipid peroxidation and gamma-glutamyltranspeptidase (${\gamma}-GT$) activity. The activity of ${\gamma}-GT$, the level of lipid peroxidation and serum toxicity index were measured in male ICR mice after treatment with DBP (5 g/kg, po). Administration of DBP was found to significantly increase the level of lipid peroxidation approximately 2 fold in liver. The activity of ${\gamma}-GT$ in the liver of DBP-exposed animals was also increased approximately 2.5 fold. However, DBP did not alter the parameters for hepatotoxicity and nephrotoxicity such as alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine. These results indicate that DBP can induce oxidative stress in mice. The ${\gamma}-GT$ activity is considered to be increased as one of the adaptive defense mechanisms to oxidative stress induced by DBP.