Cypermethrin exposure during puberty induces oxidative stress and endocrine disruption in male mice.

Cypermethrin (CYP) is one of the most common contaminants in the ecosystem. The effects of CYP exposure on the induction of oxidative stress and endocrine disruption were studied in adolescent male ICR mice. The hepatic activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT) and total antioxidant capacity (T-AOC) increased significantly after 3 weeks (postnatal day 21-42) of oral administration of 20 mg kg(-1) CYP. In accordance with the enzyme activities, the mRNA levels for the genes encoding these antioxidant proteins, such as Sod1, Sod2, Gpx1 and Gpx2, were also up-regulated significantly in the 10 and 20 mg kg(-1) CYP treatment groups. Furthermore, we also found that the 3-week oral administration of CYP decreased transcription levels of key genes in pathways of cholesterol synthesis and transport and testosterone synthesis including HMG-CoA synthase, steroidogenic acute regulatory protein (StAR) and cytochrome P450 17α-hydroxysteroid dehydrogenase (P450 17α in the liver and testes. Serum testosterone levels also decreased significantly in mice after treatment with 20 mg kg(-1) CYP. Taken together, the results indicated that CYP can induce endocrine disruption in adolescent mice. The findings will be helpful in elucidating the mechanism of toxicity induced by CYP in adolescent mice.