Abstract

Triphenyl phosphate (TPP) and tris(2-chloroethyl) phosphate (TCEP) are two of the most common organophosphate flame retardants in the ecosystem. Effects of TPP and TCEP on the induction of oxidative stress and endocrine disruption were evaluated in five weeks old male mice. After receiving 100, 300mg/kg/bodyweight oral exposure to TPP and TCEP for 35 days, the body and testis weights decreased in 300mg/kg TPP and TCEP treated groups. Hepatic malondialdehyde (MDA) contents increased significantly in both TPP treated groups, while the contents of glutathione (GSH) decreased significantly in 300mg/kg TPP and both TCEP treated groups. In addition, the hepatic activities of antioxidant enzymes including glutathione peroxidase (GPX), catalase (CAT) and glutathione S-transferase (GST) as well as their related gene expression were affected by TPP or TECP exposure. On the other hand, 300mg/kg of TPP or TECP treatment resulted in histopathological damage and the decrease of testicular testosterone levels. Moreover, the expression of main genes related to testosterone synthesis including steroidogenic acute regulatory protein (StAR), low-density lipoprotein receptor (LDL-R), cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc) and cytochrome P450 17α-hydroxysteroid dehydrogenase (P450-17α) in the testes also decreased after the exposure to 300mg/kg TPP or TCEP for 35 days. Combined with the effects on physiology, histopathology and the expression of genes, TPP and TCEP can induce oxidative stress and endocrine disruption in mice.

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