Developmental exposure to decabrominated diphenyl ether (BDE-209): effects on sperm oxidative stress and chromatin DNA damage in mouse offspring.

Polybrominated diphenyl ethers (PBDEs) are used as brominated flame retardants and have been found in human milk in recent years. This study investigates whether prenatal exposure to decabrominated diphenyl ether (BDE-209) induces sperm dysfunction in male offspring. Pregnant CD-1 mice were gavaged once daily with corn oil (control), 10, 500, and 1500 mg kg(-1) body weight of BDE-209 from day 0 of gestation to day 17. The outcomes of male reproductive parameters were assessed on postnatal day 71. Anogenital distance, sperm-head abnormalities, and testicular histopathology were significantly affected in male offspring prenatally exposed to 1500 mg kg(-1). Significant increases in the tendency for sperm DNA denaturation (αT) induction and the DNA fragmentation index (DFI) were found in those exposed to 10, 500, and 1500 mg kg(-1) (P < 0.05). We observed a significant increase of sperm hydrogen peroxide (H(2)O(2)) generation in the 10 and 1500 mg/kg/day groups compared to the control group (P < 0.05). Although our findings suggested that the mechanisms underlying BDE-209-induced sperm DNA damage and H(2)O(2) generation might not be represented as a dose-response relationship, we found that the greater the excess production of sperm H(2)O(2), the greater the sperm αT (r = 0.65, P = 0.0155) and DFI (r = 0.53, P = 0.002). In conclusion, developmental exposure to BDE-209 induced sperm-head abnormality, oxidative stress, chromatin DNA damage, and testicular histopathological changes. These findings suggest that BDE-209-induced male reproductive effects might involve the formation of sperm H(2)O(2) which attacks nucleic acids via H(2)O(2) generation.