摘要
Information regarding decabromodiphenyl ethane （DBDPE） effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase （PROD） activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase （LBD） activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.
Information regarding decabromodiphenyl ethane （DBDPE） effects on hepatotoxicity and metabolism is limited. In the present study, Wistar rats were given oral DBDPE at different doses. DBDPE induced oxidative stress, elevated blood glucose levels, increased CYP2B2 mRNA, CYP2B1/2 protein, 7-pentoxyresorufin O-depentylase （PROD） activity, and induced CYP3A2 mRNA, CYP3A2 protein, and luciferin benzylether debenzylase （LBD） activity. UDPGT activity increased with its increasing exposure levels, suggesting that oral DBDPE exposure induces drug-metabolizing enzymes in rats via the CAR/PXR signaling pathway. The induction of CYPs and co-regulated enzymes of phase II biotransformation may affect the homeostasis of endogenous substrates, including thyroid hormones, which may, in turn, alter glucose metabolism.
基金
financial support from the National Science and Technology Programme"Research&Development on Suitable Key Technologies of the Village Environmental Monitoring(2012BAJ24B02)"
