Keywords: 
• PBDE /
• zebrafish /
• hypothalamus-pituitary-thyroidal (HPT) /
• hypothalamus-pituitary-gonadal (HPG) /
• hypothalamus-pituitary-adrenal (HPA)

Abstract: 2,4,4'-Tribromodiphenyl ether (BDE-28) and 2,2',4,4',5-pentabromodiphenyl ether (BDE-99) were widespread in natural aquatic environment. Especially, the higher concentrations of BDE-28 and BDE-99 in fish and sediment were detected in the lower reach of the Yangtze River in China. There are many reports on the endocrine disrupting effects and mechanisms of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) exposure on aquatic organisms, but the research on toxicology of BDE-28 and BDE-99 was relatively lacking. In this study, zebrafish embryos were exposed to 2, 20 and 200 μg·L^-1 of BDE-28 and BDE-99, and then the effects of BDE-28 and BDE-99 on 50 genes associated with hypothalamus–pituitary–thyroidal (HPT), hypothalamus–pituitary–gonadal (HPG) and hypothalamus–pituitary–adrenal (HPA) in zebrafish larvae were investigated by q-RT-PCR methods. At 120 hours post fertilization (hpf), the exposure of BDE-28 and BDE-99 (2, 20 and 200 μg·L^-1) caused expression alteration of genes involved in HPT, HPG and HPA axis in zebrafish larvae, among which the genes expression relevant to three axes were down-regulated after exposure to BDE-28 but up-regulated after exposure to BDE-99. The changes of three major endocrine molecular pathways induced by BDE-28 and BDE-99 exposure in early life stages of zebrafish could result in alterations of endocrine function, which may affect the growth and development of zebrafish at later stages. Moreover, principal component analysis (PCA) revealed that the adverse effects of BDE-28 and BDE-99 on zebrafish were attributed to different toxic mechanisms.