期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 336, 期 -, 页码 49-54出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2017.10.005
关键词
Triclosan; Female Yellow River carp; HPG axis; Sex steroid; Aromatase
资金
- Foundation of Henan Provincial Youth Backbone Teachers [2016GGJS-119]
- Joint Fund for Fostering Talents of National Natural Science Foundation of China [U1504303]
- Joint Fund for Fostering Talents of National Natural Science Foundation of Henan province [U1504303]
Triclosan (TCS), a member of the class of compounds called pharmaceutical and personal care products (PPCPs), is a broad antibacterial and antifungal agent found in a lot of consumer products. However, TCS hormone effect mechanism in teleost female fish is not clear. Female Yellow River carp (Cyprinus carpio) were exposed to 1/20, 1/10 and 1/5 LC50 TCS (96 h LC50 of TCS to carp) under semi-static conditions for 42 days. Vitellogenin (Vtg), 17 beta-estradiol (E-2), testosterone(T), estrogen receptor (Er), gonadotropin (GtH), and gonadotropin-releasing hormone (GnRH) levels were measured by enzyme-linked immunosorbent assay (ELISA). Meanwhile, we also examined the mRNA expressions of aromatase, GtHs-beta, GnRH, and Er by quantitative real-time PCR (qRT-PCR). The results indicated that 1/5 LC50 TCS induced Vtg in hepatopancreas of female carps by interference with the hypothalamic pituitary gonadal (HPG) axis at multiple potential loci through three mechanisms: (a) TCS exposure enhanced the mRNA expression of hypothalamus and gonadal aromatase which converts androgens into estrogens, subsequently increasing serum concentrations of E-2 to induce Vtg in hepatopancreas; (b) TCS treatment increased GnRH and GtH-13 mRNA expression and secretion, causing the disturbance of reproductive endocrine and the increase of E-2 to induce Vtg in hepatopancreas; (c) TCS exposure enhanced synthesis and secretion of Er, then it bound to Er to active Vtg synthesis. These mechanisms showed that TCS may induce Vtg production in female Yellow River carp by Er-mediated and non-Er-mediated pathways.
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