期刊
ENVIRONMENTAL SCIENCE & TECHNOLOGY
卷 53, 期 24, 页码 14709-14715出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.est.9b05669
关键词
-
资金
- National Natural Science Foundation of China [21737001, 41821005]
- International S Cooperation Program of China [2016YFE0117800]
Since triphenyl phosphate (TPhP) elicits both antiestrogenic activities via blocking the estrogen receptor (ER) and estrogenic activity by elevating 17 beta-estradiol (17 beta-IE2) synthesis, its adverse effect on female reproduction is uncertain. In this study, we exposed Japanese medaka to TPhP at 131, 363, and 1773 ng/L for 100 days following hatching. TPhP significantly induced ovary retardation in all exposure groups (incidence: from 11.9 to 37.8%) and reduced egg production by 38.9 and 50.9% in the 363 and 1773 ng/L exposure groups, respectively. Vitellogenin (vtg) transcription was significantly downregulated by 35.4-57.4% after TPhP exposure, explaining the ovary retardation. Considering that 17 beta-E2 was only significantly decreased in the 1773 ng/L exposure group, ER antagonism could be the dominant contributor to the inhibition of vtg transcription and female reproductive toxicity of TPhP. As 4-hydroxyphenyl diphenyl phosphate, a metabolite of TPhP, was detected in livers with similar concentration [68.4-1237 ng/g lipid weight (lw)] to that of TPhP (485-1594 ng/g lw) and elicited medaka ER antagonistic activity (50% inhibitory concentration = 78.1 mu M), TPhP and its metabolite should both contribute to the reproductive inhibition. We demonstrate that TPhP at environmentally relevant concentrations is toxic to female reproduction, which poses an ecological risk to wild fish at the population level.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据