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首页> 外文期刊>Environmental Science & Technology >Triphenyl Phosphate at Environmental Levels Retarded Ovary Development and Reduced Egg Production in Japanese Medaka (Oryzias latipes)
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Triphenyl Phosphate at Environmental Levels Retarded Ovary Development and Reduced Egg Production in Japanese Medaka (Oryzias latipes)

机译：在环境水平上磷酸三苯酯阻碍了日本Medaka（Oryzias latipes）的卵巢发育并降低了产蛋量

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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.
机译：由于磷酸三苯酯（TPhP）通过阻断雌激素受体（ER）引起抗雌激素活性，并通过提高17β-雌二醇（17β-IE2）的合成而产生雌激素活性，因此不确定其对女性生殖的不利影响。在这项研究中，我们在孵化后的100天中以131、363和1773 ng / L的浓度对日本进行了TPhP处理。 TPhP在所有暴露组中均显着诱导卵巢发育迟缓（发生率：从11.9至37.8％），在363和1773 ng / L暴露组中分别降低产卵量38.9和50.9％。 TPhP暴露后，卵黄蛋白原（vtg）转录显着下调35.4-57.4％，这说明卵巢发育迟缓。考虑到17β-E2仅在1773 ng / L暴露组中显着降低，因此ER拮抗作用可能是抑制vtg转录和TPhP雌性生殖毒性的主要因素。由于在肝脏中检测到TPhP的代谢产物为4-羟基苯基二苯基磷酸酯，其浓度[68.4-1237 ng / g脂质重量（lw）]与TPhP的浓度[485-1594 ng / g lw]相似，并引起了aka高ER拮抗作用活性（50％抑制浓度= 78.1μM），TPhP及其代谢产物均应对生殖抑制起作用。我们证明，与环境有关的浓度的TPhP对女性繁殖有毒，这在种群水平上对野生鱼类构成了生态风险。

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