Endocrine Disrupting Effects of Triclosan on the Placenta in Pregnant Rats.
Endocrine Disrupting Effects of Triclosan on the Placenta in Pregnant Rats.
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内分泌破坏三氯生的作用对怀孕大鼠的胎盘。
DOI：
10.1371/journal.pone.0154758
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Shao B
中科院分区：
文献类型：
--
作者：
Feng Y;Zhang P;Zhang Z;Shi J;Jiao Z;Shao B
三氯生（TCS）是一种广谱抗菌剂，常用于药品和个人护理产品。有报道表明，TCS是一种潜在的内分泌干扰物;然而，TCS对胎盘内分泌功能的潜在影响尚不清楚。本研究旨在探讨天花粉蛋白（TCS）对妊娠大鼠胎盘的内分泌干扰作用。妊娠第6天（GD）至GD 20天的妊娠大鼠接受0、30、100、300和600 mg/kg/d TCS给药，随后分析各种生化参数。在检查的七种组织中，在胎盘中观察到TCS的生物累积最大。在600 mg/kg/d TCS暴露组中观察到妊娠子宫重量减轻和流产发生。激素检测显示，高剂量TCS组血清孕酮（P）、雌二醇（E2）、睾酮（T）、人绒毛膜促性腺激素（hCG）和催乳素（PRL）水平均降低。实时定量逆转录-聚合酶链反应（Q-RT-PCR）分析显示胎盘类固醇代谢酶的mRNA水平显著增加，包括UDP-葡萄糖醛酸转移酶1A 1（UGT 1A 1）、雌激素磺基转移酶1 E1（SULT 1 E1）、类固醇5α-还原酶1（SRD 5A 1）和类固醇5α-还原酶2（SRD 5A 2）。孕激素受体（PR）、雌激素受体（ERα）和雄激素受体（AR）的转录水平上调。综上所述，这些数据表明，胎盘是TCS的靶组织，TCS诱导的循环类固醇激素产生的抑制可能与胎盘中激素代谢酶基因表达的改变有关。这种激素干扰随后可能会影响胎儿的发育和生长。
Triclosan (TCS) is a broad-spectrum antimicrobial agent that is frequently used in pharmaceuticals and personal care products. Reports have shown that TCS is a potential endocrine disruptor; however, the potential effects of TCS on placental endocrine function are unclear. The aim of this study was to investigate the endocrine disrupting effects of TCS on the placenta in pregnant rats. Pregnant rats from gestational day (GD) 6 to GD 20 were treated with 0, 30, 100, 300 and 600 mg/kg/d TCS followed by analysis of various biochemical parameters. Of the seven tissues examined, the greatest bioaccumulation of TCS was observed in the placenta. Reduction of gravid uterine weight and the occurrence of abortion were observed in the 600 mg/kg/d TCS-exposed group. Moreover, hormone detection demonstrated that the serum levels of progesterone (P), estradiol (E2), testosterone (T), human chorionic gonadotropin (hCG) and prolactin (PRL) were decreased in groups exposed to higher doses of TCS. Real-time quantitative reverse transcriptase-polymerase chain reaction (Q-RT-PCR) analysis revealed a significant increase in mRNA levels for placental steroid metabolism enzymes, including UDP-glucuronosyltransferase 1A1 (UGT1A1), estrogen sulfotransferase 1E1 (SULT1E1), steroid 5α-reductase 1 (SRD5A1) and steroid 5α-reductase 2 (SRD5A2). Furthermore, the transcriptional expression levels of progesterone receptor (PR), estrogen receptor (ERα) and androgen receptor (AR) were up-regulated. Taken together, these data demonstrated that the placenta was a target tissue of TCS and that TCS induced inhibition of circulating steroid hormone production might be related to the altered expression of hormone metabolism enzyme genes in the placenta. This hormone disruption might subsequently affect fetal development and growth.