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Effects of perfluorooctane sulfuric acid on placental PRL-family hormone production and fetal growth retardation in mice

机译:全氟辛烷硫酸对小鼠胎盘PRL家族激素生产和胎儿生长迟缓的影响

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摘要

Perfluorooctane sulfuric acid (PFOS) is a persistent organic pollutant, causes fetal growth retardation but the mechanism is still unclear. This study focused on PFOS-induced toxicity such as placental trophoblast cell histopathological changes, endocrine function (i.e., prolactin (PRL)-family hormone production) and subsequent fetal growth retardation in mice. Maternal body weight gain, placental and fetal weights were significantly decreased in proportion to PFOS dosage. Placental efficiency (fetal weight/placental weight) was significantly reduced dose-dependently. Necrotic changes were observed in PFOS-treated placental tissues, and the area of injury increased dose-dependently. Finally, mRNA levels and maternal serum concentrations of the PRL-family hormones (mPL-II, mPLP-C alpha, mPLP-K) were significantly reduced dose-dependently. In addition, the changing pattern between PRL-family hormone concentrations and fetal body weight was positively correlated. These results suggest that gestational PFOS treatment induces placental histopathological changes and disruption of endocrine function, finally may lead to fetal growth retardation in mice. (c) 2014 Elsevier Ireland Ltd. All rights reserved.
机译:全氟辛烷硫酸(PFOS)是一种持久的有机污染物,导致胎儿生长迟缓,但该机制尚不清楚。本研究重点关注PFOS诱导的毒性,如胎盘滋养细胞细胞组织病理学变化,内分泌功能(即,催乳素(PRL) - 家族式激素产生)和随后的小鼠胎儿生长迟缓。母体体重增加,胎盘和胎儿重量与PFOS剂量比例显着降低。胎盘效率(胎儿重量/胎盘重量)依赖性显着减少。在PFOS治疗的胎盘组织中观察到坏死的变化,损伤面积依赖性增加。最后,PRL家族激素(MPL-II,MPLP-Cα,MPLP-K)的mRNA水平和母体血清浓度明显减少剂量依赖性。此外,PRL家族激素浓度和胎体重量之间的变化模式是正相关的。这些结果表明,妊娠期PFOS治疗诱导胎心组织病理学变化和内分泌功能的破坏,最终可能导致小鼠的胎儿生长迟缓。 (c)2014年Elsevier Ireland Ltd.保留所有权利。

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