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氯化三苯基锡延缓大鼠青春期睾丸间质细胞成熟。

Triphenyltin Chloride Delays Leydig Cell Maturation During Puberty in Rats.

作者信息

Li Linchao, Xie Lubin, Ma Leikai, Chen Yong, Chen Xianwu, Ge Fei, Huang Tongliang, Chen Lanlan, Hong Tingting, Chen Xiaofang, Zhu Qiqi, Li Xingwang, Ge Ren-Shan

机构信息

Department of Anesthesiology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, China.

Department of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, China.

出版信息

Front Pharmacol. 2018 Aug 10;9:833. doi: 10.3389/fphar.2018.00833. eCollection 2018.

Abstract

Triphenyltin chloride (TPT) is present in a wide range of human foods. TPT could disrupt testis function as a potential endocrine disruptor of Leydig cells. However, the effect of TPT on pubertal Leydig cell development is still unclear. The objective of the current study was to explore whether exposure to TPT affected Leydig cell developmental process and to clarify the underlying mechanisms. Male Sprague-Dawley rats at 35 days of age were randomly divided into four groups and received normal corn oil (control), 0.5, 1, or 2 mg/kg/day TPT for 18 days. Immature Leydig cells isolated from 35-day-old rat testes were treated with TPT (10 and 100 nM) for 24 h . exposure to ≥0.5 mg/kg TPT lowered serum testosterone levels and lowered mRNA. TPT at 2 mg/kg also lowered , , , as well as pAKT1/AKT1, pAKT2/AKT2, and pERK1/2/ERK1/2 ratios. exposure to TPT (100 nM) increased ROS production and induced cell apoptosis rate in rat immature Leydig cells. In conclusion, TPT exposure disrupts Leydig cell development possibly via interfering with the phosphorylation of AKT1, AKT2, and ERK1/2 kinases.

摘要

三苯基氯化锡(TPT)存在于多种人类食物中。作为一种潜在的睾丸间质细胞内分泌干扰物,TPT可能会扰乱睾丸功能。然而,TPT对青春期睾丸间质细胞发育的影响仍不清楚。本研究的目的是探讨暴露于TPT是否会影响睾丸间质细胞的发育过程,并阐明其潜在机制。将35日龄的雄性Sprague-Dawley大鼠随机分为四组,分别给予正常玉米油(对照组)、0.5、1或2 mg/kg/天的TPT,持续18天。从35日龄大鼠睾丸中分离出的未成熟睾丸间质细胞用TPT(10和100 nM)处理24小时。暴露于≥0.5 mg/kg的TPT会降低血清睾酮水平并降低mRNA水平。2 mg/kg的TPT还会降低……以及pAKT1/AKT1、pAKT2/AKT2和pERK1/2/ERK1/2的比值。暴露于TPT(100 nM)会增加大鼠未成熟睾丸间质细胞中的活性氧生成并诱导细胞凋亡率。总之,暴露于TPT可能通过干扰AKT1、AKT2和ERK1/2激酶的磷酸化来破坏睾丸间质细胞的发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/30d6/6095986/ee905b9cefb7/fphar-09-00833-g001.jpg

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