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双S刺激莱迪格细胞的增殖,但通过多种机制抑制了青春期雄性大鼠的分化

Peipei Pan¹, Zina Wen², Feifei Ma³

¹Department of Reproductive Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.

Environmental toxicology

|June 26, 2023

概括

在大鼠的男性青春期中,双S (BPS) 暴露降低了丸激素和抑制素水平,扰乱了莱迪格细胞的功能. 通过激活雌激素受体和增加未成熟的莱迪格细胞中的氧化应激,BPS会导致雄激素缺乏.

科学领域:

内分泌学在内分泌学.
生殖毒理学生殖毒理学
环境健康环境健康

背景情况:

双S (BPS) 是一种常见的环境污染物,也是双A (BPA) 的类似物.
已知BPS会破坏男性生殖系统,但其对男性青春期莱迪格细胞成熟的影响尚不清楚.

研究的目的:

调查青春期暴露于Bisphenol S (BPS) 对雄性大鼠莱迪格细胞成熟和功能的影响.
阐明BPS诱导的生殖毒性背后的机制.

主要方法:

雄性Sprague-Dawley大鼠 (35天大) 从出生后的35-56天开始接受了BPS (0,1,10,100,200毫克/公斤/天) 的测量.
测量了血清激素水平 (,孕激素,雌激素,LH,抑制素A,抑制素B).
分析了莱迪格细胞标记物 (CYP11A1,HSD11B1),类固醇酶基因表达 (Cyp11a1,Cyp17a1,HSD11b1,Nr5a1) 和垂体Lhb表达.
在体外研究中评估了BPS对的产生,莱迪格细胞的增殖,氧化应激和17β-基类固醇脱酶3活性的影响.

主要成果:

暴露于BPS显著降低了血清丸激素,孕激素,抑制剂A和抑制剂B水平.
在较高的BPS剂量下观察到血清LH和雌激素水平升高.
BPS增加了不成熟的CYP11A1+莱迪格细胞数量,但没有影响成熟的HSD11B1+细胞.
类固醇酶 (Cyp11a1,Cyp17a1,Hsd11b1,Nr5a1) 和垂体Lhb的丸基因表达被BPS改变.
在体外,BPS抑制了的产生,诱导了不成熟的莱迪格细胞增殖,增加了氧化应激,并抑制了17β-类固醇脱酶3活性.
这些效应被雌激素受体对抗剂和维生素E部分或完全逆转.

结论:

在青春期暴露于BPS会诱导雄性大鼠出现高性雄性雌激素缺乏.
在不成熟的莱迪格细胞中,BPS通过激活雌激素受体α (ESR1) 和诱导活性氧物种 (ROS) 来发挥其毒性.
通过BPS直接抑制17β-hydroxysteroid脱酶3活性,有助于其对男性生殖的不利影响.

关键词:

莱迪格细胞是莱迪格细胞.双醇 S 是一种双醇.双醇类似物双醇类似物生殖功能生殖功能类固醇类固醇是什么

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