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甲基硫酸盐通过准GATA2/TGF-β1/SMAD信号轴来抑制雷迪格细胞的类固醇生成

Ke Ren¹, Liehai Hu¹, Derui Zeng¹

¹Department of Urology, Nanjing Drum Tower Hospital, State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, Jiangsu 210008, China; Jiangsu Key Laboratory of Molecular Medicine, Division of Anatomy and Histo-embryology, Medical School, Nanjing University, Nanjing, Jiangsu 210093, China.

Ecotoxicology and environmental safety

|February 1, 2026

概括

甲基硫酸盐 (MES) 的发育暴露会导致雄性小鼠的生殖毒性. 这种绿色表面活性剂通过影响GATA2/TGF-β1/LHR通路来破坏丸结构并损害丸的产生.

科学领域:

环境毒理学环境毒理学
生殖生物学生殖生物学
分子机制的分子机制

背景情况:

环境污染物的发育暴露会导致成年男性生殖功能障碍.
甲基硫酸盐 (MES) 是一种被宣传为环保的阳离子表面活性剂,缺乏彻底的生殖毒性评估.
了解污染物引起的生殖损害的分子途径至关重要.

研究的目的:

在小鼠模型中研究发育性甲基硫酸盐 (MES) 暴露的生殖毒性.
阐明MES诱导的丸损伤和受损的类固醇生成背后的分子机制.

主要方法:

从怀孕8.5天到产后56天,小鼠对MES (0.06,0.6,6 mg/L) 的发育暴露.
成年男性丸的组织病理学检查.
对血清丸激素水平和精子生成的评估.
RNA测序,分子对接和CETSA-Western涂抹用于识别分子目标和途径.

主要成果:

发育性MES暴露诱导丸组织病理学:血液丸屏障受损,精子细胞失调,真空化和纤维化.
观察到血清丸激素显著降低和精子生成受损.
MES直接结合并稳定了GATA结合蛋白2 (GATA2),激活了TGF-β1 / SMAD通路,抑制LHR表达,并抑制合成.

结论:

甲基硫酸盐 (MES) 的发育性暴露会导致哺乳动物的雄性生殖毒性显著.
确定了一种新的GATA2/TGF-β1/LHR信号轴,可以调解MES诱导的类固醇生成障碍.
这些发现挑战了MES的安全概况,并强调需要进行全面的环境风险评估.

关键词:

血液-丸屏障血液-丸屏障甲基硫酸盐的甲基硫酸盐.分子对接是分子对接.性激素障碍性激素障碍性激素障碍性激素障碍性激素障碍精子的产生是精子的产生.

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