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[a]烯通过向受体/Gαs蛋白来破坏依赖LH/hCG的老鼠莱迪格细胞的类固醇生成
Clara Lazzaretti1, Neena Roy2, Elia Paradiso2
1Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, Baggiovara Hospital, University of Modena and Reggio Emilia, via Pietro Giardini 1355, 41126, Modena, Italy. clara.lazzaretti@unimore.it.
Scientific reports
|January 8, 2024
概括
短期暴露于 (Benzo[a]pyrene (BaP)) 干扰了小鼠莱迪格细胞的生殖激素信号传递,干扰了Gαs激活,影响了类固醇生成. 然而,人体颗粒细胞没有显示出BaP暴露的显著影响.
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:
- 淋巴腺热素严格调节淋巴腺细胞的类固醇生成.
- 多环芳,如[a] (BaP) 可以引起生殖毒性.
- 短期暴露于BaP对性腺激素刺激细胞的影响尚不清楚.
研究的目的:
- 为了研究短期子[a]烯 (BaP) 暴露对黄素化激素/胆激素 (LH/hCG) 介导信号传递的影响.
- 评估BaP对小鼠莱迪格 (mLTC1) 和人类粒状黄蛋白细胞 (hGLC) 的类固醇生成的影响.
主要方法:
- 利用同质的时间解析光 (HTRF) 和生物发光能量转移 (BRET) 试验进行细胞信号传输.
- 采用西式涂抹,免疫染色和免疫试验来分析蛋白质表达和类固醇生成.
- 暴露mLTC1和hGLC细胞对1nM和1μMBaP进行8小时和24小时.
主要成果:
- [a]烯 (BaP) 降低了cAMP的产生,并干扰了淋巴激素刺激的mLTC1细胞中的Gαs激活.
- 在BaP处理的mLTC1细胞中观察到CREB酸化和孕激素生产的减少.
- 在接受淋巴激素治疗的hGLC中,BaP没有影响cAMP,类固醇生成机制或类固醇生成.
结论:
- 短期暴露于烯 (BaP) 会通过影响Gαs.显著损害小鼠莱迪格细胞中的类固醇信号传递.
- 这些发现提供了对内分泌干扰剂引起的生殖毒性机制的见解.
- 人类颗粒状黄蛋白细胞对BaP对类固醇生成的短期影响表现出耐药性.
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