氟化物诱导小鼠Leydig细胞的线粒体损伤和PINK1介导的线粒体：体内和体外研究。,Environmental Pollution

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氟化物诱导小鼠Leydig细胞的线粒体损伤和PINK1介导的线粒体：体内和体外研究。
Environmental Pollution ( IF 7.6 ) Pub Date : 2019-10-21 , DOI: 10.1016/j.envpol.2019.113438
Chen Liang ₁ , Yan Gao ₁ , Yuyang He ₁ , Yongli Han ₁ , Ram Kumar Manthari ₁ , Chiranjeevi Tikka ₁ , Chenkai Chen ₁ , Jundong Wang ₁ , Jianhai Zhang ₁

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由于氟化物在环境中的广泛分布和重大的健康风险，探索氟化物的潜在危害和潜在机理非常重要。这项研究的目的是调查氟化物是否可以诱导睾丸细胞线粒体损伤和线粒体。为此，将40只雄性小鼠随机分为四组，分别用0、0.6、1.2、2.4 mM NaF去离子水处理，连续90天。结果表明，通过透射电子显微镜观察睾丸组织中的F引起线粒体吞噬，尤其是在Leydig细胞中，通过免疫荧光检测线粒体受体PHB2的位置。此外，使用TM3 Leydig细胞系并用0、0.125、0.25和0.5mM NaF处理24小时。线粒体功能指标和线粒体制造商PHB2，通过qRT-PCR，western印迹和免疫荧光共定位方法检测Leydig细胞转录本和蛋白质水平中的COX IV和调节剂PINK1。结果表明，氟化物降低了线粒体膜电位，同时增加了溶酶体的数量。同时，氟化物暴露也增加了TM3 Leydig细胞中PINK1和PHB2的表达。这些结果表明，氟化物可以诱导睾丸细胞，特别是Leydig细胞中线粒体损伤和PINK1 / Parkin介导的线粒体过多，这可能有助于阐明F诱导的雄性生殖毒性的机制。结果表明，氟化物降低了线粒体膜电位，同时增加了溶酶体的数量。同时，氟化物暴露也增加了TM3 Leydig细胞中PINK1和PHB2的表达。这些结果表明，氟化物可以诱导睾丸细胞，特别是Leydig细胞中线粒体损伤和PINK1 / Parkin介导的线粒体过多，这可能有助于阐明F诱导的雄性生殖毒性的机制。结果表明，氟化物降低了线粒体膜电位，同时增加了溶酶体的数量。同时，氟化物暴露也增加了TM3 Leydig细胞中PINK1和PHB2的表达。这些结果表明，氟化物可以诱导睾丸细胞，特别是Leydig细胞中线粒体损伤和PINK1 / Parkin介导的线粒体过多，这可能有助于阐明F诱导的雄性生殖毒性的机制。

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Fluoride induced mitochondrial impairment and PINK1-mediated mitophagy in Leydig cells of mice: In vivo and in vitro studies.

It is very important to explore the potential harm and underlying mechanism of fluoride due to the extensive distribution and the significant health risks of fluoride in environment. The objective of this study to investigate whether fluoride can induce mitochondrial impairment and mitophagy in testicular cells. For this, 40 male mice were randomly divided into four groups treated with 0, 0.6, 1.2, 2.4 mM NaF deionized water, respectively, for 90 days continuously. The results showed that mitophagy was triggered by F in testicular tissues, especially in the Leydig cells by transmission electron microscopy and mitophagy receptor PHB2 locations by immunofluorescence. Furthermore, TM3 Leydig cells line was employed and treated with 0, 0.125, 0.25, and 0.5 mM NaF for 24 h. The mitochondrial function indicators and mitophagy maker PHB2, COX IV and regulator PINK1 in transcript and protein levels in Leydig cells were examined by the methods of qRT-PCR, western blotting, and immunofluorescence co-localization. The results showed that fluoride decreased the mitochondrial membrane potential with a concomitant increase in the number of lysosomes. Meanwhile, fluoride exposure also increased the expressions of PINK1 and PHB2 in TM3 Leydig cells. These results revealed that fluoride could induce mitochondrial impairment and excessive PINK1/Parkin-mediated mitophagy in testicular cells, especially in Leydig cells, which could contribute to the elucidation of the mechanisms of F-induced male reproductive toxicity.

更新日期：2019-10-21

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