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首页> 外文期刊>Journal of toxicology and environmental health, Part A >THE ROLE OF DEATH RECEPTOR SIGNALING IN TESTICULAR GERM-CELL APOPTOSIS TRIGGERED BY MONO-(2-ETHYLHEXYL) PHTHALATE (MEHP)-INDUCED SERTOLI CELL INJURY AND ITS IMPLICATIONS FOR RISK ASSESSMENT
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THE ROLE OF DEATH RECEPTOR SIGNALING IN TESTICULAR GERM-CELL APOPTOSIS TRIGGERED BY MONO-(2-ETHYLHEXYL) PHTHALATE (MEHP)-INDUCED SERTOLI CELL INJURY AND ITS IMPLICATIONS FOR RISK ASSESSMENT

机译：死亡受体信号在单-（2-乙基己基）邻苯二甲酸酯（MEHP）引起的SERTERI细胞损伤触发的胚性胚芽细胞凋亡中的作用及其对风险评估的意义

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摘要

The focus of this review is to highlight the participation of members of the tumor necrosis factor (TNF) superfamily of proteins, particularly FasL and Fas, in triggering apoptosis of distinct testic-ular germ-cell subtypes after mono-(2-ethylhexyl) phthalate (MEHP)-induced Sertoli cell injury Despite the well-recognized expression of FasL and Fas in the testis, their functional role in this tissue and the cellular mechanisms that regulate germ-cell apoptosis in the testis remain poorly characterized Over the last several years, evidence has been accumulating indicating the participation of the FasUFas signaling pathway in the testis as a key signaling event for triggering germ-cell apoptosis consequent to MEHP-induced Sertoli cell injury. It has also recently been revealed that the stability of the c-FLIP protein, a direct inhibitor of Fas signaling, in germ cells appears to be dependent on the activity of the p5i protein. Increased degradation of the c-FLIP protein is proposed to occur in distinct germ-cell subtypes as a secondary consequence to MEHP-induced Sertoli cell injury and may account for their sensitivity to undergo apoptosis Taken together, these findings form the basis for our current hypothesis that MEHP-induced injury to Sertoli cells results in early increases in its expression of FasL and secondary changes in the regulation of Fas in germ cells as a result of p53 activation An understanding of the primary cellular site of phthalate action in the Sertoli cell and of the extent of the resulting adverse outcomes that arise from this injury are required for an accurate appraisal of the risks of environmental phthalate exposure on human reproductive health during all phases of life.
机译：这篇综述的重点是强调蛋白质（尤其是FasL和Fas）的肿瘤坏死因子（TNF）超家族成员在邻苯二甲酸单（2-乙基己基）酯引发不同睾丸生殖细胞亚型的凋亡中的参与。 （MEHP）诱导的睾丸支持细胞损伤尽管FasL和Fas在睾丸中的表达得到公认，但在过去几年中，它们在该组织中的功能作用以及调节睾丸中生殖细胞凋亡的细胞机制仍然不明确，越来越多的证据表明，FasUFas信号通路参与睾丸是触发MEHP诱导的支持细胞损伤后生殖细胞凋亡的关键信号事件。最近还发现，c-FLIP蛋白（Fas信号的直接抑制剂）在生殖细胞中的稳定性似乎取决于p5i蛋白的活性。有人认为c-FLIP蛋白降解的增加在不同的生殖细胞亚型中发生，是MEHP诱导的Sertoli细胞损伤的次要结果，并且可能解释了它们对细胞凋亡的敏感性综上所述，这些发现构成了我们当前假说的基础MEHP诱导的对支持细胞的损伤导致其FasL的早期表达增加，以及由于p53激活而导致生殖细胞中Fas调节的继发性变化。了解支持细胞和邻苯二甲酸对邻苯二甲酸酯作用的主要细胞部位要准确评估在生活的各个阶段中环境邻苯二甲酸酯暴露对人类生殖健康的风险，就需要确定由这种伤害引起的不良后果的程度。

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