Humans are occasionally exposed to extreme environmental heat for a prolonged period of time. Here, we investigated testicular responses to whole‐body heat exposure by placing mice in a warm chamber. Among the examined tissues, the testis was found to be most susceptible to heat stress. Heat stress induces direct responses within germ cells, such as eukaryotic initiation factor 2α phosphorylation and stress granule (SG) formation. Prolonged heat stress (42°C for 6 hr) also disturbed tissue organization, such as through blood‐testis barrier (BTB) leakage. Germ cell apoptosis was induced by heat stress for 6 hr in a cell type‐ and developmental stage‐specific manner. We previously showed that spermatocytes in the early tubular stages (I–VI) form SGs for protection against heat stress. In the mid‐tubular stages (VII–VIII), BTB leakage synergistically enhances the adverse effects of heat stress on pachytene spermatocyte apoptosis. In the late tubular stages (IX–XII), SGs are not formed and severe leakage of the BTB does not occur, resulting in mild apoptosis of late‐pachytene spermatocytes near meiosis. Our results revealed that multiple stress responses are involved in germ cell damage resulting from prolonged heat stress (42°C for 6 hr).

中文翻译：

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全身热暴露导致雄性生殖细胞发育阶段特异性凋亡。

有时，人类会长时间暴露于极端的环境热中。在这里，我们通过将小鼠放在温暖的房间里研究了睾丸对全身热暴露的反应。在被检查的组织中，发现睾丸最容易受到热应激。热应激诱导生殖细胞内的直接反应，例如真核起始因子2α磷酸化和应激颗粒（SG）形成。长时间的热应激（42°C，持续6小时）还会干扰组织的组织，例如通过血液-睾丸屏障（BTB）泄漏。热应激以细胞类型和发育阶段特定的方式诱导生殖细胞凋亡6小时。我们以前曾证明，早期肾小管阶段（I–VI）的精母细胞会形成SGs，以抵抗热应激。在肾小管中期（VII–VIII），BTB泄漏协同增强了热应激对粗精子细胞凋亡的不利影响。在肾小管晚期（IX–XII），SGs不会形成，BTB不会严重泄漏，从而导致减数分裂附近的晚粗精细胞的轻度凋亡。我们的研究结果表明，长时间的热应激（42°C持续6小时）会导致生殖细胞受损，而多种应激反应都参与其中。