Departments of Histology and Embryology, Faculty of Engineering, Akdeniz University, Antalya, Turkey.
Faculty of Medicine, Department of Histology and Embryology, Bozok University, Yozgat, Turkey.
Histochem Cell Biol. 2024 Oct;162(4):311-321. doi: 10.1007/s00418-024-02308-7. Epub 2024 Jul 12.
Long-term radiofrequency radiation (RFR) exposure, which adversely affects organisms, deteriorates testicular functions. Misfolding or unfolding protein accumulation in the endoplasmic reticulum (ER) initiates an intracellular reaction known as ER stress (ERS), which activates the unfolded protein response (UPR) for proteostasis. Since both RFR exposure and ERS can cause male infertility, we hypothesized that RFR exposure causes ERS to adversely affect testicular functions in rats. To investigate role of ERS in mediating RFR effects on rat testis, we established five experimental groups in male rats: control, short-term 2100-megahertz (MHz) RFR (1-week), short-term sham (sham/1-week), long-term 2100-MHz RFR (10-week), and long-term sham (sham/10-week). ERS markers Grp78 and phosphorylated PERK (p-Perk) levels and ERS-related apoptosis markers Chop and caspase 12 were investigated by immunohistochemistry, immunoblotting, and quantitative real-time polymerase chain reaction (qPCR). Long-term RFR exposure increased Grp78, p-Perk, and Chop levels, while short-term RFR exposure elevated Chop and caspase 12 levels. Chop expression was not observed in spermatogonia and primary spermatocytes, which may protect spermatogonia and primary spermatocytes against RFR-induced ERS-mediated apoptosis, thereby allowing transmission of genetic material to next generations. While short and long-term RFR exposures trigger ERS and ERS-related apoptotic pathways, further functional analyses are needed to elucidate whether this RFR-induced apoptosis has long-term male infertility effects.
长期射频辐射（RFR）暴露会对生物体造成不良影响，从而损害睾丸功能。内质网（ER）中错误折叠或未折叠蛋白的积累会引发一种称为内质网应激（ERS）的细胞内反应，该反应会激活未折叠蛋白反应（UPR）以维持蛋白质稳态。由于 RFR 暴露和 ERS 都会导致男性不育，因此我们假设 RFR 暴露会导致 ERS 对大鼠睾丸功能产生不良影响。为了研究 ERS 在介导 RFR 对大鼠睾丸影响中的作用，我们在雄性大鼠中建立了五个实验组：对照组、短期 2100MHz（兆赫）RFR（1 周）、短期假照（sham/1 周）、长期 2100MHz RFR（10 周）和长期假照（sham/10 周）。通过免疫组织化学、免疫印迹和定量实时聚合酶链反应（qPCR）研究了 ERS 标志物 Grp78 和磷酸化 PERK（p-Perk）水平以及 ERS 相关凋亡标志物 Chop 和 caspase 12。长期 RFR 暴露会增加 Grp78、p-Perk 和 Chop 水平，而短期 RFR 暴露会升高 Chop 和 caspase 12 水平。在精原细胞和初级精母细胞中未观察到 Chop 表达，这可能会保护精原细胞和初级精母细胞免受 RFR 诱导的 ERS 介导的凋亡，从而使遗传物质传递给下一代。虽然短期和长期 RFR 暴露会引发 ERS 和 ERS 相关的凋亡途径，但需要进一步的功能分析来阐明这种 RFR 诱导的凋亡是否会对男性产生长期不育的影响。
