关键词: Apoptosis Endoplasmic reticulum stress Grp78 Male infertility Radiofrequency radiation

来  源:   DOI:10.1007/s00418-024-02308-7

Abstract:
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.
摘要:
长期射频辐射(RFR)暴露,对生物体产生不利影响,睾丸功能恶化。内质网(ER)中的错误折叠或解折叠蛋白积累引发称为ER应激(ERS)的细胞内反应,激活未折叠的蛋白质反应(UPR)的蛋白质稳定。由于暴露于RFR和ERS都会导致男性不育,我们假设暴露于RFR会导致ERS对大鼠睾丸功能产生不利影响.探讨ERS在介导大鼠睾丸RFR效应中的作用。我们在雄性大鼠中建立了五个实验组:对照组,短期2100兆赫(MHz)RFR(1周),短期假(假/1周),长期2100-MHzRFR(10周),和长期假(假/10周)。ERS标记Grp78和磷酸化PERK(p-Perk)水平和ERS相关的凋亡标记Chop和caspase12通过免疫组织化学研究,免疫印迹,和定量实时聚合酶链反应(qPCR)。长期RFR暴露增加了Grp78,p-Perk,和切碎的水平,而短期RFR暴露会升高Chop和caspase12水平。在精原细胞和原代精母细胞中未观察到Chop表达,这可能保护精原细胞和原代精母细胞免受RFR诱导的ERS介导的细胞凋亡,从而允许遗传物质传递给下一代。虽然短期和长期RFR暴露会触发ERS和ERS相关的凋亡途径,需要进一步的功能分析来阐明这种RFR诱导的细胞凋亡是否对男性不育有长期影响.
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