Esma Kirimlioglu, Asli Okan Oflamaz, Enis Hidisoglu, Sukru Ozen, Piraye Yargicoglu, Necdet Demir
{"title":"短期和长期 2100 兆赫射频辐射导致大鼠睾丸内质网应激。","authors":"Esma Kirimlioglu, Asli Okan Oflamaz, Enis Hidisoglu, Sukru Ozen, Piraye Yargicoglu, Necdet Demir","doi":"10.1007/s00418-024-02308-7","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":null,"pages":null},"PeriodicalIF":2.1000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364557/pdf/","citationCount":"0","resultStr":"{\"title\":\"Short and long-term 2100 MHz radiofrequency radiation causes endoplasmic reticulum stress in rat testis.\",\"authors\":\"Esma Kirimlioglu, Asli Okan Oflamaz, Enis Hidisoglu, Sukru Ozen, Piraye Yargicoglu, Necdet Demir\",\"doi\":\"10.1007/s00418-024-02308-7\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":13107,\"journal\":{\"name\":\"Histochemistry and Cell Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364557/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Histochemistry and Cell Biology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1007/s00418-024-02308-7\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/7/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Histochemistry and Cell Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s00418-024-02308-7","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/12 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
长期暴露于射频辐射(RFR)会对生物体产生不利影响,并导致睾丸功能退化。内质网(ER)中错误折叠或未折叠蛋白质的积累会引发一种称为ER应激(ERS)的细胞内反应,从而激活未折叠蛋白质反应(UPR)以促进蛋白稳态。由于暴露于射频辐射和ERS都会导致雄性不育,我们假设暴露于射频辐射会导致ERS对大鼠的睾丸功能产生不利影响。为了研究ERS在介导射频辐射对大鼠睾丸影响中的作用,我们在雄性大鼠中设立了五个实验组:对照组、短期2100兆赫射频辐射组(1周)、短期假体组(假体/1周)、长期2100兆赫射频辐射组(10周)和长期假体组(假体/10周)。通过免疫组化、免疫印迹和实时定量聚合酶链反应(qPCR)研究了ERS标志物 Grp78 和磷酸化 PERK(p-Perk)的水平以及与ERS相关的细胞凋亡标志物 Chop 和 caspase 12。长期暴露于射频辐射会提高 Grp78、p-Perk 和 Chop 的水平,而短期暴露于射频辐射会提高 Chop 和 caspase 12 的水平。在精原细胞和初级精母细胞中未观察到 Chop 的表达,这可能会保护精原细胞和初级精母细胞免受射频辐射诱导的 ERS 介导的凋亡,从而使遗传物质得以传给下一代。虽然短期和长期暴露于射频辐射会触发ERS和与ERS相关的凋亡途径,但还需要进一步的功能分析来阐明射频辐射诱导的凋亡是否会对男性不育产生长期影响。
Short and long-term 2100 MHz radiofrequency radiation causes endoplasmic reticulum stress in rat testis.
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.
期刊介绍:
Histochemistry and Cell Biology is devoted to the field of molecular histology and cell biology, publishing original articles dealing with the localization and identification of molecular components, metabolic activities and cell biological aspects of cells and tissues. Coverage extends to the development, application, and/or evaluation of methods and probes that can be used in the entire area of histochemistry and cell biology.