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<p>Early-life environmental stressors may influence long-term organ development and cellular homeostasis. This study investigated whether prenatal exposure to 3.5&#xa0;GHz radiofrequency radiation (RFR) is associated with renal structural alterations, autophagy-related changes, and DNA damage in adult rat offspring. A total of 24 pregnant Wistar Hannover rats were randomly assigned to sham control, exposure during the last 2 weeks of gestation (D2T: exposure during the last 2 weeks of gestation), or exposure throughout gestation (D3T: exposure throughout gestation) groups (<i>n</i> = 8 dams per group). Male offspring were selected and euthanized at 6 months of age. Kidney tissues were examined histopathologically for structural alterations. Autophagy-related markers (Beclin-1 and LC3) were assessed by immunohistochemistry, and DNA damage was evaluated using the comet assay. Statistical analyses were performed using one-way analysis of variance (ANOVA) followed by appropriate post hoc tests. Peak spatial specific absorption rate (psSAR) values in the uterine region were 0.06622 mW/g (1&#xa0;g averaging) and 0.03825 mW/g (10&#xa0;g averaging). Prenatal RFR exposure was associated with significant renal histopathological alterations in offspring, most pronounced in the D3T group, including glomerular atrophy, tubular dilation, epithelial vacuolization, and cast formation (<i>p</i> &lt; 0.01–0.001 versus controls). Beclin-1 and LC3 expression levels were significantly increased in both exposure groups (<i>p</i> &lt; 0.001), suggesting altered autophagy-related marker expression. The comet assay demonstrated significantly increased DNA fragmentation in D2T and D3T groups compared with controls (<i>p</i> &lt; 0.001), indicating increased genomic stress. Overall, prenatal exposure to 3.5&#xa0;GHz RFR is associated with renal structural alterations, increased DNA damage, and changes in autophagy-related markers in adult rat offspring.</p>

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Prenatal 3.5 GHz radiofrequency exposure induces renal histological changes and DNA damage in 6-month-old rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月9日

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  • Elif Gelenli Dolanbay,
  • Fazile Canturk Tan,
  • Hava Bektas,
  • Sumeyye Koc,
  • Salih Varol,
  • Omer Kilic,
  • Unal Uslu,
  • Suleyman Dasdag

摘要

Early-life environmental stressors may influence long-term organ development and cellular homeostasis. This study investigated whether prenatal exposure to 3.5 GHz radiofrequency radiation (RFR) is associated with renal structural alterations, autophagy-related changes, and DNA damage in adult rat offspring. A total of 24 pregnant Wistar Hannover rats were randomly assigned to sham control, exposure during the last 2 weeks of gestation (D2T: exposure during the last 2 weeks of gestation), or exposure throughout gestation (D3T: exposure throughout gestation) groups (n = 8 dams per group). Male offspring were selected and euthanized at 6 months of age. Kidney tissues were examined histopathologically for structural alterations. Autophagy-related markers (Beclin-1 and LC3) were assessed by immunohistochemistry, and DNA damage was evaluated using the comet assay. Statistical analyses were performed using one-way analysis of variance (ANOVA) followed by appropriate post hoc tests. Peak spatial specific absorption rate (psSAR) values in the uterine region were 0.06622 mW/g (1 g averaging) and 0.03825 mW/g (10 g averaging). Prenatal RFR exposure was associated with significant renal histopathological alterations in offspring, most pronounced in the D3T group, including glomerular atrophy, tubular dilation, epithelial vacuolization, and cast formation (p < 0.01–0.001 versus controls). Beclin-1 and LC3 expression levels were significantly increased in both exposure groups (p < 0.001), suggesting altered autophagy-related marker expression. The comet assay demonstrated significantly increased DNA fragmentation in D2T and D3T groups compared with controls (p < 0.001), indicating increased genomic stress. Overall, prenatal exposure to 3.5 GHz RFR is associated with renal structural alterations, increased DNA damage, and changes in autophagy-related markers in adult rat offspring.