Stress-responsive MAPK signaling pathway with proliferation and apoptosis in the rat testis after 2100 MHz radiofrequency radiation exposure

Er H., Tas G. G., Soygur B., Özen Ş., Sati L.

EUROPEAN JOURNAL OF THERAPEUTICS, vol.2024, no.1, pp.1-3, 2024 (SCI-Expanded)

  • Publication Type: Article / Article
  • Volume: 2024 Issue: 1
  • Publication Date: 2024
  • Doi Number: 10.58600/eurjther2009
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), TR DİZİN (ULAKBİM)
  • Page Numbers: pp.1-3
  • Akdeniz University Affiliated: Yes


Objective: Mobile phone technology has progressed quickly in recent years. Cell phones operate using radiofrequency radiation (RFR), and the complete biological impacts of RFR remain unidentified. Thus, we aimed to investigate the potential effects of 2100 MHz radiofrequency radiation exposure on the stress-responsive JNK/p38 MAPK pathway, apoptosis and proliferation in rat testis. Methods: RFR groups were created with 2100 MHz RFR exposure for acute (2 h/day for 1 week) and chronic (2 h/day for 10 weeks) periods. Sham groups were kept under identical conditions without RFR. The cell apoptosis and histopathological changes in testis were evaluated. Immunolocalization of PCNA, active caspase-3, Bcl-xL, p-JNK and p-p38 were analyzed by immunohistochemistry, the total protein expressions were identified by Western blot. Results: There were no differences between RFR and sham groups by means of histopathology and TUNEL analysis. Also, the expression levels and the immunolocalization patterns of PCNA, active caspase-3 and Bcl-xL proteins were not altered. p-JNK and p-p38 protein expressions were prominently elevated in acute and chronic RFR groups. Conclusion: In conclusion, 2100 MHz RFR exposure had no considerably deleterious consequences on cellular proliferation and apoptosis processes in rat testis. However, increased expression of stress-activated protein kinases, p-JNK and p-p38, suggests the involvement of the MAPK signaling pathway as a critical (may be detrimental) cellular response.