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Melatonin ameliorates RF-EMR-induced reproductive damage by inhibiting ferroptosis through Nrf2 pathway activation

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Wang J, Dong J, Xu Q, Yan S, Wang H, Lei H, Ma X, Yang T, Wang K, Li Z, Wang X · 2025

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Melatonin mitigated RF-EMR-induced oxidative harm and ferroptosis in mouse testes and inhibited ROS production by stimulating the Nrf2 pathway via MT1/MT2 receptors.

Plain English Summary

Summary written for general audiences

Researchers exposed male mice to 2.45 GHz RF-EMR at 2.5 W/m2 for 8 weeks, which induced ferroptosis and oxidative stress in testicular tissue and reduced sperm quality. Melatonin administration reduced the oxidative damage and ferroptosis in the testes of exposed mice. The protective effect was mediated by melatonin stimulating the Nrf2 signaling pathway through MT1/MT2 receptors, inhibiting ROS production and ferroptosis.

Why This Matters

The authors concluded that melatonin could potentially improve RF-EMR-induced reproductive damage in male mice by blocking ferroptosis through activation of the Nrf2 pathway. Exposure to RF-EMR at 2.45 GHz with a power density of 2.5 W/m2 and SAR of 0.125-0.5 W/kg induced ferroptosis and oxidative stress in testicular tissue, leading to a decrease of sperm quality in male mice.

Cite This Study
Wang J, Dong J, Xu Q, Yan S, Wang H, Lei H, Ma X, Yang T, Wang K, Li Z, Wang X (2025). Melatonin ameliorates RF-EMR-induced reproductive damage by inhibiting ferroptosis through Nrf2 pathway activation.
Show BibTeX
@article{wang_j_dong_j_xu_q_yan_s_wang_h_lei_h_ma_x_yang_t_wang_k_li_z_wang_x_ce2636,
  author = {Wang J and Dong J and Xu Q and Yan S and Wang H and Lei H and Ma X and Yang T and Wang K and Li Z and Wang X},
  title = {Melatonin ameliorates RF-EMR-induced reproductive damage by inhibiting ferroptosis through Nrf2 pathway activation},
  year = {2025},
  
  
}

Quick Questions About This Study

The study used 2.45 GHz RF-EMR at a power density of 2.5 W/m2 with a whole-body SAR of 0.125-0.5 W/kg for 8 weeks.
RF-EMR exposure induced ferroptosis and oxidative stress in testicular tissue and decreased sperm quality in male mice.
Melatonin administration mitigated the oxidative harm to the testicles and ferroptosis caused by RF-EMR in mice.
Melatonin inhibits ROS production and ferroptosis by stimulating the Nrf2 signaling pathway through its MT1/MT2 receptors.
The authors concluded that melatonin could potentially improve RF-EMR-induced reproductive damage in male mice by blocking ferroptosis through activation of the Nrf2 pathway.