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Cumulative Low-Dose-Rate Radiation Induces Oxidative Stress, Apoptosis, and Fibrosis in Mouse Testis
Eun-Jin Kim1,2, Anjas Happy Prayoga1,3, Jina Ha1,3
1Department of Physiology, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea.
Antioxidants (Basel, Switzerland)
|August 28, 2025
Summary
Chronic low-dose-rate radiation exposure damages mouse testes, causing fibrosis and germ cell death. Oxidative stress (ROS) increased only at higher doses, indicating a threshold effect in male reproductive toxicity.
Area of Science:
- Reproductive Biology
- Radiation Biology
- Toxicology
Background:
- Ionizing radiation generates reactive oxygen species (ROS), causing oxidative damage.
- Oxidative stress is linked to male reproductive dysfunction.
- Long-term effects of low-dose-rate (LDR) radiation on testes are not well understood.
Purpose of the Study:
- To investigate the long-term effects of chronic LDR radiation on testicular structure and oxidative status in mice.
- To assess dose-dependent testicular damage, including histopathology, fibrosis, and apoptosis.
Main Methods:
- Mice were exposed to continuous LDR radiation (0.39, 1.29, 3.46 mGy/h) for 21 days.
- Testicular histopathology, collagen deposition (Masson's Trichrome, Sirius Red), apoptosis (TUNEL assay), and ROS levels were evaluated.
Main Results:
- No significant changes in testis weight were observed.
- Histology showed basal membrane disruption and reduced spermatogenic cells in irradiated groups.
- Dose-dependent collagen deposition indicated progressive testicular fibrosis.
- Increased germ cell apoptosis was confirmed in mid- and high-dose groups.
- Elevated ROS levels were observed only at the highest dose.
Conclusions:
- Chronic LDR radiation induces testicular damage via apoptosis and fibrosis.
- Oxidative stress may contribute to testicular damage at higher LDR radiation exposure levels.
- These findings highlight the reproductive risks associated with prolonged low-dose radiation exposure.
