Cumulative Low-Dose-Rate Radiation Induces Oxidative Stress, Apoptosis, and Fibrosis in Mouse Testisopen access
- Authors
- Kim, Eun-Jin; Prayoga, Anjas Happy; Ha, Jina; Kang, Deok Gyeong; Yang, Jinsung; Kang, Sohi; Kim, Jin-Mok; Ahn, Byeonggyu; Cao, Dang Long; Yun, Seung Pil; Lee, Bo Hyun; Kim, Joong-Sun; Kang, Dawon
- Issue Date
- Aug-2025
- Publisher
- MDPI AG
- Keywords
- epididymis; fibrosis; low-dose-rate radiation; reactive oxygen species; testis
- Citation
- Antioxidants, v.14, no.8
- Indexed
- SCIE
SCOPUS
- Journal Title
- Antioxidants
- Volume
- 14
- Number
- 8
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/79935
- DOI
- 10.3390/antiox14081028
- ISSN
- 2076-3921
2076-3921
- Abstract
- Ionizing radiation is a well-known environmental stressor capable of generating excessive reactive oxygen species (ROS), leading to oxidative damage in sensitive tissues, including the reproductive system. While oxidative stress is increasingly implicated in male reproductive dysfunction, the long-term effects of low-dose-rate (LDR) radiation on testicular structure and oxidative status remain underexplored. In this study, mice were exposed to continuous LDR radiation (0.39, 1.29, and 3.46 mGy/h) for 21 days to assess testicular histopathology and oxidative status. Although testis weight did not significantly differ among groups, histological analysis revealed basal membrane disruption and reduced spermatogenic cell populations in irradiated groups. Masson’s Trichrome and Sirius Red staining demonstrated dose-dependent collagen deposition, indicating progressive testicular fibrosis. TUNEL assays confirmed increased germ cell apoptosis in the mid- and high-dose-rate groups. ROS levels were significantly elevated only in the highest-dose group, suggesting a threshold-dependent oxidative stress response. These findings indicate that chronic LDR radiation induces testicular damage primarily through apoptosis and fibrosis, with oxidative stress potentially contributing at higher exposure levels.
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