The role of oxidative stress in sleep deprivation-induced reproductive dysfunction: A rationale for anti-oxidant intervention

Articles in Press

Document Type : Review Article

Authors

1 Department of Cell Biology and Genetics, School of Basic Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China

2 Department of Biochemistry and Molecular Biology, School of Basic Medicine, Guangxi Medical University, Nanning, Guangxi, 530021, China

3 The Reproductive Medical Center of Nanning Second People’s Hospital, the Third Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530031, China

10.22038/ijbms.2025.90559.19517

Abstract

Sleep deprivation (SD) is a significant risk factor for reproductive dysfunction. This review aims to synthesize evidence establishing that oxidative stress (OS) is the key pathological mediator of SD-induced reproductive impairments in both sexes and to provide a comprehensive rationale for anti-oxidant intervention. We conducted a narrative review of peer-reviewed studies (2000-2025) from PubMed, ScienceDirect, Scopus, and Google Scholar. We examined the evidence linking SD, OS, and reproductive health, with a specific focus on recent preclinical and clinical studies that directly investigate the mechanistic role of OS and the efficacy of anti-oxidant therapies. The evidence demonstrates that SD induces systemic OS, which in turn drives reproductive pathology. In males, SD leads to increased testicular OS, resulting in impaired sperm quality and hormonal disruption. In females, SD is associated with diminished ovarian reserve and reduced oocyte quality, mediated by ovarian OS. Crucially, preclinical studies show that various anti-oxidants, including bromelain, vitamin C, and zinc, can successfully ameliorate SD-induced testicular damage. In women, clinical evidence links sleep disorders to lower melatonin levels in follicular fluid and decreased ovarian reserve, supporting a similar OS-mediated mechanism. The synthesized evidence strongly suggests that OS is a key pathological mechanism through which SD impairs reproductive function. This provides a strong scientific foundation for anti-oxidant therapies as a promising strategy to mitigate these harms. Future clinical trials are warranted to develop effective anti-oxidant regimens for individuals whose fertility is compromised by SD.

Keywords

Main Subjects

References

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