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

Authors

Keke Chen, Kaixing Huang, Xiaoyu Liu, Fengyou Luo, Qiping Hu, Changlong Xu

Published in

Iranian journal of basic medical sciences. Volume 29. Issue 2. Pages 191-201.

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.

PMID:
42004508
Bibliographic data and abstract were imported from PubMed on 13 Sep 2026.

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