Abstract

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia, which contributes 
to systemic complications including cardiovascular, renal, and reproductive dysfunction. Reproductive impairments 
in both males and females are increasingly recognized as significant consequences of DM, largely mediated by 
oxidative stress. Oxidative stress arises from an imbalance between the production of reactive oxygen species (ROS) 
and the capacity of endogenous antioxidant defenses, resulting in damage to lipids, proteins, and nucleic acids. In 
males, oxidative stress disrupts spermatogenesis, reduces sperm motility, and induces DNA fragmentation, all of 
which impair fertility. In females, oxidative damage affects ovarian follicles, granulosa cells, and oocyte quality, 
compromising ovulation and increasing the risk of early pregnancy loss. Antioxidant interventions, both 
endogenous and exogenous, offer potential therapeutic strategies to mitigate these effects. Endogenous antioxidants 
such as superoxide dismutase, catalase, and glutathione peroxidase are critical for neutralizing ROS, whereas dietary 
and pharmacological antioxidants, including vitamins C and E, polyphenols, and selenium, can further restore redox 
balance. These interventions have demonstrated improvements in gamete quality, hormone regulation, and 
reproductive outcomes in experimental and clinical studies. However, challenges such as bioavailability, optimal 
dosing, timing of administration, and individual variability influence therapeutic efficacy. This review explores the 
molecular mechanisms by which oxidative stress impairs reproductive function in diabetes and highlights current 
and emerging antioxidant strategies that may preserve or restore reproductive potential, emphasizing the need for 
targeted, individualized therapeutic approaches.