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Abstract
The abnormal accumulation of reactive oxygen species (ROS) has been identified as a key culprit in the pathogenesis of male infertility. ROS are mainly derived from leukocytes and sperm mitochondria. At physiological concentrations, ROS can positively regulate sperm physiological functions such as capacitation and the acrosome reaction. However, excessive ROS that exceed the body's antioxidant
compensatory capacity will induce oxidative stress, ultimately leading to male infertility. It is worth noting
that although antioxidants can neutralize the damaging effects of ROS, excessive supplementation of
antioxidants may trigger reductive stress, which is equally harmful to oxidative stress. Therefore, clarifying
the molecular mechanisms underlying the impact of ROS concentration imbalance on male infertility, and
further formulating precise antioxidant therapeutic regimens and reducing clinical prognostic risks, have
become important research directions in the field of male infertility. This review provides a comprehensive
overview of the mechanisms by which ROS lead to the decline of male reproductive function, encompassing damage to sperm mitochondrial proteases, alterations in mitochondrial membrane potential, mtDNA injury, and the induction of calcium ion release from sperm mitochondria.
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2026, Vol. 14 
