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At low concentrations, ROS positively influence physiological processes, including sperm mature and motility. However, elevated ROS levels can harm human spermatozoa through oxidative stress, primarily due to the absence of effective DNA damage repair mechanisms and inadequate antioxidant defenses. In this review, we summarize the physiological and pathophysiological roles, endogenous and exogenous sources, and therapeutic strategies related to ROS in idiopathic asthenozoospermia. 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