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Oxidative stress pathways in male reproductive tissues involve the delicate balance between reactive oxygen species (ROS) and the antioxidant defense system, which is crucial for maintaining male fertility [5, 7]. While physiological levels of ROS, such as superoxide and hydrogen peroxide, are required for sperm maturation processes like capacitation and the acrosome reaction, excessive ROS leads to oxidative damage [10, 11]. This damage manifests as lipid peroxidation of the polyunsaturated fatty acid-rich sperm membrane, protein carbonylation, and DNA strand breaks, collectively contributing to male infertility [1, 8]. Therapeutic interventions often target these pathways using exogenous antioxidants like Vitamin E, Coenzyme Q10, and N-acetyl-cysteine to neutralize free radicals and protect sperm integrity [6, 11]. Monitoring these pathways typically involves biomarkers such as malondialdehyde (MDA) for lipid damage and 8-hydroxy-2-deoxyguanosine (8-OHdG) for DNA oxidation [1, 3].
Scavenging of reactive oxygen species (ROS), enhancement of endogenous antioxidant enzyme activity (e.g., SOD, GPx), reduction of lipid peroxidation, and protection of sperm DNA integrity from oxidative fragmentation.
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