Oxidative stress (OS) is a significant factor in male infertility, caused by an imbalance between reactive oxygen species (ROS) and the body's antioxidant defenses. ROS, which include molecules like superoxide, hydrogen peroxide, and hydroxyl radicals, can damage sperm DNA, lipids, and proteins, impairing sperm function and fertility. OS is linked to reduced sperm motility, morphology, and fertilization capacity, and is a major cause of idiopathic male infertility. ROS production in spermatozoa occurs through mechanisms such as the nicotinamide adenine dinucleotide phosphate oxidase system and mitochondrial processes. Endogenous sources of ROS include leukocytes and immature spermatozoa, while exogenous sources include radiation, toxins, smoking, and alcohol. ROS can also be generated by varicocele, a common cause of male infertility. Physiologically, low levels of ROS are essential for sperm functions like capacitation, hyperactivation, and the acrosome reaction. However, excessive ROS leads to lipid peroxidation, DNA damage, and apoptosis, all of which contribute to male infertility. ROS levels in seminal plasma are associated with impaired semen parameters, and elevated ROS levels are linked to increased sperm DNA damage and reduced fertility. Measurement of ROS in semen is crucial for diagnosing male infertility, with methods including chemiluminescence assays and nitroblue tetrazolium tests. Antioxidants, both enzymatic (e.g., SOD, catalase, glutathione peroxidase) and non-enzymatic (e.g., vitamins C and E, carotenoids), are used to reduce ROS levels and improve sperm function. Lifestyle changes, such as avoiding heat exposure, smoking, and excessive alcohol consumption, are also recommended to prevent OS. Antioxidant supplementation is a key strategy in managing OS and improving male fertility.Oxidative stress (OS) is a significant factor in male infertility, caused by an imbalance between reactive oxygen species (ROS) and the body's antioxidant defenses. ROS, which include molecules like superoxide, hydrogen peroxide, and hydroxyl radicals, can damage sperm DNA, lipids, and proteins, impairing sperm function and fertility. OS is linked to reduced sperm motility, morphology, and fertilization capacity, and is a major cause of idiopathic male infertility. ROS production in spermatozoa occurs through mechanisms such as the nicotinamide adenine dinucleotide phosphate oxidase system and mitochondrial processes. Endogenous sources of ROS include leukocytes and immature spermatozoa, while exogenous sources include radiation, toxins, smoking, and alcohol. ROS can also be generated by varicocele, a common cause of male infertility. Physiologically, low levels of ROS are essential for sperm functions like capacitation, hyperactivation, and the acrosome reaction. However, excessive ROS leads to lipid peroxidation, DNA damage, and apoptosis, all of which contribute to male infertility. ROS levels in seminal plasma are associated with impaired semen parameters, and elevated ROS levels are linked to increased sperm DNA damage and reduced fertility. Measurement of ROS in semen is crucial for diagnosing male infertility, with methods including chemiluminescence assays and nitroblue tetrazolium tests. Antioxidants, both enzymatic (e.g., SOD, catalase, glutathione peroxidase) and non-enzymatic (e.g., vitamins C and E, carotenoids), are used to reduce ROS levels and improve sperm function. Lifestyle changes, such as avoiding heat exposure, smoking, and excessive alcohol consumption, are also recommended to prevent OS. Antioxidant supplementation is a key strategy in managing OS and improving male fertility.