DNA Damage and Oxidative Stress

Many theories were proposed to explain the molecular mechanism of sperm DNA damage of spermatozoa; these are: (a) apoptosis occurring mainly during spermatogenesis [56, 57] with DNA double-strand breaks (DSBs) in spermatozoa arising through an abortive apoptotic pathway [58]; (b) ROS [59-61];

(c) defective chromatin packaging; and (d) DNA fragmentation induced by endogenous endonucleases [62] . Sperm DNA damage may result from various physiological and pathological conditions including advanced age [63], varicocele [64], cancer [65], leukocytospermia [66]. or high prolonged fever [67]. In addition, environmental factors can also be involved such as smoking and air pollution [59, 68], radiation [43, 69], pesticides, chemicals, heat, and hydrogen peroxide [70]. In addition, spermatozoa DNA damage may result due to lack of the antioxidant protection or excessive exposure to ROS or both. Antioxidants also might be achieved by extracellular antioxidants provided by the secretions of the male reproductive tract, e.g., vitamin C, uric acid, tryptophan, spermine, and taurine [71, 72]. A reduction in the incidence of sperm DNA fragmentation by oral antioxidant treatment with such scavengers (vitamin C and E) has been also reported [73],

It has also been shown that in vitro separation of the spermatozoa from the seminal plasma in ART setting leaves them unprotected and vulnerable to ROS damage from leukocytes [74] . Removal of leukocytes and adding antioxidants to the ART medium such as reduced glutathione may reverse the action of leukocytes and decrease the negative effect of ROS on spermatozoa DNA [75-77]. However, the presence of sperm DNA damage has been closely associated with impaired sperm function as well as male infertility [56] .

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