Figure 2 The central role of oxidative stress in the pathophysiology of varicocele induced male infertility Figure 2 | The central role of oxidative stress.

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Figure 2 The central role of oxidative stress in the pathophysiology of varicocele induced male infertility Figure 2 | The central role of oxidative stress in the pathophysiology of varicocele induced male infertility. Although varicocele pathogenesis is multifactorial, oxidative stress seems to have a central role. Increased oxidative stress can be a result of the combination of increased ROS and decreased TAC. Increased pressure on venous walls might result in release of ROS and higher grades of varicoceles have been shown to correlate with higher levels of oxidative stress. Oxidative stress can harm germ cells directly or indirectly through influencing nonspermatogenic cells and the basal lamina of the seminiferous tubules resulting in induction of apoptosis. In addition, spermatozoa DNA and lipid membranes are attacked directly by ROS, resulting in sperm DNA damage, increased DNA fragmentation, and lipid peroxidation. Other potential mechanisms involved in varicocele-induced male infertility include scrotal hyperthermia, hypoxia, reflux of renal and adrenal metabolites, hormonal imbalances, and the formation of antisperm antibodies; these mechanisms might act on their own to cause negative testicular effects, or they might also influence the level of oxidative stress, highlighting the central role of this pathophysiological mechanism. Heat stress has been shown to increase oxidative stress by production of ROS from mitochondrial membranes, cytoplasm, and peroxisomes, and likewise hypoxia might increase oxidative stress through inflammatory reactions. Jensen, C. F. S. et al. (2017) Varicocele and male infertility Nat. Rev. Urol. doi:10.1038/nrurol.2017.98