Oxidative Molecular and Cellular Pathways

The exact mechanism by which varicocele induces testicular failure and sperm dysfunction is still under debate; however, oxidative stress seems to play a principal role in reproductive dysfunction. In addition, the oxidative cellular and

Table 18.2 Seminal antioxidant capacity in men with varicocele

Study

Semen antioxidant

Findings

Hendin et al. [53] Sharma et al. [54] Pasqualotto et al. [55] TAC Pasqualotto et al. [56] TAC

Hurtado de Catalfo et al. [58]

Ascorbate, urate, tocopherol.

and glutathione TAC

Nonenzymatic antioxidants. SOD.CAT

Pasqualotto et al. [55] TAC Sakamoto et al. [60] SOD

SOD. CAT. GPx. vitamins C and E

Infertile (21) and fertile men

(15) with varicocele Infertile men with varicocele (56) Infertile men with varicocele (77) Infertile normospermic men with varicocele (16) Infertile men with varicocele (36) Infertile (21) and fertile (15)

men with varicocele Oligospermie (15) and normospermic men with varicocele (15) Infertile (42) and fertile (45) men with varicocele

Sperm donors without varicocele (17) Sperm donors (24)

Healthy men (19)

Healthy donors (19)

Fertile men (33)

Fertile men (17)

Oligospermie and normospermic infertile men (15) without varicocele Fertile men without varicocele (45)

Lower TAC in men with varicocele vs. controls Lower TAC in men with varicocele vs. controls Lower TAC in men with varicocele vs. controls Lower TAC in varicocele group vs. controls Lower antioxidant levels in infertile men with varicocele Lower TAC in varicocele groups vs. controls Higher SOD activity in varicocele group vs. men without varicocele Lower antioxidant levels in varicocele groups vs. fertile men

CAT Catalase; GPx glutathione peroxidase; ROS reactive oxygen species; SOD superoxide dismutase; TAC total antioxidant capacity molecular pathways, which may be abnormally activated in men with varicocele, are not completely understood. One possible mechanism is the compensatory release of nitric oxide (NO), in response to testicular venous congestion, with associated elevation in malondialdehyde (MDA) that together contribute to excessive lipid peroxidation and defective spermatogenesis [72] . Another hypothesis is cytokine-mediated oxidative stress. The expression of IL-1 and IL-6, both potent proinflammatory activators, has been shown to be upregulated in experimental and clinical varicocele, respectively [72, 73]. Leptin expression has been associated with oxidative stress (lipid peroxidation) in obesity [74] . Studies have shown an increased expression of leptin in Leydig cells and germ cells in men with vari-cocele, suggesting a possible role of leptin in inducing OS in infertile men with varicocele [72, 75]. Glial cell line-derived neurotropic factor receptor-alpha-1, a growth factor that protects neuron from OS, has been shown to play a role in sper-matogenesis and DNA synthesis [ 76 ] . This neurotropic factor is expressed at lower cellular levels in spermatids and Leydig cells in patients with untreated varicocele [77], which may account for OS in the testis. Other mechanisms that could explain the association between varicocele and OS include the antagonistic effect of cadmium on zinc (an antioxidant) [78], whereby increased levels of cadmium in infertile men with varicocele [ 79] could reduce seminal antioxidant capacity [72]. Finally, a reduced expression of HO-isoenzyme 1 may result in an increased vulnerability of testicular germ cell to oxidative injury in the presence of varicocele [80].

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