Oxidative Stress Induced Infertility in Varicocele

The pathophysiology of varicocele still remains controversial involving factors like altered testicular thermo-dynamics, changes in testicular blood flow and venous pressure, leydig cell dysfunction and presence of autoantibodies against spermatozoa. Reflux of warm blood from the abdominal cavity into the scrotum, resulting from malfunctioning of valves in spermatic and cremasteric veins attributes to the raised intra-testicular temperature.

Several theories have been proposed for the mechanism involved in defective spermatogenesis because of altered testicular thermodynamics. According to one theory, anatomical disparity between the right and left spermatic veins leads to increased hydrostatic pressure in the left spermatic vein causing dilatation of the pampiniform plexus. Another theory suggests that dysfunctional valves of the internal spermatic veins cause regression of blood. Naughton  proposed that compression of the left renal vein between the superior mesenteric artery and aorta causes partial obstruction of the left spermatic vein leading to varicocele formation. It was also suggested that spermatogenic dysfunction seen in varicocele was the result of thermal damage to spermatozoal proteins and DNA within the seminiferous tubules. The normal anatomical asymmetry and valvular dysfunction causes pooling of blood more in the left spermatic vein.

This phenomenon called the “nutcracker effect” seen as increased compression of the left renal vein between superior mesenteric artery and descending aorta causes retrograde flow of blood down the cremasteric and internal spermatic veins. The right varicocele is considered rare but with the use of modern diagnostic techniques e.g., colored Doppler ultrasound, increased frequency of bilateral localization of varicocele has now been documented in recent studies.