Effect of Varicocele Treatment on Oxidative Stress Markers and Sperm DNA Fragmentation

Varicocele manifests as a dilatation and convolution of the pampiniform plexus, which results in venous stasis that induces heat stress and hypoxia in the male reproductive tract. These insults increase the burden of oxidative stress by promoting production of reactive chemical species, depleting cellular stores of antioxidants, and altering activities of enzymes responsible for cellular metabolism. As a consequence of these derangements, direct and indirect markers of oxidative stress are elevated in the testes and semen of men with clinically significant varicocele. Sperm nuclear DNA is also damaged in this oxidative milieu, most commonly through strand breaks that result in fragmentation. Varicocele repair via surgical intervention or percutaneous embolization aims to occlude the internal spermatic vein and ameliorate the heat stress and hypoxia that accompany venous reflux. Antioxidant therapy aims to reduce oxidative stress by augmenting the cellular capacity to neutralize reactive chemical species. Current data support varicocele repair in infertile men with clinically detectable disease and abnormal semen parameters. There is a wealth of evidence demonstrating that varicocelectomy ameliorates markers of oxidative stress and sperm DNA fragmentation, effects that are sustained throughout the postoperative period. Though antioxidants have also been shown to temporarily improve these metrics, it is unclear how medical therapy alone affects fertility in men with varicocele. Use of antioxidants as adjuvant to surgical repair is an active area of investigation, with some evidence supporting augmentation of male fertility following varicocelectomy.