Varicocele is one of the commonest surgically reversible causes of infertility and affects about 40 per cent males with primary infertility and 70-80 per cent males with secondary infertility. The pathophysiology of varicocele induced infertility remains unknown. One of the mechanisms by which it causes a decline in semen quality is increased testicular temperature due to dilation and tortuosity of pampiniform plexus of veins (1). In addition, a number of men with varicocele harbour genetic abnormalities like Yq microdeletions (2). However, it is unknown whether these are causally related or simply an incidental finding because of the high prevalence of varicocele among infertile men. Supraphysiological reactive oxygen species (ROS) levels have been reported in men with varicocele and is one of the potential aetiological factors in varicocele mediated deterioration in sperm concentration, motility and morphology (3-5). Agarwal et al (6) reported that sperm dysfunction is multifactorial in varicocele but oxidative stress is the main cause. Oxidative stress can cause an alteration in the dynamics of testicular microvascular blood flow, endocrine signaling and germ cell apoptosis (7).