O-1: Study The Effect of Oral Zinc Supplementation on Enzymes of Urate Pathway in Spermatozoa of Patients with Asthenospermia

Background: The generation of reactive oxygen species (ROS) in the male reproductive tract has become an actual concern because of their probable noxious effects, at high levels, on physical properties of sperm quality. ROS are extremely reactive oxidizing agents, which a member of the class of free radicals. It was found that uric acid can act as an essential water soluble antioxidant and therefore has a possible function in protection of spermatozoa against oxidative damage. Materials and Methods: Semen samples were obtained from 60 fertile and 60 subfertile men with asthenozoospermia between July 2011 to July 2012, from couples who consulted the infertility clinic of the Babil hospital of maternity (Hilla city/ IRAQ). The subfertile group consist of the patients which treated with zinc sulfate, every participant took two capsules of zinc sulfate per day for three months (each one 220 mg). Semen samples were obtained (before and after zinc sulfate supplementation). After liquefaction seminal fluid at room temperature, routine semen analyses were performed. The levels of uric acid (UA), 5--nucleotidase (5--NU) activity, adenosine deaminase (ADA) activity and Xanthine oxidase (XO) activity are measured in the spermatozoa and seminal plasma of patients with asthenospermia and healthy subjects. Results: Compared with healthy controls, uric acid levels were found to significantly decrease in seminal plasma and spermatozoa of patients with asthenozoospermia. Zinc supplementation elevates uric acid levels in seminal plasma of asthenozoospermic subjects to normal value. This study recorded highest decrease in seminal 5'-NU activity in asthenospermic patients. The decreased activity of this marker enzyme exposed spermatozoal damage from stress induced oxidative damage possibly causing disruption in membrane function and integrity. The values of ADA were significantly higher in asthenospermic specimens as compared to the controls. The values of XO were significantly higher in asthenospermic specimens as compared to the controls. The zinc supplementation induced decrease of XO activity is of particular interest. Volume of semen, progressive sperm motility percentage, and total normal sperm count were increased after zinc sulfate supplementation. Conclusion: Zinc treatment decreases asthenozoospermia through several mechanisms such as reduction of oxidative stress and apoptosis.