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Published-Ahead-of-Print December 8, 2005, DOI:10.2164/jandrol.05136

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ROLE OF OXIDATIVE STRESS IN PATHOPHYSIOLOGY OF ERECTILE DYSFUNCTION

Ashok Agarwal , Kalyana C. Nandipati , Rakesh K. Sharma , Craig D. Zippe , and Rupesh Raina

Erectile dysfunction (ED) is a highly prevalent and often underestimated problem in the general population. Systemic risk factors such as diabetes, hypertension and hyperlipidemia increase the incidence of erectile dysfunction. The pathophysiology of ED is multifactorial, and endothelial dysfunction appears to play a key role. Nitric oxide released from the endothelium is the principle mediator involved in normal erectile response. Decreased production of NO from the damaged endothelium or increased destruction at the site of action potentially can produce ED. Recently, oxidative stress has been implicated in endothelial damage or increased destruction of NO. However, the precise site of origin of these free radicals and their interactions with the endothelium is unclear. The lack of our understanding and the paucity of reports have made this topic as an interesting future research option. Oxidative stress has been implicated as one of the major causes of ED. The introduction of oral phosphodiesterase inhibitors has completely changed the treatment of ED. Initial animal studies demonstrated the beneficial effect of combination therapy with antioxidants (vitamin E) and sildenafil. This may help improve the efficacy of oral PDE-5 inhibitors in the near future. In addition, gene therapy and NO donors may also play important roles.




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