Oxidative Stress in ED Associated with Cigarette Smoking

Cigarette smoke is a complex mixture of chemical compounds containing a high concentration of ROS, NO, peroxynitrite, and free radicals of organic compounds. These constituents get into the bloodstream and can directly activate vascular ROS production. In the general vasculature, cigarette smoking (or products of cigarette smoke) increases superoxide generation by both endothelial and smooth muscle cells from NADPH oxidase and uncoupled eNOS, and upregulates proinflammatory cytokines and the RhoA/ROCK contractile pathway. This results in reduced NO bioavailability, increased vasoconstriction, and endothelial dysfunction [82, 83].

Cigarette smoking, both active and passive, is a risk factor for ED [84, 85]. Increasing evidence provided by basic science studies supports the concept that smoking-related ED is associated with reduced bioavailability of NO due to increased oxidative stress. Chronic cigarette smoke exposure impairs neuroregula-tory control of penile erection and impairs NO bioavailability [86] . Many of the vascular effects of chronic smoking are attributed to nicotine. In rabbit cavernosal smooth muscle cells, nicotine increases superoxide formation apparently by inducing NADPH oxidase [87].

Epidemiologic evidence suggests that not only active, but passive, exposure to cigarette smoke also significantly predicts incident ED [88, 89]. Chronic passive cigarette smoking decreases NO bioavailability [90], decreases penile eNOS activity, and increases ROS production in penile arterial and corporeal vascular endothelium and smooth muscle cells [91]. These studies demonstrate that oxidative stress and endothe-lial dysfunction are the fundamental pathophysiological mechanisms linking both active and passive cigarette smoke exposure to ED. However, the exact pathogenic mechanisms underlying cigarette smoking-related ED, the sources of ROS, and cellular targets in the penis are not well understood and require further investigation.

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