Oxidative Stress in Aging Associated ED

ED is highly associated with aging, with prevalence increasing from 6.5% in men aged 20-39 years to 77.5% in those 75 years and older, and it is projected to affect 322 million men worldwide by 2025 [12, 36].

Oxidative stress is an important factor contributing to ED associated with aging. Endothelial and smooth muscle cells of the aged rat penis produce ROS [37-40]. The sources and mechanisms responsible for ROS formation in the aged penis remain mostly unknown. It has recently been demonstrated that eNOS uncoupling is a source of ROS associated with age-related ED. Supplementation with sepiap-terin, which prevents eNOS uncoupling, prevents age-associated ED and prevents increased oxidative stress [40 ] . Future studies are needed to determine in more detail the contribution and mechanism of eNOS uncoupling, as well as other possible sources of ROS in age-related ED.

Molecular mechanisms underlying decreased neurogenic-mediated corpus cav-ernosum relaxation associated with aging involve disturbances in the central and peripheral systems of neurotransmission. Central neuropathy involves increased apoptosis and excessive ROS production in the hypothalamic areas involved in the control of penile erection. Peripheral mechanisms have been attributed to a reduction in nitrergic nerve fibers in the penis and decreased nNOS expression and activity [33]. However, the sources of ROS and the mechanisms of ROS-induced impairment of nitrergic neurotransmission in age-associated ED are not known.

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