Oxidative Stress in ED

Oxidative stress has been implicated in vasculogenic and neurogenic ED, although the former has been evaluated in much more detail. Superoxide is generated from several vascular sources in the diseased penis, as discussed below. Furthermore, the reaction of superoxide and NO results in the formation of reactive nitrogen species such as the highly toxic molecule peroxynitrite, which causes oxidative damage to DNA, proteins, and lipids. ROS, produced in vascular smooth muscle cells and endothelial cells, may induce vasculogenic ED by scavenging NO or affecting eNOS expression and activity [17, 29], depleting NOS cofactors [30], generating vasoconstrictors, affecting smooth muscle cell integrity, inactivating antioxidants, and causing structural and functional changes within the vasculature [22, 27] .

Increased oxidative stress may promote atherosclerotic disease through the oxidation of LDL, the major carrier of plasma cholesterol, with further potentiation of superoxide generation [31]. Several of these pathways have been described in the penis in association with ED, as detailed in further sections.

ROS also affect nitrergic neurotransmission via apoptosis of nitrergic nerves and decreased nNOS signaling, resulting in ED [32-35].

In the following sections, we describe the known sources of ROS and targets of ROS action in the penis in vasculogenic and neurogenic ED associated with aging and major disease states, detailing known molecular mechanisms of ROS production and action associated with each health condition.

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