Oxidative Stress in Hypercholesterolemia Associated ED

Hypercholesterolemia is a significant risk factor for ED attributed to both vasculo-genic and neurogenic factors, although the molecular mechanisms of the latter are largely unknown.

Increased oxidative stress has been postulated to be major molecular factors contributing to hypercholesterolemia-induced vasculogenic ED [72-74]. Corpus caver-nosal tissue of cholesterol-fed animals exhibits increased production of ROS [75-79]. In the mouse penis, hypercholesterolemia increases protein expressions of NADPH oxidase subunits p67p hox, p47phox. and gp91p hox [76], while inhibition of NADPH oxidase by diphenyleneiodonium chloride and apocynin inhibits ROS production and preserves erectile function [76, 77] . These findings indicate a crucial role for NADPH oxidase as a ROS-producing enzyme in ED associated with hyper-cholesterolemia. In addition to NADPH oxidase, eNOS uncoupling [75, 76], but not xanthine oxidase [77], also serves as a source of ROS in the penis of experimental hypercholesterolemic animals.

Oxidative modification of LDL has a major role in hypercholesterolemia-associated atherosclerosis development and ED. Oxidized LDL (oxLDL) is present in penile tissues of patients with vasculogenic ED [80] and animal models of hypercholesterolemia-induced ED [75]. In the general vasculature, oxLDL itself increases superoxide generation via the induction of NADPH oxidase, xanthine oxidase, mitochondrial electron transport chain, and uncoupled eNOS [81], but its effect in the penile vasculature is not known.

The effect of hypercholesterolemia on neurogenic neurotransmission remains largely unknown [73]. Future studies are needed to further understand the pathology of both neurogenic and vasculogenic ED associated with hypercholesterolemia and specifically the role of oxidative stress.

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