Oxidative stress and cardiovascular risk: the role of vascular NAD(P)H oxidase and its genetic variants.

摘要: Several risk factors for coronary artery disease (CAD) induce atherosclerosis through endothelial activation and dysfunction, ample evidence now suggests that the balance between production removal of reactive oxygen species (ROS) - a condition termed oxidative stress is implicated in such processes. A main source ROS vascular cells reduced nicotinamide adenine dinucleotide/nicotinamide dinucleotide phosphate (NAD(P)H) oxidase system. This membrane-associated enzyme, composed five subunits, catalyzing one-electron reduction oxygen, using NADH or NADPH as electron donor. One system p22-phox, has polymorphic site on exon 4, associated with variable enzyme activity. polymorphism generated by point mutation (C(242)T) producing substitution histidine tyrosine at position 72, which affects one heme binding sites essential NAD(P)H The consequent decrease superoxide thus characterizes phenotype candidate conferring to carrier susceptibility CAD. At present, however, body from current literature not yet sufficient confirm exclude hypothesis C(242)T protects functional effects this potential its pathophysiological consequences also need further investigation.