Oxidative stress in endothelial cell dysfunction and thrombosis.
Endothelial dysfunction (ECD) is the earliest phenotypic change in the vasculature following exposure to atherothrombotic risk factors. ECD is associated with decreased synthesis and increased oxidative inactivation of nitric oxide (NO). Critical antioxidant enzymes essential for eliminating reactive oxygen species that can inactivate NO include the superoxide dismutases, the glutathione peroxidases, catalase, and glucose-6-phosphate dehydrogenase. Deficiencies of these enzymes increase oxidative stress and NO inactivation and, as such, can either lead to ECD or account for the underlying mechanism of ECD associated with a given atherothrombotic risk factor. Selected antioxidants improve intracellular redox state and reverse ECD by improving the bioavailability of NO. These observations provide mechanistic insights into the molecular basis of ECD in vascular disease and its treatment.
D000818:Animals; D001792:Blood Platelets / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D013927:Thrombosis / Q000378:metabolism*