Abstract
African Americans have high incidences of both cardiovascular disease (CVD) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Clinical studies demonstrate oxidative stress (OS) and lower blood GSH levels correlate with biomarkers of early atherosclerosis such as carotid intima media thickness and blood pressure. G6PD-deficient cells are susceptible to OS, which can lead to exhaustion/deficiency of GSH. We examined the hypothesis that G6PD-deficiency decreases GSH and Nitric oxide (NO), and upregulates cell adhesion molecules (CAMs) which can lead to excess endothelial dysfunction (ED) and atherosclerosis risk. G6PD deficiency in HUVEC and U937 monocytes was induced by using siRNA or by its pharmacological inhibitor (6-AN). G6PD-deficiency exhibited a dose-dependent increase in CAMs (ICAM-1 & VCAM-1), NADPH Oxidase 4, iNOS, MCP-1 and ROS, and reduction in GSH, eNOS and NO levels (p
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