PMC:7799378 / 14535-15421 JSONTXT

{"target":"http://pubannotation.org/docs/sourcedb/PMC/sourceid/7799378","sourcedb":"PMC","sourceid":"7799378","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7799378","text":"NO production is positively correlated with G6PD activity. G6PD deficiency in human granulocytes abolishes NO production induced by LPS and 12-myristate 13-acetate (PMA) [42]. IL-1β increases NOS expression and NO levels as well as G6PD activity in pancreatic islet cells [81]. Inhibition of G6PD by DHEA or siRNA decreases IL-1β-stimulated NO production. The bioavailability of NO and G6PD status are inversely correlated with ROS in endothelial cells [82]. Less endothelial NOS (eNOS) expression and low levels of NO and GSH are found in G6PD-deficient endothelial cells, while L-cysteine, a GSH precursor, reduces oxidative stress [83]. Peroxynitrite derived from NO is toxic to neurons. It stimulates G6PD activity and causes apoptosis in PC12 cells. NO-mediated apoptotic neuronal cell death can be rescued by G6PD overexpression, while G6PD suppression worsens the apoptosis 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