Breakthroughs and ViewsSuperoxide as a Messenger of Endothelial Function
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Cited by (63)
Oxidative stress in pregnancy complicated by preeclampsia
2020, Archives of Biochemistry and BiophysicsCitation Excerpt :In addition, ONOO− can lead to irreversible nitration of tyrosine residues in other proteins, causing altered phosphorylation and enzymatic dysfunction. The ONOO− formation not only inhibits the bioavailability of NO but also the production of prostaglandin I2 (PGI2) by tyrosine nitration and inhibition of prostaglandin synthase (PGIS) that causes smooth muscle contraction and activation of platelet and white blood cells [69,85]. Increasing asymmetric dimethyl-l-arginine (ADMA) can inhibit eNOS activity by decoupling of eNOS and reducing the uptake of l-arginine in endothelial cells.
Minerals in pregnancy and newborns
2020, Molecular Nutrition: Mother and InfantThe endothelial plasma membrane transporter bilitranslocase mediates rat aortic vasodilation induced by anthocyanins
2013, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :The source of ROS in response to flavonoids remains to be determined. It could be due to activation of oxidase enzymes, such as NADPH-oxidase, xanthine oxidase, mitochondria oxidases, or due to the flavonoids itself [25]. It can be speculated that the vasodilation activity of flavonoids is merely the side effect of the endothelium defense mechanisms, incorporating increased NO production, against the sudden increase in cellular oxidative stress.
Antioxidants to enhance fertility: Role of eNOS and potential benefits
2011, Pharmacological ResearchThe EGCg-induced redox-sensitive activation of endothelial nitric oxide synthase and relaxation are critically dependent on hydroxyl moieties
2010, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Several enzymes are known to generate intracellular superoxide anions in a controlled way in endothelial cells. The most important ones are the membrane-located NADPH oxidase, xanthine oxidase, arachidonic acid–metabolizing enzymes such as cytochrome P450, and the mitochondrial electron transport chain [18]. The present findings showing that inhibitors of these major enzymatic sources of superoxide anions did affect neither the EGCg-induced NO-mediated relaxation nor the phosphorylation of eNOS imply the involvement of another source of ROS, which, however, remains to be determined.
Down-regulation of neprilysin (EC3.4.24.11) expression in vascular endothelial cells by laminar shear stress involves NADPH oxidase-dependent ROS production
2009, International Journal of Biochemistry and Cell Biology
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