Table 1.
Mechanisms | Consequences | Impact in PE | References |
---|---|---|---|
Increased O2•−production | Peroxynitrite formation | Increased | [160,161,162,163] |
Sources:NOX2,Xanthine Oxidase, eNOS uncoupling | Decreased NO bioavailability | ||
Nitration, inflammation | |||
Increased arginaseactivity | l-arginine depletion | Increased | [[164], [165], [166], [167]] |
Increased ADMA levels | eNOS uncoupling | [168,169] | |
BH4 oxidation | eNOS uncoupling | No variation | [170] |
Decreased NO generation | (very few studies) | ||
Increased O2•−production | |||
eNOS S-glutathionylation | eNOS uncoupling | Increased | [171] |
Decreased NO generation | |||
Increased O2•−production | |||
LPP-adducts on eNOS | eNOS dysfunction | ||
Decreased NO generation | Increased | [127] |
O2•−, superoxide anion; NOX2, NADPH oxidase 2; NO, nitric oxide; ADMA, asymmetric dimethylarginine; BH4, tetrahydrobiopterin; eNOS, endothelial nitric oxide synthase; LPP, lipid peroxidation products.