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Model of radiation-induced endothelial dysfunction. Radiation-induced oxidative stress may decrease the availability of the eNOS cofactor BH4 due to rapid oxidation of BH4 to 7,8-BH2. Diminished BH4 availability may induce eNOS uncoupling and thereby limit NO production and increase O2− production. Endothelial NOS–dependent O2− may reduce BH4 levels even further.
