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The oxidative stress, typically observed in pathological conditions determining endothelial dysfunction, might induce endothelial NO depletion and reduced endothelial NO availability, mediated by the interaction of reactive oxygen species with NO to generate oxidative agents potentially damaging cell DNA and proteins, namely reactive nitrogen-containing species [51], or by a direct decrease of NO synthesis, therefore suggesting potential benefit from the administration of NOS substrates, such as l-ARG, as a therapeutic strategy to increase NO production and improve CVD-related endothelial dysfunction [19, 52]