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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]

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how they translate across routes is an open research question, not a solved one

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Dosing errors caused by the confusion between milligrams (mg) and milliliters (mL) have resulted in unintended overdoses/fatalities (61)

Whether the Fe-S cluster on FECH has additional functions remains to be explored