Abstract
Catalytic reduction of ABTS•– to ABTS2– was achieved by a ruthenium complex using a variety of biologically-relevant alcohols, such as amino acids, sugars, or citric acid cycle metabolites, as terminal reductants. Rate law and deuterium labeling studies revealed that radical reduction was performed by a ruthenium–hydride intermediate formed via hydride transfer from the alcohol to ruthenium. With this knowledge, it was subsequently shown that NAD+ also functioned as a terminal reductant via its ribose subunit, representing the first demonstration that NAD+ could function as a hydride donor under biologically-relevant conditions. This ruthenium complex shows promise for applications in oxidative stress and redox therapeutics.
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