We have found that N-acetylneuraminic acid (NANA) consumes toxic hydrogen peroxide (H2O2) under physiological conditions. Close investigation of this finding revealed that NANA was oxidized by an equimolar amount of H2O2 to provide its decarboxylated product, 4-(acetylamino)-2,4-dideoxy-D-glycero-D-galacto-octonic acid (ADOA). To date, there have been little data on this reaction, and its physiological significance has not been discussed. Examining the detoxification of H2O2 in cultured cells with NANA, we were able to confirm that the cell death caused by H2O2 was suppressed by NANA in a dose-dependent manner. These results revealed a novel role for NANA as a reactive oxygen scavenger. It is known that terminal NANA residues are removed by neuraminidase and that free NANA molecules are recycled or degraded by enzymes. We propose that released monomeric NANA is the potent defense molecule against oxidative damage.
