The effect of hydrogen sulfide on glycolysis-based energy production and mouse red blood cell survival

Abstract

Hydrogen sulfide (H2S), a gasotransmitter that modulates physiological and pathophysiological processes, has recently been shown to promote aerobic energy production in the mitochondrion in response to hypoxia. Its effect on anaerobic energy production, however, has yet to be established. Glycolysis is the anaerobic process by which ATP is produced through the metabolism of glucose. The purpose of this study was to establish the effect of H2S on glycolysis-mediated energy production in mouse RBCs, which are mitochondrion-free. This study demonstrated the capacity of mouse RBCs to produce H2S via 3-mercaptopyruvate sulfurtransferase (MST). Both exogenously administered H2S salt (NaHS) and MST-derived endogenous H2S stimulated glycolysis-mediated ATP production. The effect of NaHS on ATP levels was oxygen-independent. However, hypoxic stress stimulated MST activity in mouse RBCs. High concentrations of NaHS (300-1000 μM) prolonged cell viability but reduced ATP levels. H2S may offer a cytoprotective effect in mammalian RBCs to maintain oxygenindependent energy production.