Sulfide Oxidation Evidences the Immediate Cellular Response to a Decrease in the Mitochondrial ATP/O2 Ratio

The present article will not attempt to deal with sulfide per se as a signaling molecule but will aim to examine the consequences of sulfide oxidation by mitochondrial sulfide quinone reductase in mammalian cells. This oxidation appears first as a priority to avoid self-poisoning by endogenous sulfide and second to occur with the lowest ATP/O-2 ratio when compared to other mitochondrial substrates. This is explained by the injection of electrons in the respiratory chain after complex I (as for succinate) and by a sulfur oxidation step implying a dioxygenase that consumes oxygen but does not contribute to mitochondrial bioenergetics. Both contribute to increase cellular oxygen consumption if sulfide is provided below its toxic level (low mu M). Accordingly, if oxygen supply or respiratory chain activity becomes a limiting factor, small variations in sulfide release impact the cellular ATP/ADP ratio, a major metabolic sensor.

Automated summary

This article examines the consequences of sulfide oxidation by mitochondrial sulfide quinone reductase in mammalian cells. The oxidation of sulfide helps to avoid self-poisoning and has a lower ATP/O-2 ratio compared to other mitochondrial substrates. It increases cellular oxygen consumption and impacts the cellular ATP/ADP ratio.