| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2847210 | Respiratory Physiology & Neurobiology | 2013 | 7 Pages |
Hydrogen sulfide (H2S) metabolism has been proposed as the oxygen (O2) sensing mechanism coupling hypoxia to effector responses in a variety of tissues including vascular and chemoreceptor cells. Implicit in this sensing system is a mechanism for regulating intracellular H2S concentration, presumably through oxidation. However, verification of this mechanism, or any other pathway of H2S signaling has been hampered by the lack of suitable methods for measuring intracellular concentration and distribution profiles. Here, intracellular H2S concentration profiles are modeled using simple monoexponential diffusion equations and current knowledge of H2S biosynthetic and metabolic pathways. The models predict that; (1) while both mitochondrial oxidation and simple diffusion out of the cell can reduce H2S concentration, the former is considerably more effective as an effector of intracellular H2S and (2) exogenously applied H2S may have unanticipated effects on endogenous signaling processes. In addition, these models provide additional support for mitochondrial H2S oxidation as the key couple in H2S-mediated O2 sensing.
► Control of intracellular H2S signaling is mathematically modeled. ► Metabolic inactivation is more effective than regulating production or passive excretion. ► Mitochondrial oxidation is ideally suited to regulate H2S inactivation. ► Mitochondrial oxidation is a biologically relevant O2 sensor. ► Exogenous H2S cannot mimic intracellular H2S signaling.
