Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 186, Issue 2, Pages 173-179Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.resp.2013.01.010
Keywords
Hydrogen sulfide; RBC; Mitochondrion; Cystathionine beta-synthase; Diffusion
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Funding
- National Science Foundation [IOS 0641436, IOS 1051627]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1051627] Funding Source: National Science Foundation
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Hydrogen sulfide (H2S) metabolism has been proposed as the oxygen (O-2) 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 O-2 sensing. (C) 2013 Elsevier B.V. All rights reserved.
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