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Am J Physiol Regul Integr Comp Physiol 295: R1479-R1485, 2008. First published September 17, 2008; doi:10.1152/ajpregu.90566.2008
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RECEPTORS AND SIGNALING PATHWAYS

Whole tissue hydrogen sulfide concentrations are orders of magnitude lower than presently accepted values

Julie Furne,1 Aalia Saeed,2 and Michael D. Levitt1,2,3

1Research Service and 2Department of Medicine, Veterans Affairs Medical Center, Minneapolis; and 3Department of Medicine, University of Minnesota, Minneapolis, Minnesota

Submitted 3 July 2008 ; accepted in final form 11 September 2008

Hydrogen sulfide is gaining acceptance as an endogenously produced modulator of tissue function. The present paradigm of H2S (diprotonated, gaseous form of hydrogen sulfide) as a tissue messenger consists of H2S being released from the desulfhydration of L-cysteine at a rate sufficient to maintain whole tissue hydrogen sulfide concentrations of 30 µM to >100 µM, and these tissue concentrations serve a messenger function. Utilizing physiological concentrations of L-cysteine and aerobic conditions, we found that catabolism of hydrogen sulfide by mouse liver and brain homogenates exceeded the rate of enzymatic release of this compound such that measureable hydrogen sulfide release was less with tissue-containing vs. tissue-free buffers. Analyses of the gas space over rapidly homogenized mouse brain and liver indicated that in situ tissue hydrogen sulfide concentrations were only about 15 nM. Human alveolar air measurements indicated negligible free H2S concentrations in blood. We conclude rapid tissue catabolism of hydrogen sulfide maintains whole tissue brain and liver concentrations of free hydrogen sulfide that are three orders of magnitude less than conventionally accepted values and only 1/5,000 of the hydrogen sulfide concentration (100 µM) required to alter cellular function in vitro. For hydrogen sulfide to serve as an endogenously produced messenger, tissue production and catabolism must result in intracellular microenvironments with a sufficiently high hydrogen sulfide concentration to activate a local signaling mechanism, while whole tissue concentrations remain very low.

cell signaler; nitric oxide; cytochrome c oxidase


Address for reprint requests and other correspondence: M. D. Levitt, Research Service (151), VAMC, 1 Veterans Dr., Minneapolis, MN, 55417 (e-mail: levit015{at}umn.edu)






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