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ARTICLES: Guanghua Tang, Lingyun Wu, Wenbin Liang, and Rui Wang Direct Stimulation of KATP Channels by Exogenous and Endogenous Hydrogen Sulfide in Vascular Smooth Muscle Cells Mol Pharmacol 2005; 68: 1757-1764 [Abstract] [Full text] [PDF]

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Toxicity of hydrogen sulfide

Heikki Savolainen   (15 December 2005)

Response to Savolainen Letter

Rui Wang   (15 December 2005)

Toxicity of hydrogen sulfide 15 December 2005
Heikki Savolainen, Prof. Dept. of Occup. Safety & Hlth., Tampere, Finland Send letter to journal: Re: Toxicity of hydrogen sulfide heikki.savolainen{at}stm.fi Heikki Savolainen	Hydrogen sulfide is highly toxic because it is an inhibitor of mitochondrial cytochrome oxidase at minute concentrations. Histotoxic hypoxia associated with the inhibition initiates lipid peroxidation which also affects function of ion channel. For example, we found a decrease in veratridine-dependent transmembrane potential in synaptosomes from hydrogen sulfide-treated rat brain samples (1). Such findings lead us to wonder whether similar changes in other organs might result from this toxic effect. 1 Rafalowska U, Zitting A, Savolainen H. Metabolic changes in rat brain synaptosomes after exposure to sulfide in vivo. Toxicol Lett 34:193-200 (1986)
Response to Savolainen Letter 15 December 2005
Rui Wang Send letter to journal: Re: Response to Savolainen Letter rwang{at}lakeheadu.ca Rui Wang	It goes naturally and conveniently to ascribe biological changes induced by hydrogen sulfide to toxic phenomena. But the real issues raised in Dr. Savolainen’s letter are two-fold, distinguishing a “toxic effect” from a physiological action of H2S being one and understanding the mechanisms for H2S-induced modulation of ion channel functions being the other. Dr. Savolainen assumed that functional changes in “synaptosomes from hydrogen sulfide-treated rat brain samples” were toxic outcomes. Endogenous production of H2S is a well-documented fact. Without knowing in vivo concentration of hydrogen sulfide after sulfide injection into animals one cannot tell whether H2S in vivo has reached a toxic level or remained in a physiological range. Furthermore, the inhibition of mitochondrial cytochrome oxidase by hydrogen sulfide is not necessarily a consequence of toxic damage. Would it also be important if H2S at physiological range can modulate the activity of this enzyme? More detailed discussion on and comparison between physiological and toxicological effects of H2S have been described before (1, 2). Activation of KATP channels in smooth muscle cells by H2S (3) was not only observed with the whole-cell recording but also with the cell-free single channel recording configurations of the patch-clamp technique. In the absence of intracellular milieu, the effect of H2S on single KATP channel proteins on a membrane patch would not be affected by cellular metabolism or integrity of respiratory machinery in mitochondria. As such, different mechanisms may be involved in cellular and molecular effects of H2S, depending on metabolic status of the systems under investigation. 1. Wang R. The Evolvement of Gasotransmitter Biology and Medicine: From atmospheric toxic gases to endogenous gaseous signaling molecules. In "Signal Transduction and the Gasotransmitters: NO, CO, and H2S in Biology and Medicine", (Wang R, ed.), pp. 3-32, Totowa, Humana Press, 2004. 2. Wang R. Two’s company, three’s a crowd – Can H2S be the third endogenous gaseous transmitter? FASEB J. 16: 1792-1798, 2002. 3. Tang G, Wu L, Liang W, Wang R. Direct stimulation of KATP channels by exogenous and endogenous hydrogen sulfide in vascular smooth muscle. Mol. Pharmacol. 68: 1757-1764, 2005.