Hydrogen sulfide and ischemia-reperfusion injury

Gasotransmitters are lipid soluble, endogenously produced gaseous signaling molecules that freely permeate the plasma membrane of a cell to directly activate intracellular targets, thus alleviating the need for membrane-bound receptors. The gasotransmitter family consists of three members: nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H(2)S). H(2)S is the latest gasotransmitter to be identified and characterized and like the other members of the gasotransmitter family, H(2)S was historically considered to be a toxic gas and an environmental/occupational hazard. However with the discovery of its presence and enzymatic production in mammalian tissues, H(2)S has gained much attention as a physiological signaling molecule. Also, much like NO and CO, H(2)S's role in ischemia/reperfusion (I/R) injury has recently begun to be elucidated. As such, modulation of endogenous H(2)S and administration of exogenous H(2)S has now been demonstrated to be cytoprotective in various organ systems through diverse signaling mechanisms. This review will provide a detailed description of the role H(2)S plays in different model systems of I/R injury and will also detail some of the mechanisms involved with its cytoprotection.