1. Introduction
Hydrogen sulfide (H2S); a toxic gas, is endogenously produced, bioactive, and contributes to numerous physiological functions in mammalian systems. Studies support the possibility that H2S has therapeutic potential for treating multiple diseases including cardiovascular diseases. For example, experimental animal studies show that H2S may be effective in treating atherosclerosis and protecting against ischemia-reperfusion injury [1–3]. Interest in the cytoprotective actions of H2S has grown since the discovery that it can induce a hypometabolic state characterized by decreased O2 consumption, heart rate, and body temperature in non-hibernating rodents [4]. Although not discussed in this review, H2S-dependent hypometabolism is an O2-dependent phenom- enon [5]. The proposed mitochondrial and signaling actions of H2S make this molecule an attractive intervention for preventing and treating diseases and trauma-associated injuries. In this review article, we provide an overview of H2S redox biology as it relates to the biological and pharmacological actions of this interesting new signaling molecule in mammalian systems.