Potential importance of alterations in hydrogen sulphide (H2S) bioavailability in diabetes.

Despite its long-standing reputation as a foul smelling and toxic gas that is associated with the decay of biological matter,hydrogen sulphide (H2S) has emerged as an important regulator of cardiovascular homoeostasis. H2S promotes a number of cellular signals that regulate metabolism, cardiac function and cell survival. Endogenous H2S bioavailability is regulated by several enzymes involved in the biosynthesis of cysteine. This study by Brancaleone et al. in the current issue of the British Journal of Pharmacology provides novel insights into the impairment of H2S biosynthesis in the setting of diabetes mellitus. The authors report that enzymic H2S biosynthesis is impaired in a murine model of type 1 diabetes and the attenuation in H2S bioavailability is associated with impaired vascular reactivity. This study has profound implications for the use of pharmacological agents to augment endogenous H2S synthesis or agents that release H2S to augment the levels of this gaseous signalling molecule in cardiovascular disease.