• copd pathology
• copd pharmacology
• oxidative stress

Hydrogen sulfide (H₂S) is one of several small molecules, formerly known primarily as toxic gases (such as nitric oxide (NO) and carbon monoxide) that over the past 20 years have been shown to be endogenously generated small, signalling molecules.1 2 H₂S has accompanied life since its origin. Its toxicological potential, related to the inhibition of cellular respiration, has been known for centuries.3 Indeed, the Permian-Triassic mass extinction event has been linked to this toxicity. H₂S has been the cause of mining, industrial and sewage accidents, as well as deaths by the inhalation of gases emanating from volcanic and sulfur-rich water wells.

In spite of this felonious record, as it happens with other primeval redox processes, ancient H₂S pathways have evolved to play physiological roles in eukaryotic cells.

The rush of discovery for H₂S and its derivative compounds started in the late 1980s by reports of potential biological roles of H₂S in modulatory and signalling pathways.4 The associated probable health benefits generated a renewed interest in the study of H₂S, as reflected in the exponential increase in the number of publications.4

H₂S is produced from L-cysteine by an array of enzymes such as cystathionine β-synthase (CBS), cystathionine γ-lyase (CGL), 3-mercaptopyruvate sulfurtransferase (3MST), cysteine aminotransferase and from …