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Hydropersulfides, the new kids in the COPD inflammatory town
  1. Luis Puente-Maestu1,2,3,
  2. Walther Ivan Girón-Matute1,2
  1. 1Servicio de Neumología del Hospital Universitario Gregorio Marañón c/ Doctor Ezquerdo, Madrid, Spain
  2. 2Instituto de Investigación Sanitaria Gregorio Marañón c/ Doctor Ezquerdo, Madrid, Spain
  3. 3Facultad de Medicina de la Universidad Complutense de Madrid. Plaza Ramón y Cajal, Madrid, Spain
  1. Correspondence to Professor Luis Puente-Maestu, Servicio de Neumología del Hospital Universitario Gregorio Marañón c/ Doctor Ezquerdo, 4628007 Madrid, Spain; lpuente{at}separ.es

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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 D-cysteine …

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