Published online Jul 28, 2015. doi: 10.5320/wjr.v5.i2.152
Peer-review started: December 23, 2014
First decision: January 20, 2015
Revised: February 4, 2015
Accepted: March 5, 2015
Article in press: March 9, 2015
Published online: July 28, 2015
Processing time: 224 Days and 10.7 Hours
The toxicity of hydrogen sulfide (H2S) has been known for a long time, as it is prevalent in the atmosphere. However accumulative data suggest that H2S is also endogenously produced in mammals, including man, and is the third important gas signaling molecule, besides nitric oxide and carbon monoxide. H2S can be produced via non enzymatic pathways, but is mainly synthesized from L-cysteine by the enzymes cystathionine-γ-lyase, cystathionine-β-synthetase, cysteine amino transferase and 3-mercaptopyruvate sulfurtransferase (3MTS). The formation of H2S from D-cysteine via the enzyme D-amino acid oxidase and 3MTS has also been described. Endogenous H2S not only participates in the regulation of physiological functions of the respiratory system, but also seems to contribute to the pathophysiology of airway diseases such as chronic obstructive pulmonary disease, asthma and pulmonary fibrosis, as well as in inflammation, suggesting its possible use as a biomarker for these diseases. This review summarizes the different implications of hydrogen sulfide in the physiology of airways and the pathophysiology of airway diseases.
Core tip: Hydrogen sulfide (H2S) is a metabolite produced in mammalian organisms both in physiological and in pathological conditions. The measured levels appear differentiated in inflammatory airway diseases, showing the need to acknowledge H2S not only as a metabolic mediator but as a signaling biomarker as well. This could be of clinical importance since H2S levels could be used in order to access staging or treatment efficiency in patients suffering from airway diseases.