Protein Information

ID 3899
Name alcohol dehydrogenase 3
Synonyms ADH1C; ADH3; Alcohol dehydrogenase 1C; Alcohol dehydrogenase 3; Alcohol dehydrogenase gamma subunit; Alcohol dehydrogenase 1Cs; Alcohol dehydrogenase 3s; Alcohol dehydrogenase gamma subunits

Compound Information

ID 348
Name formaldehyde
CAS formaldehyde

Reference

PubMed Abstract RScore(About this table)
18097950 Thompson CM, Grafstrom RC: Mechanistic considerations for formaldehyde-induced bronchoconstriction involving S-nitrosoglutathione reductase. J Toxicol Environ Health A. 2008;71(3):244-8.
Inhalation of formaldehyde vapor has long been suspected of producing airway pathophysiology such as asthma and hyperresponsivity, presumably via irritant mechanisms. Recent studies on asthma and airway biology implicate changes in nitric oxide (NO) disposition in the adverse effects of formaldehyde, principally because enzymatic reduction of the endogenous bronchodilator S-nitrosoglutathione (GSNO) is dependent upon GSNO reductase (formally designated as alcohol dehydrogenase-3, ADH3), which also serves as the primary enzyme for cellular detoxification of formaldehyde. Considering recent evidence that regulation of bronchodilators like GSNO might play a more important role in asthma than inflammation per se, formaldehyde also needs to be considered as influencing ADH3-mediated GSNO catabolism. This is due to changes in ADH3 cofactors and thiol redox state among several potential mechanisms. Data suggest that deregulation of GSNO turnover provides a plausible, enzymatically based mechanism by which formaldehyde might exacerbate asthma and induce bronchoconstriction.
113(1,2,2,3)