title: Formaldehyde dehydrogenase: beyond phase I metabolism.
abstract: Formaldehyde dehydrogenase, formally Class III alcohol dehydrogenase (ADH3), has recently been discovered to partially regulate nitrosothiol homeostasis by catalyzing the reduction of the endogenous nitrosylating agent S-nitrosoglutathione (GSNO). Several studies have implicated this enzyme, and in particular GSNO reduction, as playing an important role in conditions such as asthma, cardiovascular disease, and immune function. While ADH3 has received considerable attention in the biomedical literature where it is often referred to as GSNO reductase (GSNOR), ADH3-mediated GSNO reduction has received comparatively less attention in the environmental toxicology community. Herein, evidences for a role of ADH3 in cell signaling through thiol homeostasis is highlighted, underscoring that the enzyme functions more broadly than to metabolize formaldehyde.
authors: ToxStrategies, Inc., Katy, TX 77494, USA. cthompson@toxstrategies.com
authors: Chad M
authors: CM
authors: Thompson
authors: Rebecca
authors: R
authors: Ceder
authors: Roland C
authors: RC
authors: Grafström
mesh_terms: D000445:Aldehyde Oxidoreductases / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D006801:Humans; D019001:Nitric Oxide Synthase / Q000378:metabolism; D011499:Protein Processing, Post-Translational / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology
chemical_list: D019001:Nitric Oxide Synthase; D000445:Aldehyde Oxidoreductases; C087006:formaldehyde dehydrogenase, glutathione-independent