ADH5


Also found in: Acronyms.

ADH5

A gene on chromosome 4q23 that encodes a member of the alcohol dehydrogenase family, which metabolise various substrates, including ethanol, retinol, other aliphatic alcohols, hydroxysteroids and lipid peroxidation products. ADH5 has minimal activity for ethanol oxidation, but has a high activity for oxidation of long-chain aliphatic alcohols and oxidation of S-(hydroxymethyl) glutathione. The ADH5 protein product is critical in metabolic elimination of formaldehyde, a potent irritant and sensitising agent that causes lacrymation, rhinitis, pharyngitis and contact dermatitis.
References in periodicals archive ?
ADH5 is a cocktail of IHC markers that includes CK8/18-pink, CK5/14-brown, and p63-brown (hematoxylin-eosin, original magnifications x40 [A, E, and I], x100 [B], X200 [G], and x400 [J]; CK5, original magnifications X200 [C] and x100 [K]; p63, original magnifications X200 [D] and x100 [L]; ADH5, original magnifications x40 [F] and X200 [H]).
For example, several studies found other variations in and near the ADH1B gene, as well as in or near the ADH4, ADH1C, ADH5, ADH6, and ADH7 genes that affect risk for alcoholism or the level of alcohol consumption (see the article by Hurley and Edenberg, pp.
* The product of the ubiquitously expressed ADH5 gene is the glutathione-dependent formaldehyde dehydrogenase (also known as nitrosoglutathione reductase [GSNOR]).
Moreover, noncoding SNPs in the region of ADH1A, ADH1B, and ADH1C have been associated with alcoholism and drinking phenotypes, as have SNPs in ADH7 and ADH5. Some non-coding SNPs have been shown to affect gene expression in cultured cells and tissues (i.e., in vitro) (Chen et al 2005; Pochareddy and Edenberg 2010, 2011), and it is likely that many different variations in this region also affect the level of expression of the different ADH enzymes in the intact organism (i.e., in vivo), thereby influencing ethanol metabolism (in some cases possibly only in specific tissues), its physiological effects, and, ultimately, drinking behavior and risk for alcoholism.
Moreover, noncoding SNPs in the region of ADH1A, ADH1B, and ADH1C have been associated with alcoholism and drinking phenotypes, as have SNPs in ADH7 and ADH5. Some noncoding SNPs have been shown to affect gene expression in cultured cells and tissues (i.e., in vitro) (Chen et al 2005; Pochareddy and Edenberg 2010, 2011), and it is likely that many different variations in this region also affect the level of expression of the different ADH enzymes in the intact organism (i.e., in vivo), thereby influencing ethanol metabolism (in some cases possibly only in specific tissues), its physiological effects, and, ultimately, drinking behavior and risk for alcoholism.