2012
DOI: 10.1016/j.alcohol.2011.08.004
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Expression pattern, ethanol-metabolizing activities, and cellular localization of alcohol and aldehyde dehydrogenases in human large bowel: association of the functional polymorphisms of ADH and ALDH genes with hemorrhoids and colorectal cancer

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Cited by 41 publications
(35 citation statements)
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“…This is because the normalized active sites of heterotetramers relative to that of the normal homotetramers without correction for 50% shorter half-life, 0.25, are not quite far from that predicted with the correction (0.16). For human tissue ALDH2 contents in normal homozygotes, immunotitration studies using the class-specific purified ALDH2 antibodies have revealed the following decreasing order: liver (1,770 AE 140 lg/g tissue; n = 17) (this study), jejunal mucosa (163 AE 11 lg/g; n = 7) (Chiang et al, 2012b), pancreas (130 AE 25 lg/g; n = 5) (Chiang et al, 2009), duodenal mucosa (93.0 AE 8.5 lg/g; n = 7) (Chiang et al, 2012b), and rectal mucosa (24.2 AE 5.3 lg/g; n = 9) (Chiang et al, 2012a), indicating that liver is the primary site for conversion of acetaldehyde to acetate in the human body during EtOH metabolism.…”
Section: Discussionmentioning
confidence: 98%
See 1 more Smart Citation
“…This is because the normalized active sites of heterotetramers relative to that of the normal homotetramers without correction for 50% shorter half-life, 0.25, are not quite far from that predicted with the correction (0.16). For human tissue ALDH2 contents in normal homozygotes, immunotitration studies using the class-specific purified ALDH2 antibodies have revealed the following decreasing order: liver (1,770 AE 140 lg/g tissue; n = 17) (this study), jejunal mucosa (163 AE 11 lg/g; n = 7) (Chiang et al, 2012b), pancreas (130 AE 25 lg/g; n = 5) (Chiang et al, 2009), duodenal mucosa (93.0 AE 8.5 lg/g; n = 7) (Chiang et al, 2012b), and rectal mucosa (24.2 AE 5.3 lg/g; n = 9) (Chiang et al, 2012a), indicating that liver is the primary site for conversion of acetaldehyde to acetate in the human body during EtOH metabolism.…”
Section: Discussionmentioning
confidence: 98%
“…Pharmacokinetic and pharmacodynamic studies support the notion that differing impairments of hepatic acetaldehyde metabolism between ALDH2*2 homozygotes and heterozygotes after alcohol intake can largely explain differential protections against alcoholism with regard to the ALDH2*2 allelic status (Chen et al, 1999b;Peng et al, 1999Peng et al, , 2007 and that heterozygous alcoholics overcoming acetaldehyde-induced aversive reactions may be attributed to physiological tolerance and/or innate insensitivity rather than an adapted acetaldehyde metabolism (Chen et al, 2009a). Recently, ALDH2 deficiency has also been associated with the increased risks of esophageal and colorectal cancer (Brooks et al, 2009;Chiang et al, 2012a) as well as a reduced efficacy of nitroglycerin (Chen and Stamler, 2006), whereas activation of ALDH2 may reduce the ischemia reperfusion cardiac injury (Chen et al, 2008).…”
mentioning
confidence: 89%
“…However, the results have been inconsistent (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). The present comprehensive meta-analysis of currently published studies aimed to identify the relationships between the ADH1B and ALDH2 polymorphisms and the risk of CRC.…”
Section: Introductionmentioning
confidence: 99%
“…For example, acetaldehyde is produced in the epithelium by mucosal ALDH 2 , while higher levels are derived from microbial oxidation of ethanol by oral microflora such as Candida species 9 , 10 , 12 , 17 , 23 . Thus, the effects of acetaldehyde on the oral cavity can be local, and oral hygiene may be linked to local production of acetaldehyde by oral microflora.…”
Section: Introductionmentioning
confidence: 99%