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Additional info for Acetaldehyde-Related Pathology: Bridging the Trans-Disciplinary Divide (Novartis Foundation Symposium 285)
While one would expect that the Km of acetaldehyde as a substrate would be the same as the Ki for acetaldehyde when it functions as a competitive substrate, this also has not been studied carefully. This consideration may be important in our understanding not only of the pathways of acetaldehyde removal, but also of the many effects that acetaldehyde has via the surrogate aldehydes allowed to escape metabolism by their preferred enzyme. This would result in a ‘multiplying’ or ‘amplification’ effect of the relatively small amount of acetaldehyde present.
Alcohol and Aldehyde Metabolizing Systems. Plenum Press, New York, p 125–135 Deitrich RA, Erwin VG 1975 Involvement of biogenic amine metabolism in ethanol addiction. Fed Proc 34:1962–1968 Deitrich RA, Erwin V 1980 Biogenic amine-aldehyde condensation products: tetrahydroisoquinolines and tryptolines (beta-carbolines). Annu Rev Pharmacol Toxicol 20:55–58 Deitrich RA, Hellerman L, Wein J 1962 Diphosphopyridine nucleotide-linked aldehyde dehydrogenase. I. Specificity and sigma-rho function. J Biol Chem 237:560–564 Deitrich RA, Collins AC, Erwin VG 1972 Genetic influence upon phenobarbital induced increase in rat liver supernatant aldehyde dehydrogenase activity.
The conclusion is that there is an increased risk factor for ALDH2-deficient individuals for head and neck cancer. There are also reports of increased incidence of cancer of the gastrointestinal tract (reviewed in Salaspuro 2003) in hepatocellular carcinoma (Kato et al 2003, Sakamoto et al 2005), oesophageal cancer (Morita et al 2005, Watanabe et al 2002) but not in colorectal adenomas (Hirose et al 2005). There is enhanced oxidative stress (Ohsawa et al 2003) perhaps related to late onset Alzheimer’s disease (Ohta et al 2004) although this is disputed (Kim et al 2004, Shin et al 2005).