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ALDH2Aldehyde Dehydrogenase 2 Family
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Preventing reduced formation of acetaldehyde by alcohol oxidation via the mitochondrial ALDH2, subsequent reactions of mitochondrial ETC and adduct formation can promote addiction recovery.
Inhibition of aldehyde dehydrogenase 2 activity, through the silencing of ALDH2, results in the build-up of acetaldehyde.
Associations of ADH and ALDH2 gene variation with self report alcohol reactions, consumption and dependence: An integrated analysis.
The associations between the ADH2 or ALDH2 genotype and the risk factors for CHD were further assessed by multiple logistic regression analysis (Table 3).
UChA animals, in contrast, carry less efficient ALDH2 variants and less active mitochondria, which result in transient elevations of acetaldehyde levels after alcohol ingestion.
Recent studies reported by Hesselbrock and colleagues (2005) also have used the alcohol clamp to examine the influence of ALDH2 genetic polymorphisms on AERs and the associated time-course of the concentration of the alcohol metabolism byproduct acetaldehyde in the blood of healthy Japanese male and female subjects.
Convivia(TM) is Raptor's proprietary oral formulation of 4-MP designed to reduce systemic acetaldehyde exposure and related symptoms in ALDH2 deficient persons following alcohol consumption.
Currently there are no approved treatments for ALDH2 deficiency, and people with this disorder could potentially benefit by lessening their exposure to acetaldehyde, a known carcinogen, and mitigating the unpleasant reactions to drinking.
Acetaldehyde, produced by alcohol oxidation through any of the mechanisms outlined above, is rapidly metabolized to acetate, mainly by ALDH2 (in cell bodies called mitochondria), to form acetate and NADH.
Another approach to interfering with ALDH activity was used by Isse and colleagues (2005), who generated mice that no longer produced active ALDH2 (i.
The ALDH enzyme most likely to be responsible for the majority of the oxidation of acetaldehyde to acetate is ALDH2, the form found in the mitochondria, an internal component of the cell.
ALDH2 wasn't one of the well-studied antioxidant players that the scientists expected to find fighting free-radical damage.