Aldehyde Dehydrogenase Deficiency as Cause of Facial Flushing Reaction to Alcohol in Japanese

Harada, Shoji; Agarwal, D. P.; Goedde, H. W.

doi:10.1016/s0140-6736(81)91172-7

Cited by 427 publications

(201 citation statements)

References 12 publications

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“…Recent studies revealed the existence of genetic deficiency in some enzyme species that can convert acetaldehyde to acetate in the human body (13,14). About 50% of Oriental people are deficient in the aldehyde-dehydrogenase 2 isozyme (ALDH2) that can most efficiently detoxify acetaldehyde (12,14,15). It is therefore possible that cells in individuals who are genetically deficient in such an aldehyde dehydrogenase activity might show an elevated level of chromosome alterations if they drink too heavily.…”

Section: Introductionmentioning

confidence: 99%

Low Km aldehyde dehydrogenase (ALDH2) polymorphism, alcohol-drinking behavior, and chromosome alterations in peripheral lymphocytes.

Morimoto

Takeshita

1996

Environ Health Perspect

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Excessive drinking of alcohol is now widely known to be one of the major lifestyle choices that can affect health. Among the various effects of alcohol drinking, cytogenetic and other genotoxic effects are of major concern from the viewpoint of prevention of alcohol-related diseases. Alcohol is first metabolized to acetaldehyde, which directly causes various types of chromosomal DNA lesions and alcohol-related diseases, and is then further detoxified to the much less toxic metabolite acetate. About 50% of Oriental people are deficient in the aldehyde-dehydrogenase 2 isozyme (ALDH2) that can most efficiently detoxify acetaldehyde. We have performed a series of experiments to investigate how the genetic deficiency in ALDH2 affects the behavioral pattern for alcohol drinking and the sensitivity of peripheral lymphocytes to the induction of chromosome alterations by exposure to alcohol and alcohol-related chemicals. We found great effects of the ALDH2 genotypes on alcohol sensitivity and alcohol-drinking behavior. We also show that lymphocytes from habitual drinkers with the deficient ALDH2 enzyme had significantly higher frequencies of sister chromatid exchanges than those from ALDH2-proficient individuals.

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Section: Introductionmentioning

confidence: 99%

Low Km aldehyde dehydrogenase (ALDH2) polymorphism, alcohol-drinking behavior, and chromosome alterations in peripheral lymphocytes.

Morimoto

Takeshita

1996

Environ Health Perspect

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“…= 22, c 2 = 268.343). The three-group (0, 1-7, [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] or the two-group (0-7, 8-22) score distribution also showed significant proportional differences between AUD Past histories of diabetes mellitus (DM), chronic liver diseases (liver cirrhosis, chronic hepatitis, hepatic dysfunction and alcoholic liver dysfunction), AUD and blood transfusion were more prevalent among AUD patients (Table 1).…”

Section: Resultsmentioning

confidence: 99%

“…The enzyme encoded by ADH2*2 has high activity as indicated by maximum velocity values on kinetics, 6,7 and ADH3 has been found to be very rare in Oriental subjects. 8 Acetaldehyde dehydrogenase2 encodes the principal isoenzyme responsible for the majority of acetaldehyde oxidation 9 and exists in two allelic forms, ALDH2*1 and ALDH2*2 . The variant subunit, encoded by ALDH2*2 , decreases the activity in the tetrameric enzyme.…”

Section: Introductionmentioning

confidence: 99%

Alcohol drinking frequency is more directly associated with alcohol use disorder than alcohol metabolizing enzymes among male Japanese

Nishiyori

Shibata

Ogimoto

et al. 2005

Psychiatry Clin Neurosci

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The development of alcohol use disorder (AUD) is related to various social, economic, cultural, environmental and hereditary factors. Several potential risk factors have been proposed for AUD in addition to alcohol consumption, including alcohol dehydrogenase2 (ADH2), acetaldehyde dehydrogenase2 (ALDH2), marital status, educational, occupational or past medical history (e.g. diabetes mellitus, hypertension, lung, digestive tract, or chronic liver disease) or smoking habits. The present study was performed to investigate the relationship between the aforementioned potential risk factors and AUD in Japan. A case-control study was performed on 153 male Japanese AUD patients and age-, gender-, or other confounder-matched controls to investigate the relation multivariately between ADH2 , ALDH2 or alcohol drinking and AUD. Genomic DNA were extracted from nail clippings by the guanidium method, and genotyping of ADH2 and ALDH2 were performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. Univariate analyses by the conditional logistic regression model revealed statistically significant odds ratios due to ADH2*1/1 genotype, ALDH2*1/1 genotype, middle school as the final school attended, longest occupations as farmers, fishermen, craftsmen, miners, production process or construction workers, and past histories of chronic liver disease and AUD. However, multivariate analyses under a hierarchically well-formulated model strategy with interaction and confounding assessment indicated that (i) heavy alcohol intake was a significant risk factor (odds ratio per 1.0 g of daily ethanol intake; 1.096, 95% confidence interval; 1.026-1.171) for developing AUD after adjusting for other confounders; and (ii) ADH2*1/1 genotype and ALDH2*1/1 genotype were not risk factors after adjusting for daily ethanol intake and other confounders. The present study shows that AUD was more directly and strongly associated with alcohol drinking than with alcohol metabolizing enzymes among male Japanese.

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“…4 Subjects with the ALDH2*2 allele, both homozygous and heterozygous, experience more intense reactions to alcohol than subjects with only ALDH2*1. 5,6 These individuals are alcohol sensitive and have a markedly reduced risk to develop alcoholism and alcoholic liver diseases. Accordingly, there exist three genotypes, ie, ALDH2*1/ALDH 2*1, ALDH2*1/ALDH2*2, and ALDH2*2/ALDH2*2.…”

Section: Introductionmentioning

confidence: 99%

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Mongconthawornchai¹,

Nanakorn²,

Nishiyori³

2002

ScienceAsia

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A genetic study on aldehyde dehydrogenase 2 (ALDH2) genotype was performed in a rural area of Khon Kaen province, northeastern Thailand. One hundred and twenty four fingernail specimens of probable non-alcoholics were obtained from unrelated male villagers 18-65 years old. The alcoholism screening test named "the Michigan Alcoholism Screening Test-Thai version (MAST-T)" was used for inclusion of probable-non-alcoholic subjects. Genomic DNA was extracted from clipped fingernails and ALDH2 genotypes were determined by PCR, Ksp 632I, digested and polyacrylamide gel electrophoresis. Most of the subjects (91.1%) were of the normal homozygous genotype (ALDH2*1/ ALDH2*1), 8.9%, heterozygous genotype (ALDH2*1/ALDH2*2), and none of them were the mutant homozygous genotype (ALDH2*2/ALDH2*2). Gene frequencies of ALDH2*1 and ALDH2*2 alleles calculated from the genotype frequencies were 0.956 and 0.044, respectively. Deviation from the HardyWeinberg' s equilibrium was not statistically significant. The present study confirms the high frequency of ALDH2*1 gene (0.950-0.956) in non-alcoholic Thai population. Interestingly, the ALDH2*2 gene is not prevalent among Thai population compared with the Japanese and Chinese, though, they are of Mongoloid origin. The information on ALDH2 gene frequency of Oriental populations and Caucasoids were discussed.

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Aldehyde Dehydrogenase Deficiency as Cause of Facial Flushing Reaction to Alcohol in Japanese

Cited by 427 publications

References 12 publications

Low Km aldehyde dehydrogenase (ALDH2) polymorphism, alcohol-drinking behavior, and chromosome alterations in peripheral lymphocytes.

Low Km aldehyde dehydrogenase (ALDH2) polymorphism, alcohol-drinking behavior, and chromosome alterations in peripheral lymphocytes.

Alcohol drinking frequency is more directly associated with alcohol use disorder than alcohol metabolizing enzymes among male Japanese

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