Correlation between human erythrocyte aldehyde dehydrogenase activity and sensitivity to alcohol

Inoue, Ken‐ichiro; Fukunaga, Manabu; Yamasawa, Kichihei

doi:10.1016/0091-3057(80)90087-8

Cited by 40 publications

(7 citation statements)

References 9 publications

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“…The rate of acetaldehyde uptake is markedly inhibited in blood from disulfiramtreated patients [35,361. Furthermore, in Japanesewho exhibit a genetic deficiency of aldehyde dehydrogenase-there exists an inverse correlation between their acetaldehyde-induced flushing and their red blood cell aldehyde dehydrogenase activity [37]. Our present experiments offered the possibility to measure the capacity of blood of normal Caucasian individuals (with uninhibited aldehyde dehydrogenase activity) to eliminate ethanol-derived acetaldehyde and to compare this with incubations of ethanol-free blood supplemented with acetaldehyde.…”

Section: Discussionmentioning

confidence: 89%

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol‐intoxicated alcoholics and controls*

Nuutinen

Salaspuro

Valle

et al. 1984

Eur J Clin Investigation

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After ethanol (0.8 g kg-1 body weight orally) significant concentrations of acetaldehyde (2-20 mumol 1(-1] were found in hepatic venous blood of moderately intoxicated non-alcoholic male Caucasians in spite of the absence of detectable levels (less than 2 mumol 1(-1] in simultaneously taken antecubital blood. In thirteen chronic alcoholics the elevation of blood acetaldehyde was more constant in the hepatic than in the peripheral vein. Fructose infusion caused a marked elevation of acetaldehyde both in the hepatic and peripheral vein of four controls, but not of four alcoholics, who eliminated ethanol about 50% faster than controls. The rate of disappearance of acetaldehyde from sampled and in vitro incubated hepatic venous blood was similar to that observed after addition of acetaldehyde in vitro to ethanol-free control blood (2 nmol ml-1 min-1 at 20 mumol 1(-1) acetaldehyde; Km about 30 mumol 1(-1]. Uptake of acetaldehyde in blood was calculated to explain maximally 30-40% of the concentration gradient between central and peripheral blood.

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Section: Discussionmentioning

confidence: 89%

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol‐intoxicated alcoholics and controls*

Nuutinen

Salaspuro

Valle

et al. 1984

Eur J Clin Investigation

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“…Less con- Weigand (1982) a All reports describe the typical effects of acetaldehyde; b original finding made with Coprinus atramentarius (inky cap mushroom); c effect limited to cephalosporins with the N-methyltetrazolethiol substitute (Kitson, 1987). Ueda et al (1967) Flushing prevalent in Asians but not in white subjects b Wolff (1972) AcH1 and flushing in Asians but not in white subjects Ewing et al (1974) ADH2 polymorphism may explain Asian flushing b,c Stamatoyannopoulos et al (1975) Inactive ALDH phenotype may explain Asian flushing b,c Goedde et al (1979) Erythrocyte ALDH12 associated with Asian flushing Inoue et al (1980) Inactive ALDH phenotype explains Asian flushing Harada et al (1981) Flushing in white subjects is reported b Schwitters et al (1982) Genetic ALDH polymorphism explains Asian flushing Goedde and Agarwal (1986) ADH2*2 alleles tend to associate with Asian flushing Shibuya et al (1989) Erythrocyte ALDH12 associated with flushing in white subjects Yoshida et al (1989) ADH2*2 alleles elevate flushing in ALDH2*1/1 Asians b Thomasson et al (1990) Alcohol sensitivity is common in Jewish men b,c Monteiro et al (1991) Flushing in white subjects more common in women than in men b Ward et al (1994) AcH1 found in women but not in men c Eriksson et al (1996) ADH2*2 alleles elevate flushing in ALDH2*1/*2 Asians b Takeshita et al (1996) ADH2*2 alleles common in Jewish populations b,c Neumark et al (1998) ADH3*1 alleles associated with flushing in white subjects b Yamamoto et al (1998) a Arrows describe increases (1) and decreases (2) in levels on activities; b AcH not determined; c flushing not determined.…”

Section: Acute Effects Of Alcohol Drinkingmentioning

confidence: 97%

The Role of Acetaldehyde in the Actions of Alcohol (Update 2000)

Eriksson

2001

Alcoholism Clin & Exp Res

228

116

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Background: Recent advances in the field of acetaldehyde (AcH) research have raised the need for a comprehensive review on the role of AcH in the actions of alcohol. This update is an attempt to summarize the available AcH research.Methods: The descriptive part of this article covers not only recent research but also the development of the field. Special emphasis is placed on mechanistic analyses, new hypotheses, and conclusions.Results: Elevated AcH during alcohol intoxication causes alcohol sensitivity, which involves vasodilation associated with increased skin temperature, subjective feelings of hotness and facial flushing, increased heart and respiration rate, lowered blood pressure, sensation of dry mouth or throat associated with bronchoconstriction and allergy reactions, nausea and headache, and also reinforcing reactions like euphoria. These effects seem to involve catecholamine, opiate peptide, prostaglandin, histamine, and/or kinin mechanisms. The contribution of AcH to the pathological consequences of chronic alcohol intake is well established for different forms of cancer in the digestive tract and the upper airways. AcH seems to play a role in the etiology of liver cirrhosis. AcH may have a role in other pathological developments, which include brain damage, cardiomyopathy, pancreatitis, and fetal alcohol syndrome. AcH creates both unpleasant aversive reactions that protect against excessive alcohol drinking and euphoric sensations that may reinforce alcohol drinking. The protective effect of AcH may be used in future treatments that involve gene therapy with or without liver transplantation.Conclusions: AcH plays a role in most of the actions of alcohol. The individual variability in these AcH-mediated actions will depend on the genetic polymorphism, not only for the alcohol and AcHmetabolizing enzymes but also for the target sites for AcH actions. The subtle balance between aversive and reinforcing, protecting and promoting factors will determine the overall behavioral and pathological developments.

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“…Erythrocytes have been reported to contain aldehyde dehydrogenase activity but the isoforms present has not been determined 18,22 . ALDH1A1 is the only isoform identified by proteomics 23 , but it has been reported to have a low affinity for short chain aldehydes 24 .…”

Section: Commentmentioning

confidence: 99%

Oxalate Formation From Glyoxal in Erythrocytes

Knight

Wood

Lange

et al. 2016

Urology

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OBJECTIVES To determine whether glyoxal can be converted to oxalate in human erythrocytes. Glyoxal synthesis is elevated in diabetes, cardiovascular disease and other diseases with significant oxidative stress. Erythrocytes are a good model system for such studies as they lack intracellular organelles and have a simplified metabolism. METHODS Erythrocytes were isolated from healthy volunteers and incubated with varying concentrations of glyoxal for different amounts of time. Metabolic inhibitors were used to help characterize metabolic steps. The conversion of glyoxal to glycolate and oxalate in the incubation medium was determined by chromatographic techniques. RESULTS The bulk of the glyoxal was converted to glycolate but ~1% was converted to oxalate. Inclusion of the pro-oxidant, menadione, in the medium increased oxalate synthesis, and the inclusion of disulfiram, an inhibitor of aldehyde dehydrogenase activity, decreased oxalate synthesis. CONCLUSIONS The glyoxalase system, which utilizes glutathione as a cofactor, converts the majority of the glyoxal taken up by erythrocytes to glycolate but a small portion is converted to oxalate. A reduction in intracellular glutathione increases oxalate synthesis and a decrease in aldehyde dehydrogenase activity lowers oxalate synthesis and suggests that glyoxylate is an intermediate. Thus, oxidative stress in tissues could potentially increase oxalate synthesis.

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Correlation between human erythrocyte aldehyde dehydrogenase activity and sensitivity to alcohol

Cited by 40 publications

References 9 publications

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol‐intoxicated alcoholics and controls*

Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol‐intoxicated alcoholics and controls*

The Role of Acetaldehyde in the Actions of Alcohol (Update 2000)

Oxalate Formation From Glyoxal in Erythrocytes

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