Increased frequency of acetaldehyde-induced sister-chromatic exchanges in human lymphocytes treated with an aldehyde dehydrogenase inhibitor

Helander, Anders; Lindahl-Kiessling, Kerstin

doi:10.1016/0165-7992(91)90124-m

Cited by 88 publications

(36 citation statements)

References 28 publications

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“…This conclusion is supported by the reported potential biological function of the ADH1C *1/*2 polymorphism, which was found to influence enzyme activity (Bosron and Li, 1987). Because the enzyme encoded by ADH1C *1/*1 showed higher activity and produced larger amounts of acetaldehyde, toxicity can occur and stable DNA adducts can be generated (Bosron ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 15267-15275 (2015) and Li, 1987;Helander and Lindahl-Kiessling, 1991). Thus, the ADH1C *1/*2 polymorphism may influence chronic alcoholic pancreatitis risk by affecting the enzyme activity of ADH1C.…”

Section: Discussionsupporting

confidence: 64%

Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis

Feng¹,

Pan²,

Gh³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Numerous studies have focused on the relationship between alcohol dehydrogenase 1C gene (ADH1C) *1/*2 polymorphism (Ile350Val, rs698, also known as ADH1C *1/*2) and pancreatitis risk, but the results have been inconsistent. Thus, we conducted a meta-analysis to more precisely estimate this association. Relevant publications were searched in several widely used databases and 9 eligible studies were included in the meta-analysis. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the strength of the association. Significant associations between ADH1C *1/*2 polymorphism and pancreatitis risk were observed in both overall metaanalysis for 12 vs 22 (OR = 1.53, 95%CI = 1.12-2.10) and 11 + 12 vs 22 (OR = 1.44, 95%CI = 1.07-1.95), and the chronic alcoholic pancreatitis subgroup for 12 vs 22 (OR = 1.64, 95%CI = 1.17-2.29) and 11 + 12 vs 22 (OR = 1.53, 95%CI = 1.11-2.11). Significant pancreatitis risk variation was also detected in Caucasians for 11 + 12 vs 22 (OR = 1.45, 95%CI = 1.07-1.98). In conclusion, the ADH1C *1/*2 polymorphism F. Fang et al. 15268©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 15267-15275 (2015) is likely associated with pancreatitis risk, particularly chronic alcoholic pancreatitis risk, with the *1 allele functioning as a risk factor.

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Section: Discussionsupporting

confidence: 64%

Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis

Feng¹,

Pan²,

Gh³

et al. 2015

Genet. Mol. Res.

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“…Moreover, drinking or inhaling acetaldehyde has mutagenic and carcinogenic effects and induced nasal and laryngeal carcinomas in experimental animals. [4][5][6][7][8] Ethanol is primarily (80%) oxidized to acetaldehyde by alcohol dehydrogenase (ADH), and most of this acetaldehyde is then eliminated by aldehyde dehydrogenase (ALDH). However, ethanol and acetaldehyde also are metabolized through the microsomal ethanol-oxidizing system and the microsomal acetaldehyde-oxidizing system, and cytochrome P450 2E1 (CYP2E1) is a major contributor to those systems.…”

Section: Discussionmentioning

confidence: 99%

Susceptibility to lung cancer and genetic polymorphisms in the alcohol metabolite‐related enzymes alcohol dehydrogenase 3, aldehyde dehydrogenase 2, and cytochrome P450 2E1 in the Japanese population

Minegishi

Tsukino²,

Muto

et al. 2007

Cancer

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BACKGROUND.It is believed that acetaldehyde plays an important role in alcohol‐related carcinogenesis; although current epidemiologic studies have provided inconsistent findings on the association between alcohol consumption and the risk of lung cancer.METHODS.To clarify the hypothesis that genetic polymorphisms in alcohol‐metabolizing enzymes may influence susceptibility to lung cancer, the authors conducted a hospital‐based case‐control study and examined genetic polymorphisms in the alcohol dehydrogenase 3, aldehyde dehydrogenase 2 (ALDH2), and cytochrome P450 2E1 genes in 505 patients with histologically confirmed lung cancer and in a group of 256 noncancer controls who provided complete cigarette and alcohol consumption histories. Genotyping was conducted by polymerase chain reaction‐restriction fragment‐length polymorphism assay.RESULTS.A significant association was noted between alcohol consumption and lung cancer risk. Thus, using the median value for the controls as the cut‐off point, the odds ratios (OR) for light and heavy drinkers were 1.76 and 1.95, respectively (P for trend = .012), compared with nondrinkers. In addition, there was a significant trend toward increased risk of lung cancer in drinkers with ALDH2 variant alleles (P for trend <.0001). The adjusted OR for heavy drinkers was 6.15 compared with nondrinkers. Regarding associations between histologic type and genotypes, the ALDH2 variant allele was significantly less common in patients who had adenocarcinoma compared with controls.CONCLUSIONS.The current observations suggested a positive association between alcohol consumption and the risk of lung cancer: Drinking may increase the risk, especially among individuals who have the variant ALDH2 alleles. Cancer 2007. © 2007 American Cancer Society.

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“…Numerous in vitro and in vivo experiments in prokaryotic and eukaryotic cell cultures, as well as in animal models, have shown that acetaldehyde has direct mutagenic and carcinogenic effects. It causes point mutations in the hypoxanthineguanine-phosphorybosyl transferase locus in human lymphocytes, and induces sister chromatide exchanges and gross chromosomal aberration (Obe et al, 1986;Dellarco, 1988;Helander and Lindahl-Kiessling, 1991). It induces inflammation and metaplasia of tracheal epithelium, delays cell cycle progression and enhances cell injury associated with hyperregeneration (Simanowski et al, 1994;Seitz et al, 2001).…”

Section: Acetaldehydementioning

confidence: 99%

Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress

Seitz

Stickel

2006

Biological Chemistry

283

178

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Hepatocellular cancer is the fifth most frequent cancer in men and the eighth in women worldwide. Established risk factors are chronic hepatitis B and C infection, chronic heavy alcohol consumption, obesity and type 2 diabetes, tobacco use, use of oral contraceptives, and aflatoxin-contaminated food. Almost 90% of all hepatocellular carcinomas develop in cirrhotic livers. In Western countries, attributable risks are highest for cirrhosis due to chronic alcohol abuse and viral hepatitis B and C infection. Among those with alcoholic cirrhosis, the annual incidence of hepatocellular cancer is 1-2%. An important mechanism implicated in alcohol-related hepatocarcinogenesis is oxidative stress from alcohol metabolism, inflammation, and increased iron storage. Ethanolinduced cytochrome P-450 2E1 produces various reactive oxygen species, leading to the formation of lipid peroxides such as 4-hydroxy-nonenal. Furthermore, alcohol impairs the antioxidant defense system, resulting in mitochondrial damage and apoptosis. Chronic alcohol exposure elicits hepatocyte hyperregeneration due to the activation of survival factors and interference with retinoid metabolism. Direct DNA damage results from acetaldehyde, which can bind to DNA, inhibit DNA repair systems, and lead to the formation of carcinogenic exocyclic DNA etheno adducts. Finally, chronic alcohol abuse interferes with methyl group transfer and may thereby alter gene expression.

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Increased frequency of acetaldehyde-induced sister-chromatic exchanges in human lymphocytes treated with an aldehyde dehydrogenase inhibitor

Cited by 88 publications

References 28 publications

Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis

Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis

Susceptibility to lung cancer and genetic polymorphisms in the alcohol metabolite‐related enzymes alcohol dehydrogenase 3, aldehyde dehydrogenase 2, and cytochrome P450 2E1 in the Japanese population

Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress

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Increased frequency of acetaldehyde-induced sister-chromatic exchanges in human lymphocytes treated with an aldehyde dehydrogenase inhibitor

Cited by 88 publications

References 28 publications

Association between alcohol dehydrogenase 1C gene *1/*2 polymorphism and pancreatitis risk: a meta-analysis

Association between alcohol dehydrogenase 1C gene *1/*2 polymorphism and pancreatitis risk: a meta-analysis

Susceptibility to lung cancer and genetic polymorphisms in the alcohol metabolite‐related enzymes alcohol dehydrogenase 3, aldehyde dehydrogenase 2, and cytochrome P450 2E1 in the Japanese population

Risk factors and mechanisms of hepatocarcinogenesis with special emphasis on alcohol and oxidative stress

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Product

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Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis

Association between alcohol dehydrogenase 1C gene 1/2 polymorphism and pancreatitis risk: a meta-analysis