Effects of alcohol consumption on DNA methylation reactions and gene expression

Aj, Garro; Espina, Noel; McBeth, Dani L.; Sl, Wang; Cy, Wu-Wang

doi:10.1097/00008469-199210003-00003

Cited by 14 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…33) Furthermore, it enhances folate deficiency and thus may induce DNA hypomethylation of the intestinal mucosal cells. 34,35) Such hypomethylation would generate transcriptional activation of various genes, and might lead to accelerated cell cycles or unlimited cell growth. As stated earlier, ALDH2 mediates the catabolism of acetaldehyde and plays a major role in the blood concentration of acetaldehyde.…”

Section: Discussionmentioning

confidence: 99%

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Murata

Tagawa

Watanabe

et al. 1999

Japanese Journal of Cancer Research

View full text Add to dashboard Cite

A case-control study was conducted to explore the possible etiologic role of alcohol and aldehyde dehydrogenase 2 (ALDH2) gene among Japanese colorectal cancer patients. Information on their drinking, smoking and dietary habits was collected from 265 colon and 164 rectum cancer patients, and 794 non-cancer patients as a control group. Genotypes of the ALDH2 gene at codon 487, glutamic acid (ALDH2 * 1) as a wild-type or lysine (ALDH2 * 2) as a mutated type with reduced enzyme activity, were analyzed by polymerase chain reaction in 160 colon and 110 rectum cancer patients and 121 control persons. Univariate analysis with the χ χ χ χ 2 statistical test showed that heavy alcohol drinking (P < < < <0.01), frequent meat intake (P < < < <0.001), and irregular (P < < < <0.01), hasty (P < < < <0.01) and excessive (P < < < <0.001) eating habits were associated with the incidence of both colon and rectum cancers, whereas heavier smoking (P < < < <0.05) and infrequent fish (P < < < <0.03) and fruit (P < < < <0.01) intake were solely associated with incidence of rectum cancer. Infrequent green vegetable intake was not correlated with the incidence of colorectal cancer. Multivariate unconditional logistic regression analysis confirmed the association of alcohol consumption (P < < < <0.01) and meat intake (P < < < <0.05).Homozygous and heterozygous carriers of ALDH2 * 2 allele tended to be found in colon (trend P = = = =0.04) but not in rectum cancer patients compared to controls. Risk elevation for colon cancer due to alcohol consumption was pronounced among the heterozygotes and it was statistically significant especially for distal colon cancer (trend P = = = =0.02). We conclude that alcohol consumption is a risk factor for colorectal cancer and the risk can be enhanced in ALDH2 heterozygotes.

show abstract

Section: Discussionmentioning

confidence: 99%

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Murata

Tagawa

Watanabe

et al. 1999

Japanese Journal of Cancer Research

View full text Add to dashboard Cite

show abstract

“…The immunosuppressive effect of chronic ethanol is well documented. There is a strong association between ethanol consumption and both increased cancer risk and infection morbidity (Garro et al, 1992;Imhof and Koenig, 2003;Watson et al, 1994). Sarkar's laboratory has recently reported that mRNA and protein levels of the cytolytic factors Granzyme B and perforin, as well as the cytokine interferon (IFN)-␥, follow a physiological circadian rhythm that concurrently drives the circadian rhythm in natural killer (NK) cell cytolytic activity (Arjona et al, 2004).…”

Section: Alcohol Effects On Clocks Governing Immune Functionsmentioning

confidence: 99%

Alcohol Consumption and the Body???s Biological Clock

Spanagel¹,

Rosenwasser²,

Schumann³

et al. 2005

Alcoholism: Clinical & Experimental Research

154

122

View full text Add to dashboard Cite

This review summarizes new findings on the bidirectional interactions between alcohol and the clock genes, underlying the generation of circadian rhythmicity. At the behavioral level, both adult and perinatal ethanol treatments after the free-running period and light response of the circadian clock in rodents; genetic ethanol preference in alcohol-preferring rat lines is also associated with alterations in circadian pacemaker function. At the neuronal level, it has been shown that ethanol consumption alters the circadian expression patterns of period (per) genes in various brain regions, including the suprachiasmatic nucleus. Notably, circadian functions of beta-endorphin-containing neurons that participate in the control of alcohol reinforcement become disturbed after chronic alcohol intake. In turn, per2 gene activity regulates alcohol intake through its effects on the glutamatergic system through glutamate reuptake mechanisms and thereby may affect a variety of physiological processes that are governed by our internal clock. In summary, a new pathologic chain has been identified that contributes to the negative health consequences of chronic alcohol intake. Thus, chronic alcohol intake alters the expression of per genes, and as a consequence, a variety of neurochemical and neuroendocrine functions become disturbed. Further steps in this pathologic chain are alterations in physiological and immune functions that are under circadian control, and, as a final consequence, addictive behavior might be triggered or sustained by this cascade.

show abstract

“…There is a strong association between ethanol consumption and both increased cancer risk and infection morbidity (18,19). We have recently shown how chronic ethanol reduces granzyme B, perforin, and NK cell cytolytic activity (20,21), however, there is no report showing a direct influence of ethanol on the circadian rhythm of NK cells.…”

mentioning

confidence: 99%

Circadian Rhythms of Granzyme B, Perforin, IFN-γ, and NK Cell Cytolytic Activity in the Spleen: Effects of Chronic Ethanol

Arjona

Boyadjieva

Sarkar

2004

The Journal of Immunology

View full text Add to dashboard Cite

Recent studies show that alterations in the body’s biological rhythms can lead to serious pathologies, including cancer. Acute and chronic ethanol consumption impairs the immune system by causing specific defects in the cellular components of the innate immune response and by creating increased risk and susceptibility to infections and cancer. NK cells are critical for immune surveillance against infected and malignant cells. To assess whether NK cell function follows a circadian trend and to determine ethanol effects on this rhythm, we measured, over a 24-h period, mRNA and protein levels of granzyme B, perforin, and the cytokine IFN-γ, as well as NK cell activity, in the splenocytes of ad libitum-fed, pair-fed, and ethanol-fed Sprague Dawley male rats. Circadian rhythms were found in mRNA and protein levels of granzyme B, perforin, and IFN-γ. A circadian pattern was also detected in NK cell cytolytic activity. Our data further demonstrated how chronic ethanol suppressed NK cell activity by directly disrupting the circadian rhythms of granzyme B, perforin, and IFN-γ. These findings identify the circadian functions of splenic NK cells and show the vulnerability of these rhythms to chronic ethanol.

show abstract

Effects of alcohol consumption on DNA methylation reactions and gene expression

Cited by 14 publications

References 0 publications

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Genotype Difference of Aldehyde Dehydrogenase 2 Gene in Alcohol Drinkers Influences the Incidence of Japanese Colorectal Cancer Patients

Alcohol Consumption and the Body???s Biological Clock

Circadian Rhythms of Granzyme B, Perforin, IFN-γ, and NK Cell Cytolytic Activity in the Spleen: Effects of Chronic Ethanol

Contact Info

Product

Resources

About