Biomarkers to assess the genetic damage induced by alcohol abuse in human lymphocytes

Maffei, Francesca; Forti, Giorgio; Castelli, E; Stefanini, Giuseppe Francesco; Mattioli, Stefano; Hrelia, Patrizia

doi:10.1016/s1383-5718(01)00318-7

Cited by 45 publications

(24 citation statements)

References 54 publications

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“…The evidence regarding an effect of drinking alcoholic beverages on increased MN is inconclusive. An increase in MN has been observed in alcoholics consuming alcoholic beverages but not in abstainers of a year or more [6,8].…”

Section: Discussionmentioning

confidence: 99%

Micronucleus Test in Exfoliated Buccal Cells from Chromium Exposed Tannery Workers

Sudha¹,

Prathyumnan²,

Joseph³

et al. 2011

IJBBB

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Abstract-Our aim was to investigate the adverse effects of occupational exposure to trivalent chromium in tannery workers and unexposed persons. Trivalent chromium used in tanning industry is an environmental contaminant that acts as a carcinogen towards humans and animals. The carcinogenic potential of metals is a major issue in defining human health risk from exposure. In the present investigation, 84 tannery workers and 52 control subjects with similar mean ages, smoking prevalences and alcohol consumption were enrolled for DNA damage analysis in buccal cells by Micronucleus assay (MN). Workers showed a significant increase in micronucleated cells when compared to controls with respect to their smoking habits, alcohol consumption, age and years of exposure. The current study suggests that chronic occupational exposure to Chromium during tanning could lead to increased levels of DNA damage. The results of the present investigation are in agreement with those obtained with the same Cr (III) compounds in mutagenicity assays in bacteria and carcinogenicity tests in rodents. A re-evaluation of the mechanisms of chromium carcinogenisis is proposed.

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Section: Discussionmentioning

confidence: 99%

Micronucleus Test in Exfoliated Buccal Cells from Chromium Exposed Tannery Workers

Sudha¹,

Prathyumnan²,

Joseph³

et al. 2011

IJBBB

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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 AA has direct mutagenic and carcinogenic effects. It causes point mutations in the hypoxanthineguanine-phosphoribosyl transferase locus in human lymphocytes, induces sister chromatid exchanges, and gross chromosomal aberrations [8][9][10][11][12][13]. It induces inflammation and metaplasia of tracheal epithelium and enhances cell injury associated with hyperregeneration in the esophageal and colorectal mucosa [14][15][16].…”

Section: Toxic and Carcinogenic Effects Of Acetaldehydementioning

confidence: 99%

Acetaldehyde as an underestimated risk factor for cancer development: role of genetics in ethanol metabolism

2009

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Chronic ethanol consumption is a strong risk factor for the development of certain types of cancer including those of the upper aerodigestive tract, the liver, the large intestine and the female breast. Multiple mechanisms are involved in alcohol-mediated carcinogenesis. Among those the action of acetaldehyde (AA), the first metabolite of ethanol oxidation is of particular interest. AA is toxic, mutagenic and carcinogenic in animal experiments. AA binds to DNA and forms carcinogenic adducts. Direct evidence of the role of AA in alcohol-associated carcinogenesis derived from genetic linkage studies in alcoholics. Polymorphisms or mutations of genes coding for AA generation or detoxifying enzymes resulting in elevated AA concentrations are associated with increased cancer risk. Approximately 40% of Japanese, Koreans or Chinese carry the AA dehydrogenase 2*2 (ALDH2*2) allele in its heterozygous form. This allele codes for an ALDH2 enzyme with little activity leading to high AA concentrations after the consumption of even small amounts of alcohol. When individuals with this allele consume ethanol chronically, a significant increased risk for upper alimentary tract and colorectal cancer is noted. In Caucasians, alcohol dehydrogenase 1C*1 (ADH1C*1) allele encodes for an ADH isoenzyme which produces 2.5 times more AA than the corresponding allele ADH1C*2. In studies with moderate to high alcohol intake, ADH1C*1 allele frequency and rate of homozygosity was found to be significantly associated with an increased risk for cancer of the upper aerodigestive tract, the liver, the colon and the female breast. These studies underline the important role of acetaldehyde in ethanol-mediated carcinogenesis.

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“…Apart from the occupational setting, other examples have been published where CA can efficiently be used in surveying subjects potentially at risk of cancer. The use of CA was proposed in programs for cancer prevention in alcoholics (Maffei et al, 2002) and in cancer screening of small groups where the estimates of relative risks may be impossible, like astronauts during space missions (Durante et al, 2001). …”

Section: Biomarkers Of Cancer Risk In Human Populations: From Researcmentioning

confidence: 99%

Chromosomal aberrations and risk of cancer in humans: an epidemiologic perspective

Bonassi

Znaor²,

Norppa

et al. 2004

Cytogenet Genome Res

188

104

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The pioneering papers published more than one century ago by Theodor Boveri opened the way to extensive research on the mechanism linking chromosomal abnormalities to the pathogenesis of cancer. As a result of this effort, robust theoretical and empirical evidence correlating cytogenetic damage to early stages of cancer in humans was consolidated, and an increased cancer risk was postulated in healthy subjects with high levels of chromosomal aberrations (CA). The first epidemiological investigation aimed at validating CA as predictor of cancer risk was carried out in the early 1990s. In that report the Nordic Study Group described an 80% increased risk of cancer in healthy subjects with high frequencies of CA. The results of this first study were replicated a few years later in a parallel research initiative carried out in Italy, and the subsequent pooled analysis of these two cohorts published in 1998 contributed to refine the quantitative estimate of the CA/cancer association. A small case-control study nested in a cohort of subjects screened for CA in Taiwan found an increased risk in subjects with high frequency of chromosome-type CA, while in 2001 a significant increase of cancer incidence associated with high levels of CA was described in a new independent cohort of radon exposed workers from the Czech Republic. Despite some common limitations affecting study design, the studies cited above have provided results of great interest both for the understanding of mechanisms of early stages of carcinogenesis, and for their potential implication for cancer prevention. The recent evolution of molecular techniques and the refinement of high throughput techniques have the potential to improve the knowledge about the role of specific sub-types of CA and to provide further insight into the mechanisms. Finally, the most challenging perspective in the field is the passage from research to regulation, with the implementation of preventive policies based on the accumulated knowledge.

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Biomarkers to assess the genetic damage induced by alcohol abuse in human lymphocytes

Cited by 45 publications

References 54 publications

Micronucleus Test in Exfoliated Buccal Cells from Chromium Exposed Tannery Workers

Micronucleus Test in Exfoliated Buccal Cells from Chromium Exposed Tannery Workers

Acetaldehyde as an underestimated risk factor for cancer development: role of genetics in ethanol metabolism

Chromosomal aberrations and risk of cancer in humans: an epidemiologic perspective

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