Chromosomal damage in chronic alcohol users

Obe, Günter; Herha, J.

doi:10.1007/bf00297623

Cited by 60 publications

(4 citation statements)

References 9 publications

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“…The reproductive and possible mutagenic effects of ethanol consumption have been well documented; however, few studies have evaluated the paternal role in the fetal alcohol syndrome (Jones and Smith, 1973;Obe and Herha, 1975;Hanson, 1980;Czajka et al, 1980). Long-term ingestion of ethanol results in testicular atrophy accompanied by reduced levels of androgen steroids (Van Thiel et al, 1975;Klassen and Persaud, 1978;Anderson et al, 1980;Cicero et al, 1981).…”

Section: Introductionmentioning

confidence: 97%

Paternal effects of ethanol in the long‐Evans rat

Mankes

LeFevre

Benitz

et al. 1982

Journal of Toxicology and Environmental Health

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Ten male Long-Evans rats were given 20% v/v ethanol in the drinking water for 60 consecutive days. Ten other males were given distilled water and served as controls. Each male was then allowed to mate with three virgin female Long-Evans rats, once per week for three consecutive weeks. The males were necropsied after the third mating, the females were killed on d 20 of gestation, and the offspring were examined for parameters of fetal growth, skeletal ossification, and soft-tissue anomalies. Ethanol caused testicular weight reductions and gross testicular atrophy in 1 of 10 males. Five matings of alcoholic male rats proved infertile. Total embryonic deaths (resorptions and preimplantation loss) were increased by ethanol, while implantations and litter size were significantly decreased. Fetuses fathered by alcoholic male rats were malformed: 55% had soft-tissue anomalies (microcephalus, microphthalmia, cranial fissure, and hydronephrosis). Litter weight and average pups weights were also reduced by paternal ethanol consumption. No recovery in reproductive function was evident over the 21-d post-ethanol mating period.

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Section: Introductionmentioning

confidence: 97%

Paternal effects of ethanol in the long‐Evans rat

Mankes

LeFevre

Benitz

et al. 1982

Journal of Toxicology and Environmental Health

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“…One chemical that has been implicated in chromosome changes is alcohol . Obe and Herha (1975) found increased chromosome aberrations in alcoholics. In further investigations, found that acetaldehyde, a metabolic derivative of alcohol, induced SCEs while SCE induction did not occur with ethanol in in vitro studies.…”

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confidence: 95%

Increased frequency of sister-chromatid exchanges in alcoholics

Butler

Sanger

Veomett

1981

Mutation Research/Environmental Mutagenesis and Related Subject

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The frequency of SCES was significantly increased in the alcoholics analyzed (10.6 &/- SD 0.66) when compared to the frequency of a control group (8.4 &/- SD 0.51). Statistical analysis of the data obtained showed that the increase was not apparently related to age, sex, cigarette smoking, duration in years of alcohol abuse, nutritional status or type of alcoholic beverage commonly consumed by the individual. Alcoholics recovering for at least one year from alcohol abuse were examined and the frequency of SCES was found to be equal to the SCE frequency in the control group. There was no statistical significance between the age, sex of the individual, smoking history and years of abstention from alcohol abuse with respect to the frequency of SCES. Therefore, one year of abstention appears sufficient to allow the SCE frequency to return to that found in the control group. In order to keep extraneous factors at a minimum and to analyze the effect of a particular factor, such as alcohol, on the number of SCES, a careful medical history and screening program was followed. However, more information is needed to determine which factors play a role in causing genetic damage and inducing SCES and to determine the significance SCES may have with respect to genetic information and function.

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“…Nevertheless, various psychotropic drugs are reported to induce chromosomal aberrations [17], As for ethanol, some papers report that an elevation of structural [18] and genome aberration [6] has been found in the lym phocytes of alcoholics compared with those of nonalco holics. In the present study, we have shown that chronic alcohol users exhibit a significantly higher frequency of various types of chromosome structural aberrations in peripheral leukocytes as compared to the control group.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal Aberrations in the Lymphocytes of Alcoholics and Former Alcoholics

Matsushima¹

1987

Neuropsychobiology

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An elevation of chromosomal aberrations has been found in the lymphocytes of alcoholics compared with those of nonalcoholics. In this study, structural aberrations of chromosomes in peripheral lymphocytes of alcoholics and former alcoholics were examined in order to study the chromosome-breaking activity of alcohol and effects of long-term sobriety on chromosomal aberrations in alcoholics. We have presumed initially that chromosomal aberrations in alcoholics would remain for a long time after abstinence from alcohol. Nevertheless we found a spontaneous reduction of the chromosomal aberrations in former alcoholics who had been dry for periods of 2 years or more. These observations suggest that chromosomal aberrations appearing in alcoholics probably formed by a chronic activity of alcohol and/or its metabolic products and cellular repair mechanisms may recover within a few years of abstinence.

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Chromosomal damage in chronic alcohol users

Cited by 60 publications

References 9 publications

Paternal effects of ethanol in the long‐Evans rat

Paternal effects of ethanol in the long‐Evans rat

Increased frequency of sister-chromatid exchanges in alcoholics

Chromosomal Aberrations in the Lymphocytes of Alcoholics and Former Alcoholics

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