DNA-repair capacity and lipid peroxidation in chronic alcoholics
Language English Country Netherlands Media print
Document type Journal Article
PubMed
2067553
DOI
10.1016/0165-7992(91)90052-6
PII: 0165-7992(91)90052-6
Knihovny.cz E-resources
- MeSH
- Alcoholism blood metabolism MeSH
- DNA biosynthesis drug effects MeSH
- Adult MeSH
- Cells, Cultured MeSH
- Ascorbic Acid blood MeSH
- Middle Aged MeSH
- Humans MeSH
- Methylnitrosourea pharmacology MeSH
- Methylation MeSH
- DNA Repair * MeSH
- Lipid Peroxidation * MeSH
- Regression Analysis MeSH
- Vitamin A blood MeSH
- Vitamin B 12 blood MeSH
- Vitamin E blood MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- DNA MeSH
- Ascorbic Acid MeSH
- Methylnitrosourea MeSH
- Vitamin A MeSH
- Vitamin B 12 MeSH
- Vitamin E MeSH
The possible impact of long-term overexposure to ethanol was studied in a group of chronic alcoholics in the psychiatric hospital. The level of DNA methylation and unscheduled DNA synthesis (UDS) induced by N-methyl-N-nitrosourea (MNU) in lymphocytes and lipid peroxidation (LPO) in plasma were used as markers of injury caused by alcohol abuse. The data were correlated with plasma levels of some natural antioxidants (vitamins A, C and E) and vitamin B12. The following results were obtained. The degree of DNA methylation by MNU in lymphocytes was the same in the exposed and control groups under our experimental conditions. The DNA excision-repair capacity of lymphocytes measured as UDS was decreased in alcoholics (p less than 0.01) and LPO in plasma was significantly higher (p less than 0.01) as a consequence of alcohol overconsumption. By the simple regression method, a correlation was found between LPO and vitamin C levels (LPO = -0.078 x vit. C + 1.9; p less than 0.05) and between UDS and LPO values (UDS = -0.384 x LPO + 4.1; p less than 0.05). These results support the hypothesis of a connection of cell membrane status and DNA damage and repair and the possible role of active oxygen species in cell damage caused by ethanol.
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Future research directions to characterize environmental mutagens in highly polluted area