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Chromosome Damage Induced by Vinyl Acetate through in Vitro Formation of Acetaldehyde in Human Lymphocytes and Chinese Hamster Ovary Cells

TLDR
The results indicate that vinyl acetate induces chromosome damage in cell cultures through enzyme-mediated hydrolysis to acetaldehyde, and this effect was more pronounced in cultures of isolated lymphocytes than in whole-blood cultures.
Abstract
A 48-h treatment with vinyl acetate (0.05-1 mM) induced a drastic increase in sister chromatid exchanges (SCEs) and (in first division cells) structural chromosome aberrations in cultured human lymphocytes. The effects were more pronounced in cultures of isolated lymphocytes than in whole-blood cultures. A distinct dose-dependent induction of SCEs similarly occurred in Chinese hamster ovary cells after a 24-h vinyl acetate treatment (0.125-1 mM). A pulse treatment of Chinese hamster ovary cells for 4 h also yielded a clear increase in SCEs, but at higher concentrations (0.3-5 mM). The presence of rat liver S9 mix enhanced the SCE-inducing effect of vinyl acetate in Chinese hamster ovary cells. Gas chromatographic analysis of human whole-blood lymphocyte cultures treated for 10 s-20 min with vinyl acetate (5.4 mM) revealed a rapid degradation of vinyl acetate and formation of acetaldehyde. During the 20-min observation period, no degradation of vinyl acetate or formation of acetaldehyde were observed in complete culture medium without blood, which suggested that the reaction was enzymatic. Acetaldehyde induced SCEs in human whole-blood lymphocyte cultures at concentrations (0.125-2 mM) comparable to those used for vinyl acetate. The results indicate that vinyl acetate induces chromosome damage in cell cultures through enzyme-mediated hydrolysis to acetaldehyde.

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Citations
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Aldehydes: occurrence, carcinogenic potential, mechanism of action and risk assessment

TL;DR: Overall assessment of the cancer risk of aldehydes in the diet leads to the conclusion that formaldehyde, acrolein, citral and vanillin are no dietary risk factors, and that the opposite may be true for acetaldehyde, crotonaldehyde and furfural.
Journal ArticleDOI

A mutagenicity assessment of acetaldehyde.

TL;DR: Although acetaldehyde is a genotoxic cross-linking agent, it does not appear to cause DNA strand breaks and there were no studies available regarding the potential of acetaldehyde to produce genetic damage in mammalian germ cells in vivo.
Journal ArticleDOI

Acetaldehyde: genotoxicity and cytotoxicity in human lymphocytes

TL;DR: This is the first study demonstrating DNA single- and double-strand breaks by acetaldehyde, and a significant cell loss after exposure to acetaldehyde is observed.
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TL;DR: There is a high correlation between carcinogenicity and mutagenicity: 90% (156/174) of carcinogens are mutagenic in the test and despite the severe limitations inherent in defining non-carcinogenicity, few "non-Carcinogens" show any degree of mutageniability.
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Statistics for toxicologists

TL;DR: In this article, the authors explain how the computer programs work and why and when they can be applied to problems in toxicology, and discuss the statistical models used and their applications in a general fashion.
Journal ArticleDOI

Screening of tobacco smoke constituents for mutagenicity using the Ames' test.

TL;DR: To clarify the mutagenic activity of individual smoke components, 239 compounds, representative of the gaseous and semivolatile phases of tobacco smoke, were assayed for mutagenicity towards 4 histidine-requiring mutants of Salmonella typhimurium.
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