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F Poncelet

Publications and source records attributed to F Poncelet.

At least 37 records · Page 2Linked to original sources

Metabolic activation and mutagenicity of 4 vinylic monomers (vinyl chloride, styrene, acrylonitrile, butadiene).

The mutagenic activity and the metabolism of four vinylic monomers; vinyl chloride, styrene, acrylonitrile and butadiene are reviewed. Those chemicals are converted by the mixed function oxidases system of the endoplasmic reticulum into reactive intermediates which can interact with macromolecules within the cell. In order to examine the mutagenic activity of these compounds and their metabolites, different mutagenicity testing systems have been used: tests with S. typhimurium, E. coli, Schizosaccharomyces pombe, Saccharomyces cerevisiae, V79 Chinese Hamster cells, CHO cells, Drosophila melanogaster as well as evaluations of chromosome aberrations.

Acrylonitrile↗

Influence of experimental factors on the mutagenicity of vinylic monomers.

The results obtained by testing the mutagenicity of several vinylic monomers, styrene, butadiene, acrylonitrile, vinyl chloride on strains of Salmonella typhimurium in various experimental conditions, modes of incubation, and in the presence of different metabolic activating systems, demonstrate that these parameters have a variable effect on the mutagenic potency of those monomers.

Animals↗

Genetic effects of chlorinated anilines and azobenzenes on Salmonella typhimurium.

The mutagenicity of 19 herbicide-derived chlorinated azobenzenes and structurally related chlorinated anilines and nitrobenzenes was assayed towards several strains of S. typhimurium, using the plate incorporation method and the fluctuation test, in the presence or in the absence of liver post-mitochondrial fractions, in aerobic and anerobic conditions. Positive results were obtained with 4,4'-dichloroazobenzene, 4,4'-dichloroazoxybene, 3,4-dichloronitrobenzene and, to a much lesser extent, with 3,4,3',4'-tetrachloroazobenzene. No mutagenic effect was observed with 2,3,7,8-tetrachlorodibenzo-p-dioxin in any condition.

Aerobiosis↗

Mutagenicity of urine from rats and mice treated with acrylonitrile.

Urines collected from rats and mice treated with acrylonitrile (ACN) were mutagenic towards Salmonella typhimurium strain TA 1530 in the absence of a metabolic activation system. When assayed in the presence of a liver S9 mix, this activity was suppressed when the urines were obtained from acrylonitrile treated rats, and decreased when these urines were collected from acrylonitrile treated mice. Pretreatment of the animals with phenobarbital abolished the direct mutagenicity of urines from acrylonitrile treated rats, and reduced that observed with mice urines. Addition of beta-glucuronidase to the incubation mixtures enhanced the mutagenicity of the urines from both phenobarbital untreated and treated rats and mice injected with acrylonitrile.

Acrylonitrile↗

Competitive inhibitory effect of microsomal N-hydroxylase, a possible explanation for the in vivo in inhibition of 2-acetylaminofluorene carcinogenicity by 3-methylcholanthrene.

The kinetic properties of the N-hydroxylation of 2-acetylaminofluorene (2-AAF) are studied with microsomal preparations of livers from both control and 3-methylcholanthrene (3-MC)-pretreated rats and hamsters. The level of basal enzymatic activity is higher in hamster than in rat liver; 3-MC induces the activity in both animals. When added in vitro to incubation mixture, 3-MC competitively inhibits the N-hydroxylase activity. When fed to rats simultaneously with 2-AAF, 3-MC suppresses the carcinogenicity of the acetylated arylamine by inhibiting the first step in its activation pathway. Hamster tissues are not protected by this pretreatment because the level of N-hydroxylase activity is too high.

2-Acetylaminofluorene↗

The mutagenicity of butadiene towards Salmonella typhimurium.

Gaseous butadiene (BUT) was mutagenic towards S. typhimurium strain TA 1530 when the incubation mixture was supplemented with a NADPH-fortified rat liver microsomal preparation; mutagenicity increased with the dose. A significant mutagenic effect was similarly observed when the petri dishes, containing the bacteria but no metabolic activation system, were incubated in the presence of butadiene, in a desiccator in which plates containing the S-9 rat liver fraction had been placed. This indirect mutagenic effect was attributed to the formation, by the S-9 mix, of volatile intermediate(s) that migrated and induced mutations in neighbouring bacteria.

Animals↗

Mutagenicity tests with griseofulvin.

Griseofulvin was studied for its ability to induce structural chromosomal aberrations in germ and somatic cells of the male mouse. It was also tested for its capacity to produce his+ revertants in Salmonella typhimurium. All tests yielded negative results, whereas highly significant effects were recorded in control assays with thio-TEPA.

Animals↗

Liver extract mediated mutagenicity of acrylonitrile.

The mutagenic activity of acrylonitrile vapours towards Salmonella typhimurium strains strictly depends upon the presence of a liver postmitochondrial fraction. The reversion rate varies according to the animal species from which the S9 fraction is obtained as well as to the pretreatment of the animals. The comparatively weak activating effect of the microsomal fraction and the inability of both SKF525A and carbon monoxide to inhibit the S9 mediated mutagenicity of acrylonitrile (ACN) suggest that the cytochrome P-450-dependent monooxygenases do not play a major role in the metabolic activation of ACN into a mutagenic intermediate (s).

Acrylonitrile↗