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Biomedical subjects

V W Mayer

Publications and source records attributed to V W Mayer.

32 records · Page 2Linked to original sources
PubMed1980

Induction of mitotic recombination by certain hair-dye chemicals in Saccharomyces cerevisiae.

A number of procedures were used to test for the potential of 5 hair-dye chemicals, 4-nitro-o-phenylenediamine, 2-nitro-p-phenylenediamine, m-phenylenediamine 2,4-diaminoanisole sulfate and 2,5-diaminoanisole sulfate, to induce genetic damage in yeast strains D3 and D4 of Saccharomyces cerevisiae. Various plate-test procedures, short-term suspension assays in phosphate buffer and suspension assays with liver enzyme activation all proved to be ineffective for demonstrating genetic effects of these chemicals. Only suspension assays in which the yeast cells were treated with the test chemical under growing conditions for up to 72 h were effective in demonstrating the genetic activity of 4-nitro-o-phenylenediamine and 2,4-diaminoanisole sulfate. The implications of these results for testing of mutagens in yeast systems are discussed along with other supportive evidence from the literature.

Culture Media↗
PubMed1977

Induction of mitotic crossing over in Saccharomyces by p-Toluidine.

p-Toluidine, a carcinogen for rats, does not cause genetic damage when tested directly in Saccharomyces cerevisiae; however, certain chemical derivatives of p-toluidine do induce gene conversion when tested directly. It may be suspected by analogy with other aromatic amines that p-toluidine, a monocyclic aromatic amine, requires conversion to breakdown products which are then the genetically active and carcinogenic entities. The Udenfriend hydroxylation medium, which has been used previously to show the genetic activity of certain other aromatic amines and nitrosamines, was used in the incubation of p-toluidine with Saccharomyces cerevisiae. The resulting breakdown products, but not the parent compound, induced reciprocal mitotic recombination in a diploid strain D-3. Recombination was monitored by using induced homozygosity of the red ade 2 marker, and the reciprocal nature of the event was confirmed by observing the simultaneous homozygosity of two peripheral markers.

Biotransformation↗
PubMed1976

Genetic effects induced in Saccharomyces cerevisiae by cyclophosphamide in vitro without liver enzyme preparations.

Cyclophosphamide induced forward mutation in Saccharomyces cerevisiae strain S288C and mitotic recombination in strains D3 and D5 but not in strain D4. The yeast cells were treated with the compound in phosphate buffer without recourse to metabolic activation protocols. Elevation of the treatment temperature increased the genetic activity of cyclophosphamide. Respiration-deficient isolates of strains S288C and D3 were more sensitive than the respiratory competent parent strains were for inducing forward mutation and mitotic recombination, respectively. Cyclophosphamide was incubated in phosphate buffer alone for increasing time intervals; strain D3 cells were added to aliquots for each time interval and incubated for an additional 30 min. The frequency of induced recombination increased as the time of compound incubation increased, showing that spontaneous degradation of cyclophosphamide to genetically active breakdown products was responsible for the genetic damage induced in the yeast cells.

Cyclophosphamide↗
PubMed1975

Legislative and technical aspects of mutagenicity testing.

A brief account is given of the history of the legislative acts that give responsibility to the U.S. Food and Drug Administration (FDA) for ensuring the safety of foods, drugs, and cosmetics. Within the present legislative framework the FDA has the authority to impose regulations which are designed to ensure the safety of all foods, drugs, and cosmetics. The existing legislative authority is adequate for this purpose; however, the difficulty lies instead with technology and the inadequacy of scientific perspective in the emerging area of mutagenicity testing. Earlier efforts in development of mutagenicity screening systems culminated only a few years ago in the proposal to use the host-mediated assay, somatic cell cytogenetics, and dominant lethal tests collectively. Subsequent research efforts indicated that there were serious practical and scientific deficiencies in using this approach. More recently a new proposal, the tier system, has been suggested as an alternative measure. The proposed tier system at FDA consists of three testing levels of increasing complexity. The first tier is an initial screening effort using techniques having maximum sensitivity that are also useful for large-scale, rapid testing. The second tier is designed to identify and confirm that the presumptive mutagens detected in the first tier are truly mutagenic for higher organisms, most especially, for mammals. The third tier would be devoted to explicit genetic tests in mammals designed to ascertain the imposed risk to man by the introduction of a mutagen in our environment. The FDA is currently involved in a number of research activities in the area of mutagenicity safety screening which will explore the adequacies and possible deficiencies of the tier system approach. These efforts are described for our in-house activities, our contract activities, and our cooperative and collaborative activities with other government agencies and institutions.

Animals↗
PubMed1973

Induction of mitotic crossing over in Saccharomyces cerevisiae by breakdown products of dimethylnitrosamine, diethylnitrosamine, 1-naphthylamine and 2-naphthylamine formed by an in vitro hydroxylation system.

Dimethylnitrosamine and diethylnitrosamine, two potent carcinogens, are nonmutagenic when tested directly in microorganisms. Likewise 1-naphthylamine and 2-naphthylamine are also nonmutagenic but the N-hydroxy derivatives are mutagenic in microorganisms. Apparently these compounds require metabolism to breakdown products which are then the proximately active agents, and microorganisms lack the enzymes necessary to effect this conversion. These compounds are mutagenic in Saccharomyces after conversion to breakdown products in an in vitro hydroxylation medium. The induction of mitotic crossing over in Saccharomyces cerevisiae by breakdown products of dimethylnitrosamine, diethylnitrosamine, 1-naphthylamine and 2-naphthylamine formed in the Udenfriend hydroxylation medium is reported in this communication. Mitotic crossing over was detected as red sectored colonies resulting from induced homozygosity of the ade2 marker. Dimethylamine and diethylamine, which lack the nitroso group of the nitrosamines, did not induce mitotic crossing over under any of the test conditions. To further confirm that the induced sectored colonies were the result of mitotic crossing over they were tested for the presence of reciprocal products. The expected reciprocal products were found in over 67% of the isolates tested. The significance and practicality of using mitotic recombination as an indicator of genetic damage potential of chemicals is discussed.

Amines↗
PubMedDate not supplied

The detection of chemically induced aneuploidy in Saccharomyces cerevisiae: an assessment of mitotic and meiotic systems.

Several systems have been evaluated for their ability to detect aneuploidy. Chromosome gain can be detected in mitotic haploid cells as well as meiotically derived haploid spores. Both chromosome gain and loss are detectable in mitotic diploid cells. Several chemicals have been identified that clearly induce aneuploidy in at least one or more of the systems.

Aneuploidy↗