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Biomedical subjects

V F Simmon

Publications and source records attributed to V F Simmon.

27 records · Page 2Linked to original sources
PubMed1979

In vitro mutagenicity assays of chemical carcinogens and related compounds with Salmonella typhimurium.

The mutagenic activity of 101 chemicals was studied with the use of the Salmonella typhimurium-microsome system described by Ames. The tester strains were TA1535, TA1536, TA1537, TA1538, TA98, and TA100. Assays were conducted in the presence and absence of a metabolic activation system prepared from the livers of randomly bred Sprague-Dawley rats that had been pretreated with Aroclor 1254. The test chemicals were incorporated into the agar with bacteria and the metabolic activation system. Mutagens were defined as chemicals that induced a reproducible dose-related increase in the number of histidine-independent revertants. With the use of these procedures, 65% of the organic carcinogens and 25% of the noncarcinogens were found to be mutagenic.

Alkylating Agents↗
PubMed1979

In vitro assays for recombinogenic activity of chemical carcinogens and related compounds with Saccharomyces cerevisiae D3.

A total of 101 carcinogens, noncarcinogens, metals, and promoters representing a wide variety of chemical classes was tested to determine whether they increased mitotic recombination in Saccharomyces cerevisiae D3. A metabolic activation system prepared from homogenates of livers from rats that had been pretreated with Aroclor 1254 (a mixture of polychlorinated biphenyls) was incorporated in the assay procedure. All of the ultimate carcinogens (20/20) and 38% of the procarcinogens (18/48) increased mitotic recombination. Of the noncarcinogens 29% (6/21) also increased mitotic recombination. A improved metabolic activation procedure appears to be required to increase the probability of detecting procarcinogens by this method. The carcinogens thioacetamide, natulan, auramine, safrole, and 1'-hydroxysafrole increased mitotic recombination in S. cerevisiae D3 (the last compound was marginally positive), but they were negative in assays with Salmonella typhyimurium.

Alkylating Agents↗
PubMed1979

Mutagenic activity of chemical carcinogens and related compounds in the intraperitoneal host-mediated assay.

The mutagenic activities of 79 carcinogens, noncarcinogens, and structurally related compounds toward Salmonella typhimurium strains TA1530, TA1535, and TA1538 and toward Saccharomyces cerevisiae D3 were investigated in the intraperitoneal host-mediated assay. Fewer than half of the carcinogens were mutagenic toward the Salmonella strains. The insensitivity of the system was most marked with the aromatic amine and polycyclic hydrocarbon procarcinogens. Under the test conditions, fewer than 10% of the carcinogens showed clear mutagenic activity toward S. cerevisiae D3. However, none of the noncarcinogens was significantly mutagenic toward either S. typhimurium or S. cerevisiae D3. Overall, the intraperitoneal host-mediated assay does not seem suitable for routine preliminary screening of large numbers of potential carcinogens. The median lethal doses to mice of 46 compounds were determined.

Alkylating Agents↗
PubMed1978

Fluroxene mutagenicity.

The commercially available volatile anesthetic fluroxene (2,2,2-trifluoroethyl vinyl ether) which contains the stabilizer N-phenyl-1-napthylamine, was tested for mutagenicity using four strains of S. typhimurium, TA1535, TA1537, TA98 and TA100, and one strain of E. coli, WP2. In addition, purified fluroxene; N-phenyl-1-napthylamine; trifluoroethanol, a major metabolite of fluoroxene; and urine from rats anesthetized with fluroxene were tested. Several procedures were utilized including exposure of bacteria to vapor in desiccators and in liquid suspension. Results indicate that fluroxene, but not its stabilizer, was mutagenic to strains TA1535, TA100 and WP2 only in liquid suspension and only in the presence of a rat-liver enzyme system. Trifluoroethanol and urine from fluroxene-treated rat were not mutagenic to any strain of bacteria. These findings indicate that fluroxene is a promutagen which requires preincubation before it is recognized. Further experiments were performed with enzymes prepared from mouse, hamster and human liver. Fluroxene was mutagenic only in the presence of enzymes prepared from Aroclor 1254 pretreated rodents. Since fluroxene was not mutagenic in the presence of enzymes prepared from three human livers, the significance of these findings to man are unclear.

Animals↗
PubMed1977

Mutagenicity of halogenated ether anesthetics.

An in vitro microbial assay system employing two histidine-dependent strains of Salmonella typhimurium, TA1535 and TA100, was used to test the mutagenicities of enflurane, methoxyflurane, isoflurane and fluroxene. Enflurane, isoflurane and fluroxene in concentrations ranging from 0.01 to 30 per cent and methoxyflurane in concentrations ranging from 0.01 to 7 per cent were incubated with bacteria in the presence or absence of homogenates of liver prepared from rats pretreated with the enzyme inducer, Aroclor 1254. Enflurane, methoxyflurane, isoflurane, and urines from patients anesthetized with these agents were not mutagenic. Fluroxene, however, was highly mutagenic, and therefore poses a possible hazard for operating room personnel and patients.

Anesthesia, Inhalation↗
PubMed1976

Mutagenicity of volatile anesthetics: halothane.

The mutagenicity of halothane was tested in an in-vitro microbial assay system employing two histidine-dependent mutants of Salmonella typhimurium, TA98 and TA100, Halothane in concentrations ranging from 0.1 to 30 per cent was incubated with bacteria in the presence or absence of a metabolic activation system prepared from either rat liver treated with Aroclor 1254 or human liver. Trifluoroacetic acid, a major metabolite of halothane, and urine from patients anesthetized with halothane also were tested. Halothane, trifluoroacetic acid, and patients' urines were not mutagenic.

Aminobiphenyl Compounds↗
PubMed1972

Degradation of bacteriophage lambda deoxyribonucleic acid after restriction by Escherichia coli K-12.

Wild-type bacteria which restrict the deoxyribonucleic acid (DNA) of infecting phage when the phage do not carry the proper host modification rapidly degrade that restricted DNA to acid-soluble products. The purified restriction enzyme acts as an endonuclease in vitro to cleave restrictable DNA and does not further degrade the DNA fragments produced. We have examined mutants of Escherichia coli K-12 which lack various nucleases in order to determine which nucleases are involved in the rapid acid solubilization in vivo of unmodified lambda DNA following restriction. Bacteria which are wild type, recA(-), or polA1(-) degrade about 50% of the unmodified phage DNA within 10 min of infection, with little subsequent degradation. Mutants which are recB(-) or recC(-) degrade unmodified DNA very slowly, solubilizing about 15% of the DNA by 10 min after infection. Two classes of phenotypic revertants of recB(-)/C(-) mutants were also tested. Bacteria which are sbcA(-) restrict poorly and do not degrade much of the restricted DNA. Bacteria which are sbcB(-) restrict normally. This mutation does not appear to affect degradation of restricted phage DNA in recB(-)/C(-) mutants, but such degradation is decreased in recB(+)/C(+) bacteria. The presence of a functional lambda exonuclease gene is not required for degradation after restriction.

Adenosine Triphosphate↗