Environmental Mutagenesis

Publisher: Environmental Mutagen Society, John Wiley and Sons

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Other titles Environmental mutagenesis (Online), Environmental mutagenesis (Online), Environmental and molecular mutagenesis
ISSN 1930-238X
OCLC 64222532
Material type Document, Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Computer File, Internet Resource

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John Wiley and Sons

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Publications in this journal

  • Article: In Memoriam

    Environmental Mutagenesis 07/2006; 9(2):107 - 109. DOI:10.1002/em.2860090202
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    ABSTRACT: The kinetics of micronucleus (MN) induction and decline in blood normochromatic erythrocytes (NCE) of mice subchronically exposed to benzene was investigated during and after exposure. Swiss (ICR) male mice (10/group) were given 0.0, 36.6, 73.2, and 146.4 mg/kg body weight benzene by gavage daily for 14 days, except for days 5 and 10. The frequency of MN increased significantly (P <.001) during benzene treatment as a function of both concentration and time. Eleven days after exposure the levels of MN were higher than those observed at the end of exposure. After an initial rapid decline in the frequency of MN from 11 to 18 days postexposure, the decline became linear with time through 60 days postexposure. Using linear regression analysis, the MN level in each treatment group was predicted to reach control levels by approximately 85 days post-treatment. Dose-dependent suppression and recovery of erythropoiesis, estimated by polychromatic erythrocyte frequency, were observed in the 1st and 2nd weeks of exposure, respectively. Red blood cell (RBC) production was markedly increased in the first 3 weeks after benzene treatment. At later times the rate of production of the RBC returned to normal and may account for the linear decline observed in MN frequency. This research indicates that the frequency of MN is dose and duration dependent, while the decline in MN frequency after the end of benzene exposure can be related to changes in the kinetics of erythropoiesis.
    Environmental Mutagenesis 01/1988; 12(3):319 - 329. DOI:10.1002/em.2860120306
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    ABSTRACT: Recent molecular analysis of in vivo-derived hprt mutant T-lymphocytes cloned from human blood show that mutants occurring at the normal frequency (˜ 5 × 10−6) in healthy young individuals generally represent independent hprt mutations. Here we report that in an individual with a high mutant frequency (86–620 × 10−6),92% (61/66) of the mutant clones are descendents of an original mature T-cell precursor that has undergone in vivo clonal expansion. Therefore, these mutants could represent as few as one original hprt mutation. If so, correcting for the clonal expansion yields a revised calculated mutant frequency (Mf) value for this individual that is near the normal range. These hprt mutant clones all showed identically rearranged T-cell receptor (TCR) β and γ gene patterns by Southern blot analysis. All the clones were surface marker CD4+, showed no obvious chromosomal aberration, and had no detectable hprt gene structural alteration. This TCR-defined T-cell clone appears to have expanded in the blood of the individual over a 6-month period and persists at high levels after nearly 4 years.This finding illustrates the need to analyze mutants from individuals with high mutant frequencies at the molecular level in order to estimate hprt mutation frequency from the calculated hprt mutant frequency. The possibility that spontaneous hprt mutants might arise in vivo preferentially in dividing cells, and implications of this, are discussed.
    Environmental Mutagenesis 01/1988; 12(3):271-284. DOI:10.1002/em.2860120302
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    ABSTRACT: No abstract is available for this article.
    Environmental Mutagenesis 01/1988; 12(3):343-344. DOI:10.1002/em.2860120309

  • Environmental Mutagenesis 01/1988; 12(2). DOI:10.1002/em.2860120214

  • Environmental Mutagenesis 01/1988; 12(S14):1 - 85. DOI:10.1002/em.2860120602
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    ABSTRACT: Tetracycline and chloramphenicol increase the number of mutant colonies of strain TA102, which carries the reverting gene on die plasmid pAQ1. Determination of the plasmid content by agarose gel analysis shows that the increase of the mutant colony number is paralleled closely by an increase of die number of pAQ1 plasmids per cell, indicating mat the two compounds do not increase the frequency of mutants “per gene,” but only enhance the number of the genes at which mutations can occur. Thus, not considering die molecular processes could result in mistakenly attributing the increase in the number of mutants per plate (respective to the number of mutants per cell) to a mutagenic activity of die antibiotics.
    Environmental Mutagenesis 01/1988; 12(4):353-363. DOI:10.1002/em.2860120404
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    ABSTRACT: Two tricyclic antidepressants, amitriptyline and imipramine, were evaluated for their in vitro cytogenetic effects in human lymphocyte cultures.Peripheral blood cultures from three normal healthy donors were set up for 72 hr for each of the drugs. The drugs were added at the start (72-hr exposure), 24 hr (48-hr exposure), and 48 hr (24-hr exposure) after initiation of the cultures. The concentrations evaluated at each exposure time were 50, 250, 1,000, and 10,000 ng/ml for amitriptyline and 25, 500, and 5,000 ng/ml for imipramine. The first two concentrations correspond to the plasma levels of the respective drugs after therapeutic doses. All treatments for a donor were given at the same time. Untreated cultures served as controls for the baseline frequency of the parameters assayed. The parameters assayed were chromosome aberrations, mitotic index, and sister chromatid exchanges (SCEs).Amitriptyline was found to be nongenotoxic at plasma levels by all the parameters assayed. However, frequencies of chromosome aberrations and SCEs were significantly increased at concentrations 4 and 40 times the plasma level (1,000 and 10,000 ng/ml) although the actual increase was small. The mitotic index was not affected at any concentration.Though imipramine showed a significant increase in chromosome damage at the upper plasma level and at concentrations higher than that, SCE frequency was significantly increased only at concentration higher than the plasma level (5,000 ng/ml), the actual increase being small for both these parameters. The mitotic index was not affected at any concentration.These results suggest mat amitriptyline may be a slightly safer drug than imipramine from a genetic point of view.
    Environmental Mutagenesis 01/1988; 12(4):421 - 430. DOI:10.1002/em.2860120410
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    ABSTRACT: Perturbation of DNA replication by chemical-DNA adducts produced by exposure to mutagenic/carcinogenic chemicals results in mutagenic or cytotoxic damage in the DNA. Demonstration of a correlation between cell cycle dependency of cytotoxicity and point mutation at the Na+/K+ ATPase gene could suggest that the two consequences of chemical exposure are caused by the same damage in the template DNA and that both are mediated through DNA replication-associated mechanisms. N-methyl-N′-nitro-N-nitrosoguanidine, N-ethyl-N′-nitro-N-nitrosoguanidine, 4-nitroquinoline-1-oxide, and benzo(a)pyrene-trans-7,8-dihydrodiol-9, 10-epoxide demonstrated cell cycle-related patterns of cytotoxicity in 10T1/2 cells, with maximal cell killing produced by exposure in early S phase, and were highly efficient mutagens of the Na+/K+ ATPase gene relative to their cytotoxic potential. In contrast, methyl methanesulfonate and N-acetoxy-N-2-fluorenylacetamide were maximally cytotoxic in ceil populations exposed in early G1 phase and were weak mutagens of the Na+/K+ ATPase gene at comparable levels of cytotoxicity. These data suggest that mutagenic/carcinogenic chemicals that are effective at producing mutations by misreplication kill cells by a related mechanism that may be associated with the perturbation of DNA replication.
    Environmental Mutagenesis 01/1988; 12(3):299 - 309. DOI:10.1002/em.2860120304
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    ABSTRACT: Using an improved microculture method, we investigated how the patterns of persistence of urethane-induced SCEs in lymphocytes differ among individuals and strains of mice (the ddY and C57BL strains), and we attempted to speculate on their relationship to carcinogen susceptibility. After a single intraperitoneal (i.p.) injection of 900 mg/kg of body weight of urethane into ten female mice each for the two strains, blood samples for the SCE analysis were collected from the tail vein at ten times during the 180 posttreatment days for each individual. Immediately after the treatment, SCE values increased to about three to four times the spontaneous values in all of the animals tested and then fell gradually. (The difference from spontaneous values was statistically significant until 120 days after the treatment.) Even after 180 days, however, some “outlier” cells with exceptionally high SCEs (>20) persisted. Although there was some difference in average SCEs between the ddY and C57BL strains, the magnitude of the difference was too small to account for the difference between the strains in the incidence of urethane-induced malignancy. Also, when autopsy data at the 200th posttreatment day were matched individually with the data of SCE values within each strain, it was difficult to predict the individual risk of the occurrence of lung adenoma or other tumors from the relative difference in SCE values.
    Environmental Mutagenesis 01/1988; 12(4):375 - 383. DOI:10.1002/em.2860120406

  • Environmental Mutagenesis 01/1988; 12(4):431 - 477. DOI:10.1002/em.2860120411
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    ABSTRACT: Human cytomegalovirus (CMV) is potentially an effective but often overlooked genotoxic agent in humans. We report here evidence that indicates that infection by CMV can induce chromosome alterations and mitotic inhibition. The frequency of chromosome aberrations induced was dependent on the input multiplicity of infection (m.o.i.) for human lung fibroblasts (LU), but not for human peripheral blood lymphocytes (PBLs) when both cell types were infected at the GO phase of the cell cycle. The aberrations induced by CMV were mostly chromatid breaks and chromosome pulverizations that resembled prematurely condensed S-phase chromatin. Pulverized chromosomes were not observed in LU cells infected with virus stocks that had been rendered nonlytic by UV-irradiation at 24,000 ergs/mm2 or from infection of human lymphocytes. In LU cells infected with UV-irradiated CMV, the frequency of aberrations induced was inversely dependent on the extent of the exposure of the CMV stock to the UV-light. In permisive CMV infection of proliferating LU cells at 24 hr after subculture, a high percentage (> 40%) of the metaphase cells were arrested at their first metaphase and displayed severely condensed chromosomes when harvested 48 hr later. A significant increase (p < 0.05) in the chromosome aberration frequency was also observed. Our study shows that CMV infection is genotoxic to host cells. The types and extent of damage are dependent on the viral genome expression and on the cell cycle stage of the cells at the time of infection. The possible mechanisms for induction of chromosome damage by CMV are discussed.
    Environmental Mutagenesis 01/1988; 12(4):409 - 420. DOI:10.1002/em.2860120409
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    ABSTRACT: A data-based approach to formulating quality-control criteria for the mouse lymphoma cell forward mutation assay is described. Quality-control guidelines for solvent controls, positive controls, and compound-treated cultures were developed based on analysis of over 800 experiments. Frequency distributions of experimental parameters of control cultures, such as mutant frequencies, cloning efficiencies, and suspension growths, were examined. Cloning efficiency and relative total growth affected the variability only when the test chemical was highly toxic. This information was used to generate the quality-control criteria, which were applied to an experiment before it was evaluated for a response. The response categories for classifying the effect of test chemicals on the assay system are defined in terms of (1) the statistically significant differences in average mutant frequency between solvent control cultures and cultures exposed to a chemical and (2) the trend of the dose-related responses.
    Environmental Mutagenesis 01/1988; 12(S13):19 - 36. DOI:10.1002/em.2860120503
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    ABSTRACT: Enhanced reactivation of Ultraviolet-irradiated virus has been reported to occur in heat-shocked host cells. Since enhanced virus reactivation is often accompanied by untargeted mutagenesis, we investigated whether such mutagenesis would occur for herpes simplex virus (HSV) in CV-1 monkey kidney cells subjected to heat shock. In addition to expressing enhanced reactivation, the treated cells were transiently more susceptible to infection by unirradiated HSV. No mutagenesis of unirradiated HSV was found whether infection occurred at the time of increased susceptibility to infection or during expression of enhanced viral reactivation.
    Environmental Mutagenesis 01/1988; 12(2):201 - 207. DOI:10.1002/em.2860120206
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    ABSTRACT: α,β-Unsaturated aldehydes are reactive compounds which are ubiquitous in the environment. This class of compounds has been tested for mutagenicity in Salmonella typhimurium by a number of groups who have obtained differing results. The present studies were undertaken to test the mutagenicity and toxicity of two novel α,β-unsaturated aldehydes, specifically trans,trans-muconaldehyde and trans-4-hydroxynonenal, and to re-examine the mutagenicity of crotonaldehyde. Trans,trans-muconaldehyde is a newly found microsomal metabolite of benzene, and trans-4-hydroxynonenal is a toxic aldehyde formed endogenously during lipid peroxidation. Compounds were tested in S. typhimurium strain TA 100 using a 30-min liquid preincubation procedure. The present mutagenicity studies indicate that these α,β-unsaturated aldehydes at first appear to be mutagenic, although only at concentrations which decrease survival counts, and result in a disappearance of the bacterial lawn. The colonies observed on mutagenicity test plates are not mutants but rather pin point survivors.
    Environmental Mutagenesis 01/1987; 9(3):289-295. DOI:10.1002/em.2860090308
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    ABSTRACT: Acrylamide was tested without exogenous activation in L5178Y/TK+/− −3.7.2C cells for mutation at the thymidine kinase locus and for clastogenicity. Acrylamide gave a positive induced mutagenic response (approximately 70 mutants/106 survivors) when tested at 600–650 μg/ml. The highest dose tested (850 μg/ml) resulted in an induced mutant frequency of approximately 380 mutants/106 survivors (survival = 13%). Acrylamide induced almost exclusively small-colony mutants, indicating that it might be acting by a clastogenic mechanism. As predicted, acrylamide was clastogenic, inducing both chromatid and chromosome breaks and rearrangements. A clearly positive clastogenic response was observed at both the 750 μg/ml and 850 μg/ml doses, which showed 16 and 64 aberrations per 100 cells, respectively (background = 3 aberrations per 100 cells). These studies indicate that the L5178Y/TK+/− mouse lymphoma assay can detect some chromosomal mutagens (clastogens) that show little activity in other single gene mutation assays, the CHO/HPRT and Salmonella.
    Environmental Mutagenesis 01/1987; 9(3):261 - 267. DOI:10.1002/em.2860090305

  • Environmental Mutagenesis 01/1987; 9(1):105-106. DOI:10.1002/em.2860090111
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    ABSTRACT: The results and data from the testing of 255 chemicals for mutagenicity in Salmonella are presented. All chemicals were tested under code using a preincubation modification of the Salmonella/microsome test in the absence of exogenous metabolic activation and in the presence of liver S-9 from Aroclor-induced male Sprague-Dawley rats and Syrian hamsters.
    Environmental Mutagenesis 01/1987; 9(S9):61 - 109. DOI:10.1002/em.2860090603
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    ABSTRACT: The ability of inhaled methyl isocyanate (MIC) to induce genotoxic and cytotoxic damage in vivo was evaluated by assessing the induction of chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs) in bone marrow metaphase cells, the induction of micronuclei in polychromatic erythrocytes (MN-PCEs), and the inhibition of bone marrow cellular proliferation and erythropoiesis. B6C3F1 mice were exposed to MIC by two exposure regiments: (a) in two experiments, male mice only were exposed to 3, 10, and 30 ppm for 2 hr(b) in four experiments, male and female mice were exposed to 1 and 3 ppm (in one experiment, to 6 ppm, also, 6 hr per day for 4 consecutive days. The various cytogenetic endpoints were analyzed in bone marrow and peripheral blood (4-day exposure regimen only) samples taken from bromodeoxyuridine tablet-implanted animals killed 11 to 22 hr after cessation of the exposure to MIC. Exposure to MIC for 2 hr induced a significant delay in cellular proliferation but did not induce a significant increase in CAs, SCEs (evaluated at 3 and 10 ppm, only) or in bone marrow MN-PCEs. Also, this exposure regimen did not inhibit the rate of erythropoiesis. Following exposure to MIC for 4 days, a weak but significant increase in CAs and SCEs was observed in male (in one experiment) and in female (in two experiments) mice. The induction was especially apparent in the single experiment in which mice were exposed to 6 ppm MIC. At this concentration, a significant increase in MN-PCEs in peripheral blood was observed in male but not female mice. Delay in bone marrow cell proliferation was observed in male mice beginning at 3 ppm and in female mice at 6 ppm. The 4-day exposure regimen resulted also in a depressed rate of erythropoiesis, with male mice appearing to exhibit greater depression than female mice. The results demonstrate that exposure to MIC by inhalation results in bone marrow damage, indicating the systemic genotoxic/cytotoxic activity of MIC and/or reactive metabolites.
    Environmental Mutagenesis 01/1987; 9(1):37 - 58. DOI:10.1002/em.2860090106