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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  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The Salmonella/microsome test developed by Ames and his coworkers has been widely used in the evaluation of chemicals for genotoxic potential. Although the value of this assay is well recognized, there have been no comprehensive studies on the interlaboratory reproducibility of the method using a standardized protocol. A program was therefore initiated to compare the results obtained in four laboratories from testing a series of coded mutagens and nonmutagens using a standardized protocol. Additional objectives of this study were to compare male Fisher 344 rat, B6C3F1 mouse, and Syrian hamster liver S-9 preparations for the activation of chemicals; to compare Aroclor 1254-induced liver S-9 from all three species with the corresponding non-induced liver S-9's; and to compare the response of Escherichia coli WP-2 uvrA with the Salmonella typhimurium tester strains recommended by Ames. Since a primary use of in vitro microbial mutagenesis tests is the identification of potential carcinogens by their mutagenicity, the authors decided to compare the animal species and strains used by the National Cancer Institute/National Toxicology Program (NCI/NTP) for animal carcinogenicity studies.
    Environmental Mutagenesis 04/2008; 6(S2):51 - 100.
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    ABSTRACT: Three independent laboratories tested eight “model” and five coded chemicals in the Syrian hamster embryo clonal transformation assay system to establish the intra- and interlaboratory reproducibility of the system and to identify sources of variability. When a common cell pool and the same lot of fetal calf serum were used, the three laboratories obtained consensus on the activity of eight model chemicals: five chemicals (benzo(a)pyrene, 7,12-dimethylbenz(a)anthracene, N-methyl-N′-nitro-N-nitrosoguanidine, nitroquinoline-N-oxide, and lead chromate) induced morphological transformation without exogenous metabolic activation and three (N-2-fluorenylacetamide, pyrene, and anthracene) produced no transformation response. Five coded chemicals (2,6-dichloro p-phenylenediamine, 4,4′-oxydianiline, cinnamyl anthranilate, dichlorvos, and reserpine), representative of environmental chemical classes, but not necessarily strong carcinogens, produced more equivocal responses in this interlaboratory study. Thus, while the assay can be used to distinguish between transforming and nontransforming chemicals in some cases, the intrinsic limitations in low transformation frequency and in achieving any dose-response results are major constraints to the use of this systsem in a routine testing program at the present time. Efforts to increase the transformation frequency or to amplify the expression of the transformed phenotype constitute some of the approaches which should be explored in order to overcome these limitations.
    Environmental Mutagenesis 07/2006; 8(1):77 - 98.
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    ABSTRACT: The genotoxicities of organic extracts of airborne particles have been studied extensively in the Salmonella/mammalian microsome (Ames) test, but in few other bioassays. In these studies, we tested benzene-acetone extracts of particulate pollutants collected in Lexington, Kentucky, for capacity to induce increases in sister chromatid exchanges (SCE) in human lymphocytes and V79 cells, as well as in the Ames assay. Extracts induced linear dose-related increases in SCE in human lymphocytes and in bacterial revertants. However, variable responses were observed in SCE assays in V79 cells with and without activation by rat liver S9 or feeder layers of irradiated Syrian hamster fetal cells. We conclude that the SCE assay in human lymphocytes may be a useful indicator of the potential risks to humans of airborne particulate pollutants, as it utilizes human cells recently taken from the host, is rapid and economical, and requires small quantities of test materials. However, thorough studies of the quantitative relationships between SCE induction and mutagenicity in human cells are needed.
    Environmental Mutagenesis 07/2006; 3(6):671 - 681.
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    ABSTRACT: While 2-nitronaphthalene was a weak direct-acting base-substitution mutagen (1.4 revertants/nanomole) for Salmonella typhimurium, the analogous nitronaphthalic acid anhydride and imides were moderate frameshift mutagens (∼20 rev/nanomole in strain TA98). Although imide derivatives are efficient DNA intercalators, mutagenicity data indicate that the bulk of the frameshift activity is derived from adduct formation between hydroxylamine intermediates and DNA. The low level of frameshift activity (∼8% of total) resulting from simple intercalation (measured in strain TA1537) is not dependent upon reduction of the nitro function.Evidence is presented that suggests that the reduction of the nitro function to the corresponding hydroylamine might not involve a free nitroso intermediate.The introduction of a second nitrofunction into nitronaphthalenes results in great positional effects of the various isomers on mutagenic activity and specificity.
    Environmental Mutagenesis 07/2006; 3(5):499 - 511.
  • Environmental Mutagenesis 07/2006; 6(2):119 - 119.
  • Environmental Mutagenesis 07/2006; 1(3):287 - 290.
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    ABSTRACT: The mutagenicities of 61 flavonoids (naturally occurring flavonoid aglycones and flavonal glycosides and synthetic flavonoids) and those of 11 compounds structurally related to flavonoids were tested with Salmonella typhimurium strains TA100 and TA98. Among the 22 flavone derivatives tested, only wogonin was strongly mutagenic, while five derivatives, apigenin triacetate, acacetin, chrysoeriol, pedalitin, and pedalitin tetraacetate, were only weakly mutagenic. Two bisflavonyl derivatives, neither of which has a 3-hydroxyl group, were not mutagenic. Of the 16 flavonol derivatives tested, all except 3-hydroxyflavone and the tetra- and penta-methyl ethers of quercetin were mutagenic. Of the five flavanone derivatives tested, only 7,4-dihydroxyflavanone was mutagenic, showing weak activity. Of the four flavanonol derivatives tested, hydrorobinetin and taxifolin were weakly mutagenic. Of the six isoflavone derivatives tested, tectorigenin was weakly mutagenic. Of the 11 compounds in the miscellaneous group structurally related to flavonoids, only iso-liquiritigenin was mutagenic, showing weak activity. For the emergence of strong mutagenicity, the double bond between positions 2 and 3 and the hydroxyl group at position 3 are required, except in wogonin, which does not have a hydroxyl group at position 3 but is strongly mutagenic to TA100. The 3-O-acetyl ester of flavonol, quercetin, was mutagenic with S9 mix, but 3-O-methyl ethers were not. Six flavonol glycosides, three quercetin glycosides and three kaempferol glycosides were mutagenic after preincubation with “hesperidinase,” a crude extract of Aspergillus niger. Of 66 flavonoid agylcones and compounds structurally related to flavonoids, quercetin was the strongest mutagen. The carcinogenicity of this compound should be clarified because it is ubiquitously found in vegetables.
    Environmental Mutagenesis 07/2006; 3(4):401 - 419.
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    ABSTRACT: The effects of nitrofurantoin and AF-2 in stationary phase cells were compared with the effects in log phase cells. The Saccharomyces cerevisiae diploid strain D7 was used. This strain can be used to monitor lethality, gene conversion, mitotic gene recombination, and reversion. Stationary phase cells were not sensitive to nitrofurantoin, but treatment of log phase cells did result in the induction of lethality and gene conversion. Log phase cells were approximately 10 times more sensitive to the lethal effects of AF-2 than were stationary phase cells. The AF-2 induced increase in frequencies of gene conversion and mitotic recombination per surviving cell were similar in both log and stationary phase cells. Gene reversion was induced by AF-2 in stationary cells, but no revertants were induced in log cells. Measurement of nitroreductase activity gave values for log phase cells which were five to sixfold greater than for stationary phase cells. The increased sensitivity of log phase cells to nitrofurans could therefore be in part due to an increased activation of these compounds. It is concluded that the use of log phase cells is optimal for the detection of induced gene conversion and recombination by nitro compounds.
    Environmental Mutagenesis 07/2006; 3(6):651 - 658.
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    ABSTRACT: The isomers of various two-, three-, and four-ring amino polycyclic aromatic hydrocarbons were tested for mutagenic activity using a microbial plate incorporation test with four Salmonella typhimurium strains (TA98, TA 100, TA1535, and TA 1537). All compounds were assayed with an S9 metabolic activating enzyme system. The two-ring compounds were tested only with TA98. All were weakly mutagenic (1–10 rev/μg) except 2-aminobiphenyl, which was not mutagenic under these test conditions. All except two of the 13 fused three-ring compounds (aminofluorenes, aminoanthracenes, and aminophenanthrenes) were active frame shift mutagens; only the aminophenanthrenes were active base-pair mutagens. The potency of this group of isomeric compounds ranged from moderately (˜ 20 rev/μg) to strongly (> 5,000 rev/μg) mutagenic. As a group, the pericondensed fourring amino compounds were the most mutagenic of the three groups tested. All of the aminofluoranthene and aminopyrene isomers showed significant mutagenic activity with TA98, TA100, and TA1537. In general, the mutagenic potency of the amino polycyclic aromatic compounds tested was highly dependent on the structural position of the amino group.
    Environmental Mutagenesis 07/2006; 6(4):497 - 515.
  • Environmental Mutagenesis 07/2006; 1(3):295 - 296.
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    ABSTRACT: Chemical and mutagenic characteristics of TRP-P-1, TRP-P-2, GLU-P-1, GLU-P-2, GLOB-P-1, and GLOB-P-2 were evaluated. We synthesized TRP-P-1 and TRP-P-2 and also obtained samples of these compounds from a commercial source. By GC-MS analysis, the samples of TRP-P-2, GLUs, and GLOBs were more than 99% pure; but the samples of TRP-P-1 contained 11–17% of different impurities. These impurities had no effect on the mutagenicity of these chemicals in the Ames test using either strain TA98 or TA100 of Salmonella typhimurium. All six compounds were inactive without metabolic activation and the γ-carbolines (TRPs) were more active in both strains than the α-carbolines (GLOBs). GLU-P-1 was the most active of the promutagens tested in both TA98 (41,000 revertants/μg) and TA100 (6,580 revertants (μg). In TA98 the order of activity was GLU-P-1 > TRP-P-2 > TRP-P-1 > GLU-P-2 ≅ GLOB-P-2 > GLOB-P-1. In TA100 the order of activity was GLU-P-1 ≫ GLU-P-2 > TRP-P-2 ≅ TRP-P-1 ≫ GLOB-P-1 ≅ GLOB-P-2. We determined the UV absorption and fluorescence characteristics of these compounds, and of HM and NHM, and established an HPLC procedure for their resolution. Sensitivities in the picogram range were attainable using fluorescence detection.
    Environmental Mutagenesis 07/2006; 3(6):639 - 649.
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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 07/2006; 9(3):261 - 267.
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    ABSTRACT: The mutagenic activity of ambient air particles from Morgantown, West Virginia, has been monitored for 6 months using the Ames Salmonella assay system. Airborne particles, collected on glass fiber filters using a Hi-Vol sampler, were extracted with dichloromethane (DCM) and/or ethyl acetate plus methanol (E + M) in sequence. A dose-dependent mutagenic response was observed in Salmonella typhimurium TA 98 for DCM extracts from all samples. E + M extracts were mutagenic only when samples were extracted with E + M before DCM extraction. The mutagenic activity of samples collected in June and July was independent of S-9 in vitro activation, whereas the mutagenicity of those collected from October to December increased in the presence of S-9 activation. The class fractionation of extracts showed that only acidic and polynuclear aromatic fractions were mutagenic. The mutagenicity of particles from Morgantown air was also detected with the Salmonella arabinose-resistant assay system.
    Environmental Mutagenesis 07/2006; 3(6):617 - 626.
  • Article: In Memoriam
    Environmental Mutagenesis 07/2006; 9(2):107 - 109.
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    ABSTRACT: Drosophila melanogaster males were treated with different doses of X-rays or ethyl methanesulfonate (EMS) and mated so that mutagenized X chromosomes could be recovered and tested for lethal mutations and for less drastic mutations affecting viability and other aspects of fitness. The lethals were detected in standard X-linked lethal tests. The less drastic mutations were detected in one generation tests for effects on viability and in multigeneration tests for effects on overall fitness. The Poisson-corrected frequencies of the lethal mutations increased linearly with dose for both X-rays and EMS. Based on the data, 1 Krad X-rays given acutely induces the same number of lethals as 0.55 mM EMS administered by feeding. For some of the X-ray and EMS doses, the mutagenized chromosomes that were nonlethal reduced the viability of their carriers by a small amount, but there was no discemable dose-effect relationship. However in every case where a viability effect was seen, the percentage reduction was less than the corresponding frequency of lethals. All the groups of mutagenized nonlethal chromosomes reduced overall fitness by a significant percentage. Wherever a meaningful comparison was possible, this reduction was 2–3 times the reduction in viability, but, as in the viability data, no dose-effect relationship was discernable.
    Environmental Mutagenesis 07/2006; 6(3):261 - 272.
  • Environmental Mutagenesis 07/2006; 4(4):499 - 519.
  • Environmental Mutagenesis 07/2006; 7(6):923 - 932.
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    ABSTRACT: Formaldehyde is a large production volume chemical widely distributed in research laboratories, industrial workplaces, and home and personal environments. Inhalation studies with formaldehyde have documented its ability to produce squamous cell carcinomas in rats. When primary hamster embryo cells were treated by gaseous exposure to formaldehyde or by incorporation into the medium, a dose-related increase in the frequency of SA7 virus transformation was produced. The length of chemical treatment and the time interval before subsequent addition of transforming virus was critical, with two-hr treatment times as the most efficient. Treatment by gaseous exposure permitted utilization of lower treatment concentrations. Determination of formaldehyde concentrations in culture media of bioassay dishes treated by this method documented that 2.2 fig/ml produced significantly enhanced viral transformation. Exposure of hamster embryo cells to formaldehyde by these methods produces reproducible and quantitative genotoxic effects.
    Environmental Mutagenesis 07/2006; 5(1):49 - 57.
  • Environmental Mutagenesis 07/2006; 5(3):255 - 261.