ISSN:0192-2521    

DOI:10.1002/em.2860070402

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

ISSN:0192-2521    

DOI:10.1002/em.2860070403

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractNiridazole, a widely used antiprotozoan agent, is mutagenic forSalmonella typhimuriumstrains that contain guanine‐cytosine as well as adenine‐thymine base pairs at their mutational sites. The mutagenic activity for both types of targets depends upon nitroreduct

ISSN:0192-2521    

DOI:10.1002/em.2860070404

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractA selective system is described that provides a simple and sensitive assay for the detection and analysis of induced mobile element transpositions inDrosophila melanogaster. The system will detect a single event in samples greater than 106and thus provides a eucaryotic assay system for monitoring the induction of transposition by a variety of agents including, but not limited to, chemical carcinogens and toxins, ionizing radiation, and various environmental pollutants. The experimental system focuses on an X‐linked rosy+transposon and a conditional lethal system that permits the detection of a single transposition event in very large samples. The results of a pilot experiment utilizing this system are presente

ISSN:0192-2521    

DOI:10.1002/em.2860070405

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractLitter‐size reduction (LSR) is a useful measure of part of the overall F1radiation‐induced damage. Extensive LSR data were obtained as a by‐product of specific‐locus experiments. Fourteen such experiments involving 158,490 F1litters have been analyzed for the extent of LSR induced by x‐ or gamma‐irradiation of spermatogonia. Litter sizes were compared between experimental and control groups at about 3 weeks after birth. In order to reduce variability, comparisons were made only with concurrent controls and between groups of litters having mothers of approximately the same age. At the high dose rate of 90 R/min, the LSRs showed a humped dose‐response curve. There was a pronounced dose‐rate effect, the mutational responses being much less at dose rates of 0.009 R/min and 0.001 R/min. It is estimated that if men were exposed to 1 R of radiation delivered at low linear energy transfer (low LET) and low dose rate, the number of deaths caused by induced dominant mutations among their children before late childhood would be about 19 per million live‐born. This can be added to the earlier estimate of an approximately equal number of viable disorders in all body systems as based on dominant skeletal mutations. This gives a total estimate of induced dominant damage, but much of this addition represents death in very early embryonic life that would not be recognized in humans. The LSR data also permit the conclusion that only an extremely small proportion of serious radiation‐induced genetic disorders among live‐born humans would be expected to result from

ISSN:0192-2521    

DOI:10.1002/em.2860070406

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractMobile and stationary combustion sources emit particle‐bound organics that, after extraction, are mutagenic toSalmonella typhimurium. In this study, the organic emissions from diesel, cigarette smoke condensate (CSC), coke oven, and roofing tar were fractionated and compared for mutagenicity in the Ames assay. This study demonstrated major differences in the distribution of mutagenicity among the four emission sources. Within each source, the relative mutagenicity of each fraction was significantly different in the presence and absence of an exogenous metabolic activation. In the diesel sample, over 90% of the mutagenic activity is located in the aromatic and polar neutral (PN) fractions; nitrated polynuclear aromatic hydrocarbons (NO2‐PNAs) can account for a significant portion of this activity. Most of the mutagenicity of the coke oven main sample was found in the organic base (BASE) and PN fractions, which contained aromatic amines and nitrogen heterocycles. The CSC sample also had a high percentage of the mutagenic activity in the BASE fraction. Chemical analysis, however, indicates that the components in the CSC differed from those of the coke oven main sample. The roofing tar sample, which was not mutagenic in the absence of metabolic activation, contained several components that were very mutagenic after fractionation. This may be due to the separation of toxic components from the mutagenic components. The roofing tar emissions contained aromatic and polar mutagenic constituents. Although the specific mutagens in these different sources are not identical, they all cause frameshift mutations and appear to be compounds that could be classified as polycyclic organic mat

ISSN:0192-2521    

DOI:10.1002/em.2860070407

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractFour environmental emissions samples were ranked by their genotoxic potency in several bioassays. Although the relative potency of a series of automotive emissions (diesel and gasoline) in the Ames assay correlated well with the relative potency in mammalian cell and mouse skin, this was not the case for the coke oven, roofing tar, and cigarette smoke condensate (CSC) emissions. This study examines the role of metabolic activation in determining the difference between a microbial and a mammalian bioassay in ranking the genotoxic potency of these environmental emissions. Uninduced and Aroclor 1254‐induced S9 from both rat and hamster liver were compared as the metabolic activator in the Ames assay withSalmonella typhimuriumTA98. The diesel emissions sample was directacting while the other samples required activation. The standard S9 concentration (only Aroclor‐induced rat, approximately 1.25 mg protein/plate) also produced the maximum mutagenic activity. Induced S9s produced higher mutagenic activity than uninduced. The hamster S9 gave significantly higher mutagenic activities than rat S9 for the coke oven and CSC. The relative potency of these four samples was not significantly different between the microbial (Ames), mammalian cell (mouse lymphoma), and tumor initiation (mouse skin) assays. These results suggest that the differences observed between the relative mutagenic activity of these emissions in the mammalian cell and microbial assays was not due to a lack of optimization of the S9 system but may be inherent in the different response of the indicator cells to different chemical clas

ISSN:0192-2521    

DOI:10.1002/em.2860070408

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

Abstract4,4′‐Methylene‐bis‐(2‐chlorobenzeneamine) (MbOCA) is a commercially important industrial chemical that is carcinogenic in three animal species and mutagenic in the Ames test. The ability of hepatic postmitochondrial supernatant from humans, dogs, mice, and rats to activate MbOCA to a bacterial mutagen has been investigated using the Ames plate incorporation test and a bacterial fluctuation test. In the Ames plate test, hepatic S9 preparations from mice and Aroclor 1254‐induced rats only were sufficiently active to produce a significant mutagenic response. Preincubation of MbOCA with S9 from human liver produced a slight increase in the number of revertants but not a doubling as compared to controls. However, using the more sensitive bacterial fluctuation test, liver S9 from all species activated MbOCA to a bacterial mutagen. The responses produced were dose‐related and, for at least part of the dose range, were double the background levels observed in controls. The increases in the mutagenicity of MbOCA produced by liver S9 from humans, dogs, and rats were significant at the 0.1% level of probability. Liver S9 preparations from all species in which MbOCA is carcinogenic have now been demonstrated to be capable of activating this compound to a bacterial mutagen. The finding that S9 from human liver can also activate MbOCA to a mutagen increases the concern that it may be a hum

ISSN:0192-2521    

DOI:10.1002/em.2860070409

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractTwenty‐five laser dyes and four analogs were tested for mutagenicity in the Ames/Salmonellatest. Seven dyes and two analogs gave positive mutagenic responses with bacterial strains TA1538 and TA98. Of two widely used families of laser dyes (coumarins and rhodamines), four coumarin samples, but none of the rhodamine samples, were mutagenic. All mutagenic compounds require enzyme activation for positive response except two terphenyl analogs, which are mutagenic with or without activation. Using high‐performance liquid chromatography (HPLC), it was determined that five mutagenic dye samples had multiple components. The dyes themselves may not be the mutagenic agents in all cases (as with Nile Blue) but may contain impurities that are mutagenic. One dye, adicyanome‐thylene (DCM) (≥95% pure), was mutagenic at doses below 0.5 μg/plate on strains TA1538 and TA98. DCM also induced reversions in strains TA96, TA97, TA100, TA102, and TA104, although less efficiently. This study indicates the need for further toxicological testing of these types of compounds. The mutagenic components of these dye mixtures, whether it is the dye or a contaminant, presents a possible hazard to those handling them. Therefore, practices and procedures for the safe handling of specific dyes should be reviewed in light of these

ISSN:0192-2521    

DOI:10.1002/em.2860070410

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY

摘要:

AbstractChemical mutagens including methyl methanesulfonate, N‐methyl‐N'‐nitro‐N‐nitrosoguanidine, iodomethane, and epichlorohydrin have been classified as “chromosomal mutagens” in the L5178Y/thymidine kinase (TK) gene mutation assay by Clive and coworkers [Mutat Res 59:61–108, 1979; and “The Predictive Value of Short‐Term Screening Tests in Carcinogenicity Evaluation.” Amsterdam: Elsevier/North Holland, pp 103–123, 1980] who observed mutagen‐dependent increases in small TK‐deficient mutant colonies with detectable damage to the chromosome (11) that carries the TK locus. In this study, we tested these four chemicals for the induction of gene mutations at the ouabain‐resistance (ouares) locus of 3.7.2C L5178Y cells to determine if presumptive chromosomal mutagens would go undetected at a gene locus that is unresponsive to chromosomal damage. A final concentration of 375 μg/ml ouabain in soft‐agar medium selected against the ouabain‐sensitive phenotype without loss of the mutagen‐induced ouabain‐resistant phenotype. Verification of the mutant phenotype was completed for six individual soft‐agar ouarescolonies derived from mutagen‐treated cultures via growth for 10–11 days in nonselective medium followed by retesting for colony formation in selective soft‐agar medium. Dose‐related reproducible increases in the frequency of ouabain‐resistant mutants were observed for 3.7.2C L5178Y cells that had been exposed for 3 hr to 24–46 μg/ml epichlorohydrin, 1.9–3.6 μg/ml iodomethane, 0.006–0.011 μg/ml N‐methyl‐N'‐nitro‐N‐nitrosoguanidine and 2.0–5.4 μg/ml methyl methanesulfonate. Also, treatments with EMS, which induced sufficient numbers of ouarescolonies to permit analysis of colony size distribution, showed the existence of a bimodal size distribution similar to those reported for TK‐deficient mutants. This discovery suggests that mutant colony size in this cell line may be independent of specific gene locus effects. We conclude that (1) chemicals that induce a high proportion of chromosomal mutants, as detected at the TK locus in earlier studies, also induce single gene mutations at the ouabain‐resista

ISSN:0192-2521    

DOI:10.1002/em.2860070411

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1985

数据来源: WILEY