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1. |
Editorial |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 305-305
Richard J. Albertini,
George R. Hoffmann,
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ISSN:0893-6692
DOI:10.1002/em.2850110302
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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2. |
Importance of animal experiments in carcinogenesis research |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 307-314
William Lijinsky,
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ISSN:0893-6692
DOI:10.1002/em.2850110303
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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3. |
Flavone mutagenicity in salmonella typhimurium: Dependence on the PKM101 plasmid and excision‐repair deficiency |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 315-322
J. T. Macgregor,
R. E. Wilson,
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摘要:
AbstractFlavones mutagenic inSalmonella typhimuriumfall into two distinct classes, characterized by different structural and metabolic activation requirements and by different strain responses. The mutagenic potencies of a prototype agent of each class, quercetin (3,3′,4′,5,7‐hydroxyflavone) and norwogonin (5,7,8‐hydroxyflavone), were determined in tester strains differing in excision‐repair capability and in the presence or absence of plasmid pKM101. Two series of strains were used, one with the hisD3052 frameshift mutation and one with the hisG46 missense mutation. With both agents and for both series of strains, the mutagenic response was markedly dependent on the absence of excision repair and the presence of the pKM10
ISSN:0893-6692
DOI:10.1002/em.2850110304
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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4. |
Effect of treatment medium on induction of aneuploidy by nocodazole insaccharomyces cerevisiae |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 323-331
Rhoda E. Taylor‐Mayer,
Vernon W. Mayer,
Carol J. Goin,
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摘要:
AbstractWhile studying ways to improve responsiveness ofSaccharomyces cerevisiaestrain D61.M to agents that induce aneuploidy, we noted that nocodazole, which strongly induces aneuploidy when yeast cells are treated in yeast extract‐peptone‐dextrose (YEPD) medium, had no effect when a synthetic complete (SC) medium was used. Further study revealed that the presence of peptone was necessary for induction. Other aneuploidy‐inducing agents, including ethyl acetate, acetone, and methyl benzimi‐dazoie‐2‐yl‐carbamate (MBC), were equally active in either medium. Benomyl, which degrades to MBC, was less active in SC than i
ISSN:0893-6692
DOI:10.1002/em.2850110305
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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5. |
Recontacting subjects in mutagen‐exposure‐monitoring studies: II. Results of a questionnaire study of mutagenesis researchers, with review of the pertinent literature |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 333-358
David B. Busch,
Douglas Easterling,
Howard Leventhal,
George T. Bryan,
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摘要:
AbstractA questionnaire on the attitudes of mutagenesis researchers regarding the health significance of and the use of data from tests of human mutagen exposure or genetic damage was completed by 71 of 312 (23%) individuals who had been participants in meetings or organizations concerned with mutagenesis research. On a point scale of 0 to 10, with 0 indicating strong disagreement, 5 indicating uncertainty, and 10 indicating strong agreement, the average respondent felt (8.31 ± 2.27) that data indicating a probable health hazard should be shared automatically with the subjects, but was also moderately concerned about psychological distress of subjects learning of study results indicating abnormally high mutagen exposure (6.14 ± 2.57) or genetic damage (6.94 ± 2.48). The average respondent felt that follow‐up of subjects could improve the quality of mutagen‐exposure‐monitoring studies (8.33 ± 1.49), disagreed that subjects whose laboratory data suggested unusually severe exposure or damage should not be asked about possible sources of exposure (1.15 ± 1.32), and disagreed that it was ethical to follow up but not discuss results with subjects having laboratory evidence of abnormal mutagen exposure (3.78 ± 3.43) or genetic damage (3.06 ± 3.17) to see how many developed cancer relative to a control group.Fifteen specific tests for measuring mutagen exposure or genetic damage were rated on a scale of 0 to 10, with 0 being “totally experimental” and 10 being “absolutely diagnostic of degree of exposure or genetic damage.” Values ranged from 6.13 ± 2.67 for karyotyping leukocytes to 3.43 ± 2.43 for quantifying frequency of rare red cel
ISSN:0893-6692
DOI:10.1002/em.2850110306
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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6. |
Chromosomal aberrations in the cotton rat, sigmodon hispidus, exposed to hazardous waste |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 359-367
Ruth A. Thompson,
Gene D. Schroder,
Thomas H. Connor,
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摘要:
AbstractThe study of chromosome damage in rodents living on hazardous‐waste sites may provide evidence of important biological consequences of chronic exposure to toxic chemical wastes. This study compared bone‐marrow cells of animals (Sigmodon hispidus) taken from two superfund waste‐disposal sites with those from an uncontaminated site and demonstrated that both populations exposed to hazardous wastes had significantly more structural and numerical aberrations than the control popul
ISSN:0893-6692
DOI:10.1002/em.2850110307
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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7. |
Selenium‐mediated reduction in the mutagenicity of cigarette smoke |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 369-378
O. T. Chortyk,
J. L. Baker,
W. J. Chamberlain,
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摘要:
AbstractCigarette smoke contains carcinogens and mutagens and affects the health of smokers. Recently, increased research has proven the potentially protective activity of selenium (Se) against heavy metal toxicity, cancer, and other health disorders. Accordingly, we have proposed the fortification of tobacco with Se to develop safer cigarettes. As a start in evaluating any biological effects of added Se, we have determined the mutagenicity of inhaled, mainstream (MS) cigarette smoke condensate (CSC), with and without Se, in the preincubation assay of the Ames test. Initially, it was shown that Se, as sodium selenite, was not mutagenic at high concentrations (up to 80 μg/plate) with strains TA1538 and TA1978. Subsequently, the effects of different levels of Se, added to MS CSC, were examined with TA98, TA100, and TA1538. On the average, addition of 10 μg Se produced mutagenicity reductions of about 50%. Higher levels of added Se yielded further reductions. Cigarette sidestream (SS) smoke, collected between puffs, was also tested. Again, Se added to SS‐CSC gave similar reductions, confirming its antimutagenic effect for both mainstream and sidestream sm
ISSN:0893-6692
DOI:10.1002/em.2850110308
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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8. |
Detection of carcinogenic glutamic acid pyrolysis products in worcestershire sauce by high‐performance liquid chromatography |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 379-388
Shigeo Manabe,
Yoshikatsu Kanai,
Hiroyuki Yanagisawa,
Kazuhiko Tohyama,
Shinsuke Ishikawa,
Yasuhisa Kitagawa,
Osamu Wada,
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摘要:
AbstractCommercially available Worcestershire sauce was analyzed for mutagenic and carcinogenic glutamic acid pyrolysis products using high‐performance liquid chromatography. These carcinogenic heterocyclic amines were found to be present in all brands of Worcestershire sauce analyzed. The identity of the carcinogens was confirmed by spectrometric analyses and the SOSumu‐test. The concentrations of 2‐amino‐6‐methyldipyrido[l,2‐a:3′,2′‐d]imidazole (Glu‐P‐1) and 2‐amino‐dipyrido‐[1,2‐a:3′,2′‐d]imidazole (Glu‐P‐2) in the Worcestershire sauce were 695 ± 329 pmol/liter (mean ± SD, n = 5) and 1,839
ISSN:0893-6692
DOI:10.1002/em.2850110309
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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9. |
Effects of cigarette smoking and solvent exposure on sister chromatid exchange frequency in painters |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 389-399
Karl T. Kelsey,
John K. Wiencke,
Frederic F. Little,
Edward L. Baker,
John B. Little,
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摘要:
AbstractA cross‐sectional study of sister chromatid exchange frequency (SCE) in peripheral blood lymphocytes from 117 members of the International Brotherhood of Painters and Allied Tradesman was conducted in union locals in two major U.S. cities. Chronic solvent exposure intensity and duration were estimated from interviewer‐administered‐questionnaire data. SCE for all of the workers in the study were scored by one reader. A second reader determined the SCE frequency from a random sample of 30 workers. No significant difference in SCE frequency was associated with reader or time of reading. Age, coffee and alcohol intake and chronic solvent exposure (both intensity and duration, estimated over the working lifetime and over the year prior to study for each worker) did not significantly elevate SCE. The effect of smoking on SCE frequency, assessed by analysis of variance controlling for other possible confounding factors, showed that smoking increased SCE frequency (P<.0001). The SCE frequency in the smoking, solvent‐exposed (estimated as lifetime exposure) painters was 6.75 SCE/cell; in the non‐smoking, solvent‐exposed workers the SCE frequency was 5.73 SCE/cell; the controls had SCE levels of 6.84 SCE/cell (smokers) and 5.90 SCE/cell (non‐smokers), respectively. These observations are consistent with other work suggesting that chronic solvent exposure in the paint trade is not associated with an elevation in SCE in peripheral blood lymphocytes. However, further work is necessary to address adequately the question of the genotoxicity of acute solvent exposure in
ISSN:0893-6692
DOI:10.1002/em.2850110310
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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10. |
Human mutagens: Evidence from paternal exposure? |
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Environmental and Molecular Mutagenesis,
Volume 11,
Issue 3,
1988,
Page 401-415
Steven A. Narod,
George R. Douglas,
Earle R. Nestmann,
David H. Blakey,
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摘要:
AbstractThe importance of inherited mutations as a cause of human disease has been established clearly through examples of well‐defined genetic anomalies, such as Down syndrome and retinoblastoma. Furthermore, it is suspected that environmental contaminants induce mutations resulting in increased risk for such defects in subsequent generations of persons exposed. The present lack of direct evidence for induced inherited genetic disorders in human beings hampers the development of risk estimation techniques for extrapolation from animal models. The most extensive prospective epidemiologic studies of inherited genetic effects have involved survivors of atomic bomb detonations and patients treated with cancer chemotherapy. In neither case has a significant elevation in inherited genetic effects or cancer been detected in the offspring of exposed individuals. Epidemiologic studies of subjects receiving chronic exposure may be confounded by the effect of maternal exposure during pregnancy. Consideration of only paternal exposure can minimize the confounding influence of teratogenicity, enhancing the resolving power of studies for inherited effects. Using this approach, retrospective (case‐control) studies of childhood cancer patients have provided limited but suggestive evidence for inheritance of induced effects. Endpoints, such as congenital malformations and spontaneous abortion following paternal exposure, can also be considered as indicators of heritable mutagenic effects. For example, there is limited evidence suggesting that paternal exposure to anaesthetic gases may cause miscarriage and congenital abnormalities as a result of induced male germ cell mutations. By comparing male‐exposure endpoints for which there are human data, as described above, with parallel or similar animal endpoints, such as dominant lethal, inherited cancer and “male teratogenic” effects, it is possible that suitable models for extrapolating to human risk can be developed. In order to establish a clearer relationship between induced mutation and genetic disease, the current surveillance systems should be expanded to include endpoints relevant to genetic study. The relaxation of regulations regarding access to census data could improve the chances of documenting such an as
ISSN:0893-6692
DOI:10.1002/em.2850110311
出版商:Wiley Subscription Services, Inc., A Wiley Company
年代:1988
数据来源: WILEY
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