Mutation Research/Reviews in Genetic Toxicology最新文献_第10页

Availability of the GENE-TOX database on the National Library of Medicine TOXNET System 国家医学图书馆TOXNET系统上基因- tox数据库的可用性

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90009-C

Michael C. Cimino, Angela E. Auletta

引用次数: 6

A review of the genotoxicity of 1-ethyl-1-nitrosourea 1-乙基-1-亚硝基脲的遗传毒性研究进展

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90005-8

T. Shibuya , K. Morimoto

{"title":"A review of the genotoxicity of 1-ethyl-1-nitrosourea","authors":"T. Shibuya , K. Morimoto","doi":"10.1016/0165-1110(93)90005-8","DOIUrl":"10.1016/0165-1110(93)90005-8","url":null,"abstract":"<div><p>1-Ethyl-1-nitrosourea (ENU) is a potent monofunctional ethylating agent that has been found to be mutagenic in a wide variety of mutagenicity test systems from viruses to mammalian germ cells. It also has been shown to induce tumors in various organs of mammals.</p><p>ENU has been used only for research purposes. ENU possesses the dual action of ethylation and carbamoylation. The ethyl group can be transferred to nucleophilic sites of cellular constituents, and the carbonyl group can be transferred to an amino group of a protein. ENU is able to produce significant levels of alkylation at oxygens, such as the O<sup>6</sup> position of guanine and the O<sup>4</sup> position of thymine of DNA. The molecular genetic data obtained from ENU-induced mutants on various species suggest that ENU produces mainly GC-AT transitions and, to a small extent, AT-GC, AT-CG, AT-TA, GC-CG and GC-TA base substitutions. This mutation spectrum of ENU is different from that of 1-methyl-1-nitrosourea, which mainly induces GC-AT transitions.</p><p>ENU is a most potent mutagen in mouse germ cells, especially in stem-cell spermatogonia. It induces intragenic mutations with high frequency in male mouse germ cells. ENU has been established as a model compound for exploring the effects of chemical mutagenesis on mouse germ cells.</p></div>","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":"297 1","pages":"Pages 3-38"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0165-1110(93)90005-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18688766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 156

A critical review of the genotoxic potential of electric and magnetic fields 对电场和磁场的基因毒性潜能的评述

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90008-B

Joyce McCann , Fred Dietrich , Charles Rafferty , Alice O. Martin

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引用次数: 196

Interaction of pine cone extract fraction VI with mutagens 松果提取物ⅵ与诱变剂的相互作用

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90007-A

Heysuk Lee , Kimiko Aoki , Hiroshi Sakagami , Takemi Yoshida , Yukio Kuroiwa

{"title":"Interaction of pine cone extract fraction VI with mutagens","authors":"Heysuk Lee , Kimiko Aoki , Hiroshi Sakagami , Takemi Yoshida , Yukio Kuroiwa","doi":"10.1016/0165-1110(93)90007-A","DOIUrl":"10.1016/0165-1110(93)90007-A","url":null,"abstract":"<div><p>Pine cone extract fraction VI (PC-VI) inhibited the mutagenicity of the promutagens tested: the polycyclic aromatic hydrocarbon benzo[<em>a</em>]pyrene (B[a]P) dose-dependently, and the aromatic amines 2-aminoanthracene (AA) and 2-acetylaminofluorene (AAF) at high concentrations. PC-VI had no effect on the mutagenicity of the direct-acting mutagens 2-(2-furyl)-3-(5-nitrofuryl)acrylamide (AF-2) and <em>N</em>-methyl-<em>N</em>′-nitro-<em>N</em>-nitrosoguanidine (MNNG), but inhibited the mutagenicity of the direct-acting mutagen <em>N</em>-hydroxy 2-acetylaminofluorene (N-OH AAF, proximate mutagen of AAF). The addition of PC-VI to rat hepatic microsomes resulted in a decrease of their enzyme activities, especially NADPH-cytochrome <em>c</em> reductase. By gas-chromatographic analysis of B[a]P or AA contents after incubation of B[a]P or AA and PC-VI and S9 mix, the inhibition of hepatic metabolizing enzymes and the interaction between AA and PC-VI were confirmed. On the other hand, PC-VI had no effect on the DNA repair systems for B[a]P- or AA-induced mutagenesis.</p><p>We conclude that PC-VI shows indirect antimutagenicity by interfering with cytochrome P-450-dependent bioactivation and by direct interaction with AA and the proximate mutagenic product of AAF.</p></div>","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":"297 1","pages":"Pages 53-60"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0165-1110(93)90007-A","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18688768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

The genetic toxicology of 5-fluoropyrimidines and 5-chlorouracil 5-氟嘧啶和5-氯尿嘧啶的遗传毒理学研究

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90006-9

Suzanne M. Morris

{"title":"The genetic toxicology of 5-fluoropyrimidines and 5-chlorouracil","authors":"Suzanne M. Morris","doi":"10.1016/0165-1110(93)90006-9","DOIUrl":"10.1016/0165-1110(93)90006-9","url":null,"abstract":"<div><p>The halogenated pyrimidines were synthesized in the 1950s as potential anti-tumor agents after the discovery that certain tumors preferentially incorporated uracil rather than thymine into the DNA. The fluorinated derivatives are widely recognized today as effective treatment modalities, especially with tumors of the head, neck and breast. Mechanistically, efficacy of the fluorinated pyrimidines results from the ability of these compounds to incoporporate into RNA and inhibit its maturation to those forms necessary for cellular metabolism and from the inhibition of the enzyme, thymidylate synthetase, which controls the biosynthesis of thymine and DNA synthesis. The 5-fluoropyrimidines can incorporate into DNA, but the contribution of this phenomenon to the overall efficacy of this class of chemotherapeutic agents is not totally resolved. Evidence exists that this class of compounds possesses the properties to induce genotoxic effects, both in bacterial and eukaryotic cells. Most notably, these effects include the induction of cellular toxicity and the induction of chromosome aberrations. The biology and chemistry of the chlorinated pyrimidines were first explored as a possible means of sensitizing the DNA to ionizing radiation in a manner similar to the sensitization observed when DNA incorporates bromodeoxyuridine. This approach was not utilized clinically. The genetic toxicology of this compound became important with the discovery of the ribonucleoside in the effluents of sewage treatment plants. Evidence is now available that the chlorinated pyrimidines, upon conversion to deoxyribonucleosides, are effective mutagens, clastogens and toxicants, as well as extremely effective inducers of sister-chromatid exchanges.</p></div>","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":"297 1","pages":"Pages 39-51"},"PeriodicalIF":0.0,"publicationDate":"1993-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0165-1110(93)90006-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18688767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 67

Publisher's notice 出版商通知

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-07-01 DOI: 10.1016/0165-1110(93)90004-7

The Publisher

引用次数: 0

Contents volume 296 (1993) 目录第296卷（1993年）

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-03-01 DOI: 10.1016/0165-1110(93)90016-G

引用次数: 0

Intrauterine growth retardation as a potential endpoint in mutation epidemiology 宫内生长迟缓作为突变流行病学的潜在终点

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-03-01 DOI: 10.1016/0165-1110(93)90012-C

Andrew E. Czeizel

引用次数: 0

The genetic toxicology of 6-mercaptopurine 6-巯基嘌呤的遗传毒理学

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-03-01 DOI: 10.1016/0165-1110(93)90015-F

Pasquale Mosesso , Fabrizio Palitti

引用次数: 35

Power frequency electric and magnetic fields: A review of genetic toxicology 工频电场和磁场：遗传毒理学综述

Mutation Research/Reviews in Genetic Toxicology Pub Date : 1993-03-01 DOI: 10.1016/0165-1110(93)90013-D

J.C. Murphy , D.A. Kaden , J. Warren , A. Sivak

引用次数: 0