Mutation Research/Reviews in Genetic Toxicology最新文献

{"title":"Dr. Hans F. Stich, Professor Emeritus of the University of British Columbia, 1927–1995","authors":"Helmut Bartsch , Lorenzo Tomatis","doi":"10.1016/S0165-1110(96)00028-0","DOIUrl":"https://doi.org/10.1016/S0165-1110(96)00028-0","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)00028-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72067962","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}

{"title":"Carbon tetrachloride: Genetic effects and other modes of action","authors":"Douglas McGregor, Matti Lang","doi":"10.1016/S0165-1110(96)00027-9","DOIUrl":"https://doi.org/10.1016/S0165-1110(96)00027-9","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)00027-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72067961","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}

{"title":"DNA adducts and chronic degenerative diseases. Pathogenetic relevance and implications in preventive medicine","authors":"Silvio De Flora ,&nbsp;Alberto Izzotti ,&nbsp;Kurt Randerath ,&nbsp;Erika Randerath ,&nbsp;Helmut Bartsch ,&nbsp;Jagadeesan Nair ,&nbsp;Roumen Balansky ,&nbsp;Frederikjan van Schooten ,&nbsp;Paolo Degan ,&nbsp;Gilberto Fronza ,&nbsp;Debra Walsh ,&nbsp;Joellen Lewtas","doi":"10.1016/S0165-1110(96)00043-7","DOIUrl":"https://doi.org/10.1016/S0165-1110(96)00043-7","url":null,"abstract":"<div><p>Chronic degenerative diseases are the leading causes of death in developed countries. Their control is exceedingly difficult due to their multiplicity and diversity, the interconnection with a network of multiple risk factors and protective factors, the long latency and multistep pathogenesis, and the multifocal localization. Adducts to nuclear DNA are biomarkers evaluating the biologically effective dose, reflecting an enhanced risk of developing a mutation-related disease more realistically than the external exposure dose. The localization and accumulation of these promutagenic lesions in different organs are the composite result of several factors, including (a) toxicokinetics (first-pass effect); (b) local and distant metabolism; (c) efficiency and fidelity of DNA repair; and (d) cell proliferation rate. The last factor will affect not only the dilution of DNA adducts but also the possible evolution towards either destructive processes, such as emphysema or cardiomyopathies, or proliferative processes, such as benign or malignant tumors at various sites. They also include heart tumors affecting fetal myocytes after transplacental exposure to DNA-binding agents, blood vessel tumors, and atherosclerotic plaques. In this article, particular emphasis is given to molecular alterations in the heart, which is the preferential target for the formation of DNA adducts in smokers, and in human aorta, where an extensive molecular epidemiology project is documenting the systematic presence of adducts to the nuclear DNA of smooth muscle cells from atherosclerotic lesions, and their significant correlation with known atherogenic risk factors. Exocyclic DNA adducts resulting from lipid peroxidation, and age-related indigenous adducts (I-compounds) may also originate from endogenous sources, chronic infections and infestations, and inflammatory processes. Type II I-compounds are bulky DNA lesions resulting from oxidative stress, whereas type I I-compounds are presumably normal DNA modifications, which display positive correlations with median life span and are decreased in cancer and other pathological conditions. Profiles of type I I-compounds strongly depend on diet and are related to the antidegenerative effects of caloric/dietary restriction. Even broader is the possible meaning of adducts to mitochondrial DNA, which have been detected in rodents exposed to genotoxic agents and complex mixtures, as well as in untreated rodents, in larger amounts when compared to the nuclear DNA of the same cells. Mutations in mitochondrial DNA increase the number of oxidative phosphorylation-defective cells, especially in energy-requiring postmitotic tissues such as brain, heart and skeletal muscle, thereby playing an important role in aging and a variety of chronic degenerative diseases. A decreased formation of DNA adducts is an indicator of reduced risk of developing the associated disease. Therefore, these molecular dosimeters can be used as biomarkers in the ","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)00043-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72067960","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}

{"title":"Product review","authors":"","doi":"10.1016/S0165-1110(96)00040-1","DOIUrl":"https://doi.org/10.1016/S0165-1110(96)00040-1","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)00040-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72067963","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}

{"title":"Nuclear architecture and the induction of chromosomal aberrations","authors":"C. Cremer, ,&nbsp;Ch. Münkel ,&nbsp;M. Granzow ,&nbsp;A. Jauch ,&nbsp;S. Dietzel ,&nbsp;R. Eils ,&nbsp;X.-Y. Guan ,&nbsp;P.S. Meltzer ,&nbsp;J.M. Trent ,&nbsp;J. Langowski ,&nbsp;T. Cremer","doi":"10.1016/S0165-1110(96)90031-7","DOIUrl":"10.1016/S0165-1110(96)90031-7","url":null,"abstract":"<div><p>Progress in fluorescence in situ hybridization, three dimensional microscopy and image analysis has provided the means to study the three-dimensional structure and distribution of chromosome territories within the cell nucleus. In this contribution, we summarize the present state of knowledge of the territorial organization of interphase chromosomes and their topological relationships with other macromolecular domains in the human cell nucleus, and present data from computer simulations of chromosome territory distributions. On this basis, we discuss models of chromosome territory and nuclear architecture and topological consequences for the formation of chromosome exchanges.</p><p>“The idea of the nucleus as a bag of broken chromosome ends flapping around seeking new partners...seems no longer to be tenable from our picture of the interphase nucleus” (J.R.K. Savage, 1990)</p></div>","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90031-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963380","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}

{"title":"Adaptive response to ionizing radiation in human lymphocytes: the problem of scoring aberrations in cells irradiated during asynchronous growth","authors":"A. Wojcik ,&nbsp;S. Aghamohammadi ,&nbsp;M. Aillaud ,&nbsp;A. Bosi ,&nbsp;G. Dai ,&nbsp;G. Olivieri ,&nbsp;B. Salone ,&nbsp;J.R.K. Savage ,&nbsp;J.D. Shadley ,&nbsp;C. Streffer","doi":"10.1016/S0165-1110(96)90034-2","DOIUrl":"10.1016/S0165-1110(96)90034-2","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90034-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963383","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}

{"title":"Nomenclature systems for FISH-painted chromosome aberrations","authors":"John R.K. Savage ,&nbsp;James D. Tucker","doi":"10.1016/S0165-1110(96)90036-6","DOIUrl":"10.1016/S0165-1110(96)90036-6","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90036-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963385","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}

{"title":"Micronuclei: a biological indicator of radiation damage","authors":"Wolfgang-Ulrich Müller ,&nbsp;Michael Nüsse ,&nbsp;Beate M. Miller ,&nbsp;Anne Slavotinek ,&nbsp;Silvia Viaggi ,&nbsp;Christian Streffer","doi":"10.1016/S0165-1110(96)90037-8","DOIUrl":"10.1016/S0165-1110(96)90037-8","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90037-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963386","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}

{"title":"Radiation induced apoptosis","authors":"Mats Harms-Ringdahl ,&nbsp;Pierluigi Nicotera ,&nbsp;Ian R. Radford","doi":"10.1016/S0165-1110(96)90038-X","DOIUrl":"10.1016/S0165-1110(96)90038-X","url":null,"abstract":"","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90038-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963387","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}

{"title":"Insight into sites","authors":"John R.K. Savage","doi":"10.1016/S0165-1110(96)90030-5","DOIUrl":"10.1016/S0165-1110(96)90030-5","url":null,"abstract":"<div><p>Spatial factors conditioning the formation of radiation-induced chromosome exchange aberrations are reviewed, and concepts such as ‘rejoining distance’ and ‘site’ are re-examined in the light of the unexpectedly high frequencies of multi-break (‘Complex’) exchanges being revealed by FISH painting. Given the anticipated densities of dsb within a nucleus, and assuming random 3-D break distribution, nearest-neighbour analysis indicates that the most likely break interaction distance is a well defined shell, several hundred nm from each break. The sharpness with which this shell is defined increases with break density, and therefore with dose. It is argued that random movement and chance meeting over such distances will not account for the Complex frequencies observed, and that other factors, or modes of formation, must be invoked.</p></div>","PeriodicalId":100940,"journal":{"name":"Mutation Research/Reviews in Genetic Toxicology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1996-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0165-1110(96)90030-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19963379","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}