{"title":"Defective DNA excision repair in cells of patients with homocystinuria","authors":"T.A. Sinelshchikova, G.N. Lvova, N.N. Shoniya, G.D. Zasukhina","doi":"10.1016/0167-8817(87)90025-3","DOIUrl":null,"url":null,"abstract":"<div><p>Fibroblasts obtained from biopsied material and lymphocytes from patients wwith homocystinuria were studied for repair activity using the criterion of repair of DNA breaks induced by 4-nitroquinoline 1-oxide and γ-irradiation and criteria of reactivation and induced mutagenesis of vaccinia virus. Lymphocytes showed defective DNA repair for all these criteria. In fibroblast cultures, the inhibition of cell-repair activity for the γ-type was retained. The number of spontaneous and γ-induced virus mutations increased as passaging of fibroblasts proceeded.</p></div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1987-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(87)90025-3","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research/DNA Repair Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0167881787900253","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Fibroblasts obtained from biopsied material and lymphocytes from patients wwith homocystinuria were studied for repair activity using the criterion of repair of DNA breaks induced by 4-nitroquinoline 1-oxide and γ-irradiation and criteria of reactivation and induced mutagenesis of vaccinia virus. Lymphocytes showed defective DNA repair for all these criteria. In fibroblast cultures, the inhibition of cell-repair activity for the γ-type was retained. The number of spontaneous and γ-induced virus mutations increased as passaging of fibroblasts proceeded.