Radiation-induced human chromosome aberrations

IF 1.9 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 1971-12-01 DOI:10.1016/0027-5107(71)90050-9

J.G. Brewen , N. Gengozian

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引用次数: 58

Abstract

Whole blood cultures from humans and from the New World primate, Saguinus fuscicollis, were irradiated with various doses of 250 kV X-rays. The resulting centric ring plus dicentric aberration yields were fitted to the three models, Y = a+bD, Y = a+bD+cD², and Y = a+cD², by least squares regression. In both instances the best fit was to the model Y = a+bD+cD², with coefficients of the one- and two-track components for human and marmoset being: b = (0.78 ± 0.09)·10⁻³, c = (5.92 ± 0.31)·10⁻⁶, and b = (1.11 ± 0.36)·⁻³, c = (7.7 ± 1.7)·10⁻⁶, respectively.

Whole-body irradiation of several marmosets was done with ⁶⁰Co γ-rays at a dose rate of 3.7 R/min. Blood samples were drawn immediately and 24 h after the irradiation, and the aberration yields in the circulating leukocytes were measured. The aberration yields at the two sampling times were identical. Concurrent with these studies, freshly drawn whole blood was irradiated in the same manner for the purpose of in vivo to in vitro radiosensitivity comparison. In this instance the in vitro irradiation produced aberration yields identical to those from in vivo irradiation.

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辐射引起的人类染色体畸变

用不同剂量的250千伏x射线照射人类全血培养物和新世界灵长类动物镰刀线虫全血培养物。通过最小二乘回归，拟合Y = a+bD、Y = a+bD+cD2和Y = a+cD2三个模型的中心环和双心像差。在这两种情况下，最适合的模型是Y = a+bD+cD2，人类和狨猴的单轨和双轨分量系数分别为:b =(0.78±0.09)·10−3,c =(5.92±0.31)·10−6,b =(1.11±0.36)·−3,c =(7.7±1.7)·10−6。用60Co γ射线以3.7 R/min的剂量率对若干狨猴进行全身照射。照射后立即和24 h采血，测定循环白细胞畸变率。两次采样时产生的像差相同。在进行这些研究的同时，新鲜抽取的全血以同样的方式照射，以比较体内和体外的放射敏感性。在这种情况下，体外辐照产生的畸变与体内辐照产生的畸变相同。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.