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Molecular analysis of T‐lymphocyte HPRT ‐ mutations in individuals exposed to ionizing radiation in Goiânia, Brazil
Author(s) -
Skandalis Adonis,
Da Cruz Aparecido D.,
Curry John,
Nohturfft Axel,
Curado Maria P.,
Glickman Barry W.
Publication year - 1997
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(1997)29:2<107::aid-em1>3.0.co;2-b
Subject(s) - hypoxanthine guanine phosphoribosyltransferase , mutagen , point mutation , biology , mutation frequency , genetics , mutant , microbiology and biotechnology , ionizing radiation , exon , gene , mutation , mutagenesis , coding region , ethyl methanesulfonate , carcinogen , irradiation , physics , nuclear physics
We have characterized 54 HPRT ‐ point mutations in T‐lymphocytes from 17 individuals exposed to ionizing radiation of 137 Cs in Goiânia, Brazil and compared this spectrum to that of 30 HPRT ‐ mutants from 9 unexposed Brazilian controls. The average internal exposure of the exposed group was 205 mCi, and the average external exposure was 1.7 Gy. The average HPRT ‐ mutant frequency for the exposed group was 13.3 × 10 ‐5 , approximately a 10‐fold increase over the mutant frequency of the unexposed controls, which was 1.56 × 10 ‐5 . The types of point mutations characterized included base substitutions, small deletions, frameshifts, in‐sertions, complex mutations, and losses of exon sequences from the mRNA. The relative frequency of the different mutation types was similar in the two studied groups. However, in our study the distribution of events within the hprt coding sequence seemed to cluster at the same regions of the gene. These observations imply that the hprt gene does not present a homogeneous target to radiation mutagenesis, and perhaps this class of information may be used to detect radiation exposure in human populations. Environ. Mol. Mutagen. 29:107‐116, 1997. © 1997 Wiley‐Liss, Inc.