High susceptibility of chromosome 16 to radiation-induced chromosome rearrangements in human lymphocytes under in vivo and in vitro exposure

被引:8
|
作者
Camparoto, ML
Takahashi-Hyodo, SA
Dauwerse, JG
Natarajan, AT
Sakamoto-Hojo, ET
机构
[1] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Pret, Dept Biol, BR-14040901 Ribeirao Preto, SP, Brazil
[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Genet, BR-14040901 Ribeirao Preto, SP, Brazil
[3] Leiden Univ, Med Ctr, Dept Human & Clin Genet, Leiden, Netherlands
[4] Leiden Univ, Med Ctr, Dept Toxicogenet, Leiden, Netherlands
关键词
D O I
10.1159/000081522
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim of the present study was to investigate whether chromosome 16p presents breakpoint regions susceptible to radiation-induced rearrangements. The frequencies of translocations were determined by fluorescence in situ hybridization (FISH) using cosmid probes C40 and C55 mapping on chromosome 16p, and a chromosome 16 centromere-specific probe (pHUR195). Peripheral lymphocytes were collected from normal individuals and from seven victims of Cs-137 in the Goiania (Brasil) accident (absorbed doses: 0.8-4.6 Gy) 10 years after exposure. In vitro irradiated lymphocytes (3 Gy) were also analyzed. The mean translocation frequency/cell obtained for the 137Cs exposed individuals was 2.4-fold higher than the control value (3.6 x 10(-3) +/- 0.001), and the in vitro irradiated lymphocytes showed a seven-fold increase. The genomic translocation frequencies (FGs) were calculated by the formula Fp = 2.05 fp(1 - fp)FG (Lucas et al., 1992). For the irradiated lymphocytes and victims of 137Cs, the FGs calculated on the basis of chromosome 16 were 2- to 8-fold higher than those for chromosomes 1, 4 and 12. Our results indicate that chromosome 16 is more prone to radiation-induced chromosome breaks, and demonstrate a non-random distribution of induced aberrations. This information is valuable for retrospective biological dosimetry in case of human exposure to radiation, since the estimates of absorbed doses are calculated by determining the translocation frequency for a sub-set of chromosomes, and the results are extrapolated to the whole genome, assuming a random distribution of induced aberrations. Furthermore, the demonstration of breakpoints on 16p is compatible with the reports about their involvement in neoplasias. Copyright (C) 2005 S. Karger AG, Basel.
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页码:287 / 292
页数:6
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