BENZENE METABOLITE, 1,2,4-BENZENETRIOL, INDUCES MICRONUCLEI AND OXIDATIVE DNA DAMAGE IN HUMAN-LYMPHOCYTES AND HL-60 CELLS

被引:72
|
作者
ZHANG, LP
ROBERTSON, ML
KOLACHANA, P
DAVISON, AJ
SMITH, MT
机构
[1] UNIV CALIF BERKELEY,SCH PUBL HLTH,DEPT BIOMED & ENVIRONM HLTH SCI,BERKELEY,CA 94720
[2] SIMON FRASER UNIV,FAC APPL SCI,BIOENERGET RES LAB,BURNABY V5A 1S6,BC,CANADA
关键词
1,2,4-BENZENETRIOL; MICRONUCLEI; OXYGEN RADICALS; 8-HYDROXY-2'-DEOXYGUANOSINE; HUMAN LEUKEMIA;
D O I
10.1002/em.2850210405
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The triphenolic metabolite of benzene, 1,2,4-benzenetriol (BT), is readily oxidized to its corresponding quinone via a semiquinone radical. During this process, active oxygen species are formed that may damage DNA and other cellular macromolecules. The ability of BT to induce micronuclei (MN) and oxidative DNA damage has been investigated in both human lymphocytes and HL60 cells. An antikinetochore antibody based micronucleus assay was used to distinguish MN containing kinetochores and potentially entire chromosomes (kinetochore-positive, K+) from those containing acentric chromosome fragments (kinetochore-negative, K-). BT increased the frequency of MN formation twofold in lymphocytes and eightfold in HL60 cells with the MN being 62% and 82% K+, respectively. A linear dose-related increase in total MN, mainly in K+-MN, was observed in both HL60 cells and lymphocytes. Addition of copper ions (Cu2+) potentiated the effect of BT on MN induction threefold in HL60 cells and altered the pattern of MN formation from predominantly K+ to K-. BT also increased the level of 8-hydroxy-2'-deoxyguanosine (8-OH-dG), a marker of active oxygen-induced DNA damage. Cu2+ again enhanced this effect. Thus, BT has the potential to cause both numerical and structural chromosomal changes in human cells. Further, it may cause point mutations indirectly by generating oxygen radicals. BT may therefore play an important role in benzene-induced leukemia.
引用
收藏
页码:339 / 348
页数:10
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