In vitro DNA damage by arsenic compounds in a human lymphoblastoid cell line (TK6) assessed by the alkaline Comet assay

被引:46
作者
Guillamet, E
Creus, A
Ponti, J
Sabbioni, E
Fortaner, S
Marcos, R [1 ]
机构
[1] Univ Autonoma Barcelona, Fac Ciencies, Dept Genet & Microbiol, Grp Mutagenesi, Bellaterra 08193, Spain
[2] Commiss European Communities, Joint Res Ctr, Inst Hlth & Consumer Protect, ECVAM Unit, I-21020 Ispra, Italy
关键词
D O I
10.1093/mutage/geh005
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Arsenic is classified as a carcinogen for humans, but as a possible genotoxic agent. Thus, taking into account the controversial data about how arsenic compounds are able to induce genetic damage, we investigated the possible genotoxic activity of different arsenic compounds in the TK6 human lymphoblastoid cell line using the alkaline Comet assay. Eight different inorganic and organic arsenical compounds have been selected as follows: three inorganic (sodium arsenite, sodium arsenate and sodium hexafluorarsenate) and five organic (monomethylarsonic and dimethylarsinic acids, arsenobetaine, tetramethylarsonium iodide and tetraphenylarsonium chloride). According to their toxicity and genotoxicity, the highest concentration tested was 10 mM, and the duration of the treatments was 30 min or 3 h. The results indicate that some compounds belonging to both the organic and inorganic species were able to induce significant increases in the tail moment, the parameter used to determine genotoxicity. Thus, the inorganic compounds sodium arsenite and sodium arsenate (but not sodium hexafluoroarsenate) were genotoxic, while among the organoarsenic species tested only tetramethylarsonium iodide and tetraphenylarsonium chloride compounds (but not monomethylarsonic, dimethylarsinic acids and arsenobetaine) induced significant increases in the tail moment. Nevertheless, genotoxic induction was generally only observed at the highest doses tested.
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页码:129 / 135
页数:7
相关论文
共 45 条
[1]   Arsenic: Health effects, mechanisms of actions, and research issues [J].
Abernathy, CO ;
Liu, YP ;
Longfellow, D ;
Aposhian, HV ;
Beck, B ;
Fowler, B ;
Goyer, R ;
Menzer, R ;
Rossman, T ;
Thompson, C ;
Waalkes, M .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1999, 107 (07) :593-597
[2]   Genetic toxicology of a paradoxical human carcinogen, arsenic: a review [J].
Basu, A ;
Mahata, J ;
Gupta, S ;
Giri, AK .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2001, 488 (02) :171-194
[3]   ARSENIC SPECIATION IN THE ENVIRONMENT [J].
CULLEN, WR ;
REIMER, KJ .
CHEMICAL REVIEWS, 1989, 89 (04) :713-764
[4]   THE COMET ASSAY - A COMPREHENSIVE REVIEW [J].
FAIRBAIRN, DW ;
OLIVE, PL ;
ONEILL, KL .
MUTATION RESEARCH-REVIEWS IN GENETIC TOXICOLOGY, 1995, 339 (01) :37-59
[5]  
FARINA M, 2003, THESIS U STUDI PAVIA
[6]  
Gradecka D, 2001, Int J Occup Med Environ Health, V14, P317
[7]  
Hartmann A, 1996, ENVIRON MOL MUTAGEN, V27, P98
[8]   COMPARATIVE INVESTIGATIONS OF THE GENOTOXIC EFFECTS OF METALS IN THE SINGLE-CELL GEL (SCG) ASSAY AND THE SISTER-CHROMATID EXCHANGE (SCE) TEST [J].
HARTMANN, A ;
SPEIT, G .
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1994, 23 (04) :299-305
[9]   Mutagenicity of arsenic in mammalian cells: Role of reactive oxygen species [J].
Hei, TK ;
Liu, SX ;
Waldren, C .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (14) :8103-8107
[10]   The ability of the Comet assay to discriminate between genotoxins and cytotoxins [J].
Henderson, L ;
Wolfreys, A ;
Fedyk, J ;
Bourner, G ;
Windebank, S .
MUTAGENESIS, 1998, 13 (01) :89-94