Update on the genotoxicity and carcinogenicity of cobalt compounds

被引:241
作者
Lison, D
De Boeck, M
Verougstraete, V
Kirsch-Volders, M
机构
[1] Univ Catholique Louvain, Ind Toxicol & Occupat Med Unit, B-1200 Brussels, Belgium
[2] Free Univ Brussels, Lab Cell Genet, Brussels, Belgium
关键词
cobalt; DNA breakage; inhibition of DNA repair;
D O I
10.1136/oem.58.10.619
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Objective-To integrate recent understandings of the mechanisms of genotoxicity and carcinogenicity of the different cobalt compounds. Method-A narrative review of the studies published since the last IARC assessment in 1991 (genotoxicity, experimental carcinogenesis, and epidemiology). Results-Two different mechanisms of genotoxicity, DNA breakage induced by cobalt metal and especially hard metal particles, and inhibition of DNA repair by cobalt (II) ions contribute to the carcinogenic potential of cobalt compounds. There is evidence that soluble cobalt (II) cations exert a genotoxic and carcinogenic activity in vitro and in vivo in experimental systems but evidence in humans is lacking. Experimental data indicate some evidence of a genotoxic potential for cobalt metal in vitro in human lymphocytes but there is no evidence available of a carcinogenic potential. There is evidence that hard metal particles exert a genotoxic and carcinogenic activity in vitro and in human studies, respectively. There is insufficient information for cobalt oxides and other compounds. Conclusion-Although many areas of uncertainty remain, an assessment of the carcinogenicity of cobalt and its compounds requires a clear distinction between the different compounds of the element and needs to take into account the different mechanisms involved.
引用
收藏
页码:619 / 625
页数:7
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