Heterocyclic aromatic amine metabolism, DNA adduct formation, mutagenesis, and carcinogenesis

被引:106
作者
Turesky, RJ [1 ]
机构
[1] Natl Ctr Toxicol Res, Div Chem, Jefferson, AR 72079 USA
关键词
D O I
10.1081/DMR-120005665
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Heterocyclic aromatic amines (HAAs) are carcinogenic compounds formed in meats, fish, and poultry prepared under common household cooking practices. Some HAAs are also formed in tobacco smoke condensate. Because of the widespread occurrence of HAAs in these daily staples, health concerns have been raised regarding the potential role of HAAs in the etiology of some human cancers associated with frequent consumption of these products. In this review, the metabolism of HAAs to biologically active metabolites that bind to DNA and provoke mutations and cancer in various biological systems is discussed. Some of the current analytical and molecular methods that are used to measure biomarkers of HAA exposure and genetic damage in experimental animal models and humans are also presented. These biochemical data combined may help to better assess the role that HAAs may have in the development of some common forms of human cancers.
引用
收藏
页码:625 / 650
页数:26
相关论文
共 126 条
[1]  
Adamson R.H., 2000, FOOD BORNE CARCINOGE, P229
[2]   MAMMALIAN-CELL MUTAGENICITY AND METABOLISM OF HETEROCYCLIC AROMATIC-AMINES [J].
AESCHBACHER, HU ;
TURESKY, RJ .
MUTATION RESEARCH, 1991, 259 (3-4) :235-250
[3]   EFFECT OF HETEROCYCLIC AMINES AND BEEF EXTRACT ON CHROMOSOME-ABERRATIONS AND SISTER CHROMATID EXCHANGES IN CULTURED HUMAN-LYMPHOCYTES [J].
AESCHBACHER, HU ;
RUCH, E .
CARCINOGENESIS, 1989, 10 (03) :429-433
[4]  
AESCHBACHER HU, 1999, 7 INT C CARC MUT N S
[5]  
AESCHBACHER HU, 1997, MUTAGENIC CARCINOGEN
[6]  
AESCHBACHER HU, 1991, POTENTIAL CARCINOGEN
[7]  
AESCHBACHER HU, 1995, HETEROCYCLIC AMINES
[8]  
AESCHBACHER HU, 2000, FOOD BORNE CARCINOGE
[9]   Intestinal tumours induced by the food carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in multiple intestinal neoplasia mice have truncation mutations as well as loss of the wild-type Apc+ allele [J].
Andreassen, Å ;
Vikse, R ;
Steffensen, IL ;
Paulsen, JE ;
Alexander, J .
MUTAGENESIS, 2001, 16 (04) :309-315
[10]   HUMAN BIOMONITORING AND THE P-32 POSTLABELING ASSAY [J].
BEACH, AC ;
GUPTA, RC .
CARCINOGENESIS, 1992, 13 (07) :1053-1074