Antimutagenic activity of tea: role of polyphenols

被引:30
作者
Ioannides, C [1 ]
Yoxall, V [1 ]
机构
[1] Univ Surrey, Mol Toxicol Grp, Sch Biomed & Mol Sci, Guildford GU2 7XH, Surrey, England
关键词
tea; catechins; flavanols; tea polyphenols; antimutagenicity; camellia sinensis;
D O I
10.1097/00075197-200311000-00008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Tea is considered to be one of the most promising dietary chemopreventive agents and, consequently, it is being studied extensively worldwide. Despite the fact that tea has proved very efficient in affording protection against chemical-induced cancer in animal models of the disease, epidemiological studies do not always support the laboratory findings, so that the value of tea as a human anticarcinogen may be considered as 'not proven'. A major mechanism of the anticarcinogenic activity of tea in animals is impairment of the interaction of carcinogens with DNA leading to mutations. The antimutagenic activity of tea as well as the underlying mechanisms will be reviewed, and the role of polyphenols, the postulated bioactive components, and caffeine will be critically evaluated. Recent findings In rats, exposure to tea modulated the disposition of heterocyclic amines, a major group of food-borne carcinogens, stimulating the pathways that lead to deactivation, and this is concordant with the established ability of tea to modulate the carcinogen-metabolizing enzyme systems. These observations provide a rational mechanism for the anticarcinogenic activity of tea in animals. Summary The beneficial activities of tea have always been attributed to the polyphenols, as these are present in tea at substantial concentrations and are endowed with antioxidant activity. It is becoming increasingly evident, however, that the bioavailability of these compounds is poor as a result of limited absorption and presystemic metabolism by mammalian and microbial enzymes. We propose that the biological activity of tea may be mediated by caffeine and microbial metabolites of polyphenols.
引用
收藏
页码:649 / 656
页数:8
相关论文
共 65 条
[1]   CAFFEINE INHIBITS HEPATIC-MICROSOMAL ACTIVATION OF SOME DIETARY GENOTOXINS [J].
ALLDRICK, AJ ;
ROWLAND, IR .
MUTAGENESIS, 1988, 3 (05) :423-427
[2]   Antimutagenic activity of selenium-enriched green tea toward the heterocyclic amine 2-amino-3-methylimidazo[4,5-f]quinoline [J].
Amantana A. ;
Santana-Rios G. ;
Butler J.A. ;
Xu M. ;
Whanger P.D. ;
Dashwood R.H. .
Biological Trace Element Research, 2002, 86 (2) :177-191
[3]   Inhibition of PhIP mutagenicity by catechins, and by theaflavins and gallate esters [J].
Apostolides, Z ;
Balentine, DA ;
Harbowy, ME ;
Hara, Y ;
Weisburger, JH .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 1997, 389 (2-3) :167-172
[4]   Modulation of hepatic cytochrome P450 activity and carcinogen bioactivation by black and decaffeinated black tea [J].
Bu-Abbas, A ;
Clifford, MN ;
Walker, R ;
Ioannides, C .
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, 1999, 7 (01) :41-47
[5]   Proliferation of hepatic peroxisomes in rats following the intake of green or black tea [J].
Bu-Abbas, A ;
Dobrota, M ;
Copeland, E ;
Clifford, MN ;
Walker, R ;
Ioannides, C .
TOXICOLOGY LETTERS, 1999, 109 (1-2) :69-76
[6]   Contribution of caffeine and flavanols in the induction of hepatic phase II activities by green tea [J].
Bu-Abbas, A ;
Clifford, MN ;
Walker, R ;
Ioannides, C .
FOOD AND CHEMICAL TOXICOLOGY, 1998, 36 (08) :617-621
[7]   MARKED ANTIMUTAGENIC POTENTIAL OF AQUEOUS GREEN TEA EXTRACTS - MECHANISM OF ACTION [J].
BUABBAS, A ;
CLIFFORD, MN ;
WALKER, R ;
IOANNIDES, C .
MUTAGENESIS, 1994, 9 (04) :325-331
[8]   Subchronic toxicity of 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX) in Wistar rats [J].
Vaittinen, SL ;
Komulainen, H ;
Kosma, VM ;
Julkunen, A ;
MakiPaakkanen, J ;
Jansson, K ;
Vartiainen, T ;
Tuomisto, J .
FOOD AND CHEMICAL TOXICOLOGY, 1995, 33 (12) :1027-1037
[9]   SELECTIVE INDUCTION OF RAT HEPATIC CYP1 AND CYP4 PROTEINS AND OF PEROXISOMAL PROLIFERATION BY GREEN TEA [J].
BUABBAS, A ;
CLIFFORD, MN ;
WALKER, R ;
IOANNIDES, C .
CARCINOGENESIS, 1994, 15 (11) :2575-2579
[10]  
BuAbbas A, 1997, J SCI FOOD AGR, V75, P453, DOI 10.1002/(SICI)1097-0010(199712)75:4&lt