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  • 标题:Polyphenols as inhibitors of carcinogenesis.
  • 作者:C S Yang ; M J Lee ; L Chen
  • 期刊名称:Environmental Health Perspectives
  • 印刷版ISSN:0091-6765
  • 电子版ISSN:1552-9924
  • 出版年度:1997
  • 卷号:105
  • 期号:Suppl 4
  • 页码:971-976
  • 语种:English
  • 出版社:OCR Subscription Services Inc
  • 摘要:Many polyphenolic compounds have demonstrated anticarcinogenic activities in animal models. These compounds include flavanone, flavonols, isoflavone, and catechins. In this article, tea catechins will be used as an example to illustrate current research in this area. Many laboratory studies have demonstrated the inhibition of tumorigenesis in animal models by different tea preparations. The animal models include tumorigenesis in the mouse lung, rat and mouse esophagi, mouse forestomach, mouse skin, mouse duodenum, rat small intestine, rat and mouse livers, and rat colon. In most of the studies, the inhibitory activity of tea could be demonstrated when tea preparations were given either during or after the carcinogen treatment period. Black tea was also effective, although the activity was weaker than green tea in some experiments. Decaffeinated tea preparations were also active in many model systems. The molecular mechanisms for these broad inhibitory actions are not fully understood. They are most likely related to the biochemical actions of the tea polyphenols, which include antioxidative activities and inhibition of cell proliferation and of tumor promotion-related activities. The effect of tea consumption on human cancers is not clear in spite of numerous investigations. The bioavailability and pharmacokinetics of tea polyphenols are being studied in animals and humans to provide a basis for more quantitative analyses on the effect of tea on carcinogenesis. More mechanistic and dose-response studies will help us to understand the effects of tea consumption on human carcinogenesis. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.2M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 971 972 973 974 975 976
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