Polyphenols As Inhibitors of Carcinogenesis
Chung S. Yang, Mao-Jung Lee, Laishun Chen, and Guang-yu Yang
Laboratory for Cancer Research, Rutgers University,
Piscataway, New Jersey
Abstract
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. -- Environ Health Perspect 105(Suppl 4):971-976 (1997)
Key words: tea, polyphenols, carcinogenesis inhibition, lung, esophageal cancer, stomach cancer
This paper is based on a presentation at the symposium on Mechanisms and Prevention of Environmentally Caused Cancers held 21-25 October 1995 in Santa Fe, New Mexico. Manuscript received at EHP 16 April 1996; accepted 20 November 1996.
The work was supported by NIH grant CA56673 and Center Grant ES05022. The authors thank D. Wong for excellent secretarial service and J.M. Landau for helpful suggestions.
Address correspondence to Dr. C.S. Yang, Laboratory for Cancer Research, College of Pharmacy, Rutgers University, Frelinghuysen Road, Piscataway, NJ 08855-0789. Telephone: (908) 445-5361. Fax: (908) 445-0687. E-mail: csyang@rci.rutgers.edu
Abbreviations used: B[a]P, benzo[a]pyrene; DBT, decaffeinated black tea; DGT, decaffeinated green tea; EC, (-)-epicatechin; ECG, (-)-epicatechin-3-gallate; EGC, (-)-epigallocatechin; EGCG, (-)-epigallocatechin gallate; NDEA, N-nitrosodiethylamine; NMBzA, N-nitrosomethylbenzylamine; NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone.
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Last Update: June 30, 1997