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Supplement: Free Radicals: The Pros and Cons of Antioxidants

Green Tea Polyphenols: Antioxidative and Prooxidative Effects^1,2

Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, State University of New Jersey, Piscataway, NJ 08854-8020

³To whom correspondence should be addressed. E-mail: csyang{at}rci.rutgers.edu.

KEY WORDS: • tea • epigallocatechin-3-gallate

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Tea consumption has been suggested to have many beneficial health effects, including the prevention of cancer and heart diseases (1). The polyphenolic catechins in green tea, such as (–)-epigallocatechin-3-gallate (EGCG), have been shown to be potent antioxidants in many chemical and biochemical studies (2). Some antioxidative effects of catechins have been demonstrated in vivo, for example, the prevention of 8-hydroxydeoxyguanosine formation. The general antioxidative functions of tea catechins in the plasma and other tissues following tea ingestion, however, are not strong and sometimes are not significant (1). One of the reasons for this is the rather low bioavailability of tea catechins in animals and humans. Tea catechins are readily methylated, glucuronidated, sulfated, and effluxed out of the cells (2). Many of the cancer preventive activities of tea and related signal transduction pathways have been attributed to antioxidative mechanisms, but direct evidence of this proposal is sparse. In fact, many of the reported effects of EGCG in cell culture could be the consequences of oxidative or prooxidative reactions involving these polyphenolic compounds (3,4). The stability of EGCG varies with the cell-culture conditions (pH 7.0–7.4). Under many cell-culture conditions, the half-life of EGCG is <2 h in the presence of cells and even shorter in the absence of cells (5). It is oxidized and dimerized; H₂O₂ and other compounds are also formed. Some of the apoptotic effects and gene-expression changes caused by EGCG may be mediated by H₂O₂, because they are prevented by coincubation with catalase. Some of the reported EGCG effects on receptors may not be due to EGCG directly. They may be caused by superoxide radical or oxidized EGCG species, because the effect is abolished in the presence of superoxide dismutase, which stabilizes EGCG. The presence of superoxide dismutase increases the effectiveness of EGCG in inhibiting cell growth, suggesting that the growth inhibition effect is caused by EGCG directly. Depending on the experimental conditions, EGCG and other polyphenolic compounds can function as either antioxidants or prooxidants. The prooxidative effect may be due to the high oxygen tension used in the cell-culture conditions. The autooxidation of polyphenols leads to the formation of radical and quinone species, which may dimerize or form thiol adducts. These types of reactions may not occur in vivo from normal tea consumption. The possible occurrence of these reactions, for example when large amounts of tea are ingested or at certain inflammation sites or organ sites, needs to be investigated. It is a challenge to determine the importance of the antioxidative and prooxidative activities of catechins after tea consumption.

	FOOTNOTES

 
¹ Presented as part of the conference "Free Radicals: The Pros and Cons of Antioxidants," held June 26–27 in Bethesda, MD. This conference was sponsored by the Division of Cancer Prevention (DCP) and the Division of Cancer Treatment and Diagnosis, National Cancer Institute, NIH, Department of Health and Human Services (DHHS); the National Center for Complementary and Alternative Medicine (NCCAM), NIH, DHHS; the Office of Dietary Supplements (ODS), NIH, DHHS; the American Society for Nutritional Science; and the American Institute for Cancer Research and supported by the DCP, NCCAM, and ODS. Guest editors for the supplement publication were Harold E. Seifried, National Cancer Institute, NIH; Barbara Sorkin, NCCAM, NIH; and Rebecca Costello, ODS, NIH.

² This study was supported by National Institutes of Health Grant P01 CA 88961.

	LITERATURE CITED

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1. Yang, C. S. & Landau, J. M. (2000) Effects of tea consumptiopn on nutrition and health. J. Nutr. 130:2409-2412.[Abstract/Free Full Text]

2. Yang, C. S., Maliakal, P. & Meng, X. (2002) Inhibition of carcinogenesis by tea. Annu. Rev. Parmacol. Toxicol. 42:25-54.

3. Yang, G. Y., Liao, J., Kim, K., Yurkow, E. J. & Yang, C. S. (1998) Inhibition of growth and induction of apoptosis in human cancer cell lines by tea polyphenols. Carcinogenesis 19:611-616.[Abstract/Free Full Text]

4. Yang, G.-Y., Liao, J., Li, C., Chung, J., Yurkow, E. J., Ho, C.-T. & Yang, C. S. (2000) Effect of black and green tea polyphenols on c-jun phosphorylation and H₂O₂ production in transformed and non-transformed human bronchial cell lines: possible mechanisms of cell growth inhibition and apoptosis induction. Carcinogenesis 21:2035-2039.[Abstract/Free Full Text]

5. Hong, J., Lu, H., Meng, X., Ryu, J.-H., Hara, Y. & Yang, C. S. (2002) Stability, cellular uptake, biotransformation, and efflux of tea polyphenol (–)-epigallocatechin-3-gallate in HT-29 human colon adenocarcinoma cells. Cancer Res 62:7241-7246.[Abstract/Free Full Text]

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