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Carcinogenesis, Vol. 21, No. 1, 63-67, January 2000
© 2000 Oxford University Press


Molecular Epidemiology and Cancer Prevention

Comparative chemopreventive mechanisms of green tea, black tea and selected polyphenol extracts measured by in vitro bioassays

Vernon E. Steele5, Gary J. Kelloff, Douglas Balentine4, Charles W. Boone, Rajendra Mehta2, Donya Bagheri3, Caroline C. Sigman3, Songyun Zhu1 and Sheela Sharma1

Chemoprevention Branch, Division of Cancer Prevention, National Cancer Institute, NIH, Bethesda, MD 20892,
1 ManTech Environmental Inc., Research Triangle Park, NC 27709,
2 University of Illinois at Chicago, Chicago, IL 60612,
3 CCS Associates, Mountain View, CA 94043,
4 Thomas J.Lipton Company, Englewood Cliffs, NJ 07632, USA

Black tea extracts (hot aqueous, polyphenols and theaflavins) and green tea extracts (hot aqueous, polyphenols, epicatechin, epicatechin gallate, epigallocatechin and epigallocatechin gallate) were tested in nine standardized cell culture assays for comparative cancer chemopreventive properties. Most black and green tea extracts strongly inhibited neoplastic transformation in mouse mammary organ cultures, rat tracheal epithelial cells and human lung tumor epithelial cells. Nearly all tea fractions strongly inhibited benzo[a]pyrene adduct formation with human DNA. Induction of phase II enzymes, glutathione-S-transferase and quinone reductase, were enhanced by nearly all tea fractions, while glutathione was induced by only a few fractions. Ornithine decarboxylase activity was inhibited by nearly all the green tea fractions, but none of the black tea fractions. 12-O-tetradecanoylphorbol-13-acetate-induced free radicals were inhibited by most tea fractions. These results provide strong evidence of both anti-mutagenic, anti-proliferative and anti-neoplastic activities for both black and green tea extracts. Such anticancer mechanisms may well be responsible for the cancer preventive efficacies seen in both experimental and human studies.

Abbreviations: B[a]P, benzo[a]pyrene; BTE, black tea extract; BTP, black tea polyphenols; DMBA, 7,12-dimethylbenz[a]anthracene; DMFO, difluoromethylornithine; DMSO, dimethyl sulfoxide; EC, epicatechin; ECG, epicatechin gallate; EGC, epigallocatechin; EGCG, epigallocatechin gallate; ETOAc, ethyl acetate; GSH, glutathione; GST, glutathione-S-transferase; GTE, green tea extract; GTP, green tea polyphenols; MMOC, mouse mammary organ culture; NADPH:QR, quinone reductase; ODC, ornithine decarboxylase; RTE, rat tracheal epithelial; TPA, 12-O-tetradecanoylphorbol-13-acetate.

5 To whom correspondence should be addressed at: EPN Room 201, MSC 7322, National Cancer Institute, 9000 Rockville Pike, Bethesda, MD 20892-7322, USA Email:vsly{at}nih.gov


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