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[Cancer Research 54, 3428-3435, July 1, 1994]
© 1994 American Association for Cancer Research

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Inhibitory Effects of Black Tea, Green Tea, Decaffeinated Black Tea, and Decaffeinated Green Tea on Ultraviolet B Light-induced Skin Carcinogenesis in 7,12-Dimethylbenz[a]anthracene-initiated SKH-1 Mice1

Zhi Y. Wang, Mou-Tuan Huang, You-Rong Lou, Jian-Guo Xie, Kenneth R. Reuhl, Harold L. Newmark, Chi-Tang Ho, Chung S. Yang and Allan H. Conney2,3,

Laboratory for Cancer Research, Department of Chemical Biology and Pharmacognosy [Z. Y. W., M-T. H., Y-R. L., J-G. X., H. L. N., C. S. Y., A. H. C.] and Pharmacology and Taxicology [K. R. R.], College of Pharmacy, Rutgers, State University of New Jersey, Piscataway, New Jersey 08855-0789, and Department of Food Science, Cook College, Rutgers, State University of New Jersey, New Brunswick, New Jersey 08901 [C-T. H.]

In a previous study (Z. Y. Wang et al., Cancer Res., 52: 1162–1170, 1992), we found that administration of a water extract of green tea leaves as the sole source of drinking fluid inhibited ultraviolet B light (UVB)-induced carcinogenesis in SKH-1 mice previously initiated with 7,12-dimethylbenz[a]anthracene (DMBA). In the present study, we compared the effects of black tea, green tea, decaffeinated black tea, and decaffeinated green tea on UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice. A 1.25% water extract of each kind of tea leaf (1.25 g tea leaf/100 ml water) was prepared by passing 4 liters of hot water through 50 g of tea leaves in a Bunn tea brewing machine. The mean concentrations of solids in multiple samples of 1.25% black tea, green tea, decaffeinated black tea, and decaffeinated green tea analyzed during the course of this study were 4.23, 3.94, 3.66, and 3.53 mg/ml, respectively. These concentrations of tea solids are similar to those present in tea brews ingested by humans. Femmale SKH-1 mice were treated topically with 200 nmol of DMBA, followed 3 weeks later by irradiation with 30 mJ/cm2 of UVB twice weekly for 31 weeks. UVB-induced formation of skin tumors was markedly inhibited by oral administration of 0.63 or 1.25% black tea, green tea, decaffeinated black tea, or decaffeinated green tea as the sole source of drinking fluid 2 weeks prior to and during 31 weeks of UVB treatment. Administration of each of the eight tea preparations not only inhibited the number of tumors, but tumor size was also markedly decreased. Histopathological examination of each tumor showed that oral administration of the eight tea preparations had a marked inhibitory effect on the formation of UVB-induced keratoacanthomas and carcinomas. Administration of 1.25% black tea, green tea, decaffeinated black tea, or decaffeinated green tea inhibited the number of keratoacanthomas per mouse by 79, 78, 73, or 70%, respectively, and the number of carcinomas per mouse was inhibited by 93, 88, 77, or 72%, respectively. In summary, administration of black tea was comparable to green tea as an inhibitor of UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice. Oral administration of decaffeinated black tea or decaffeinated green tea also had a marked inhibitory effect on UVB-induced skin carcinogenesis in DMBA-initiated SKH-1 mice, but these tea preparations were slightly less effective than the regular teas at the high dose level.

1 This study was supported in part by Grants No. CA49756 and ES05022 from the National Institutes of Health.

2 William M. and Myrle W. Garbe Professor of Cancer and Leukemia Research.

3 To whom requests for reprints should be addressed, at Department of Chemical Biology and Pharmacognosy, College of Pharmacy, Rutgers University, P.O. Box 789, Piscataway, NJ 08855-0789.

Received 1/28/94. Accepted 4/28/94.




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Copyright © 1994 by the American Association for Cancer Research.