Inhibition of Carcinogenesis by Tea: Bioavailability of Tea Polyphenols and Mechanisms of Actions

Abstract

The inhibitory activity of tea and tea polyphenols has been demonstrated in many studies with animal models in different laboratories, but such activity has been observed only in some of the epidemiological studies. A key question is whether tea consumption lowers cancer risk in humans. To answer this question, we need to know the effective components of tea and the mode of their inhibitory actions against tumorigenesis. It is important to know the levels of the putative active components in the target tissues and whether such levels are capable of inhibiting cancer formation and growth. In this report, we plan to review the inhibitory activities of tea and tea polyphenols against the development of lung tumors in animals and the growth of human cancer cells in culture, discuss the possible active components involved and mechanisms of action, and describe the tissue levels and pharmacokinetics of tea polyphenols in animal models and humans.

Inhibition of Lung Tumorigenesis in Animal Models

The tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) effectively induces adenomas and adenocarcinomas in the lungs of A/J mice. In typical experiments, decaffeinated green or black tea (DGT or DBT) was given to mice in the drinking fluid as 0.3% or 0.6% solution of tea solids. The tea solids were dehydrated water extracts of tea leaves. Tea was administered to mice during the NNK treatment period (for 3 weeks beginning 2 weeks before a single dose of NNK, 103 mg/kg, i.p.) or after the NNK treatment period (beginning 1 week after the NNK treatment until the termination of the experiment 15 weeks later). The tea treatment markedly inhibited tumorigenesis, especially tumor multiplicity (1). In these experiments, the inhibitory activities of decaffeinated green and black tea were comparable, although green tea might be slightly more effective in some experiments.