The prevention of lung cancer induced by a tobacco-specific carcinogen in rodents by green and black tea

A growing body of evidence from studies in laboratory animals indicates tha t green tea protects against cancer development at various organ sites. We have previously shown that green tea, administered as drinking water, inhib its lung tumor development in A/J mice treated with 4-(methylnitrosamino)-1 -(3-pyridyl)-I-butanone (NNK), a potent nicotine-derived lung carcinogen fo und in tobacco. The inhibitory effect of green tea has been attributed to i ts major polyphenolic compound, epigallocatechin gallate (EGCG), and, to a lesser extent, to caffeine. We have also demonstrated that while levels of O-6-methylguanine, a critical lesion in NNK lung tumorigenesis, were not af fected in lung DNA, However, the levels of 8-hydroxydeoxyguanosine (8-OH-dG ), a marker of oxidative DNA damage, were significantly suppressed in mice treated with green tea or EGCG, These studies underscore the importance of the antioxidant activity of green tea and EGCG for their inhibitory activit y against lung tumorigenesis, Unlike green tea, the effect of black tea on carcinogenesis has been scarcely studied, even though the worldwide product ion and consumption of black tea far exceeds that of green tea. The oxidati on products found in black tea, thearubigins and theaflavins, also possess antioxidant activity, suggesting that black tea may also inhibit NNK-induce d lung tumorigenesis. Indeed, bioassays in A/J mice have shown that black t ea given as drinking water retarded the development of lung cancer caused b y NNK, However, data on the relationship of black tea consumption with the lung cancer risk in humans are limited and inconclusive. There is a need fo r additional tumor bioassays in animal models to better examine the protect ive role of black tea against lung cancer. The development of adenocarcinom as and adenosquamous carcinomas in F344 rats upon chronic administration of NNK provides an important and relevant model for lung carcinogenesis in sm okers. Thus far, no information was previously available regarding the effe cts of tea on this model. We conducted a 2-year lifetime bioassay in F344 r ats to determine whether black tea and caffeine are protective against lung tumorigenesis induced by NNK. Our studies in both mice and rats have gener ated important new data that support green and black tea end caffeine as po tential preventive agents against lung cancer, suggesting that a closer exa mination of the roles of tea and caffeine on lung cancer in smokers may be warranted.