Here, we examined the effect of
black tea and
caffeine on lung
tumorigenesis in F344 rats induced by the
nicotine-derived
carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in a 2-year bioassay. NNK was administered s.c. at a dose of 1.5 mg/kg
body weight three times weekly for 20 weeks. Animals were given either
black tea as
drinking water at concentrations of 2%, 1%, or 0.5%, or
caffeine in
drinking water at concentrations identical to those in 2% and 0.5%
tea infusions for 22 weeks. The treatment period began 1 week before and ended 1 week after the NNK administration. The animals were sacrificed on week 101 for the examination of
tumors in target organs, including lung, liver, nasal cavity, and other major organs. The NNK-treated group, given 2%
black tea, showed a significant reduction of the total lung
tumor (
adenomas,
adenocarcinomas, and
adenosquamous carcinomas) incidence from 47% to 19%, whereas the group given 1% and 0.5%
black tea showed no change. The 2%
tea also reduced liver
tumor incidence induced by NNK from 34% in the group given only deionized water to 12%. The
tumor incidence in the nasal cavity, however, was not affected by either
black tea or
caffeine at any of the concentrations tested. The most unexpected finding was the remarkable reduction of the lung
tumor incidence, from 47% to 10%, in the group treated with 680 ppm
caffeine, a concentration equivalent to that found in the 2%
tea. This incidence is comparable to background levels seen in the control group. This study demonstrated for the first time in a 2-year lifetime bioassay that
black tea protects against lung
tumorigenesis in F344 rats, and this effect appears to be attributed, to a significant extent, to
caffeine as an active ingredient of
tea.