Effects of Black Tea Extract on Transplantable and Solid Tumors in Swiss Albino Mice

The chemopreventive effects of green tea and its polyphenols are well documented in the literature. Epidemiological studies have suggested that green tea consumption might be effective in the prevention of certain human cancers. About 80% of the tea is consumed as black tea. Limited studies have been carried out to assess the usefulness of black tea as anti_carcinogen. The present set of investigations were initiated to study the anti_tumorigenic potential of aqueous black tea extract (ATE) in Swiss albino mice in \%in vivo\% animal bioassay, using 7, 12 dimethyl_benzanthracene (DMBA) as carcinogen. In the experimental group, 2% ATE was given orally as sole source of drinking water, while the control were allowed to drink normal water, \%ad lib.\% The results revealed that drinking of 2% ATE could effectively inhibit the onset of tumorigenesis, cumulative number of tumors and average number of tumors per mouse. In ATE drinking group 44% animals remained tumor free till the termination of experiment, i. e. 26 weeks. In the second set of experiment the preventive efficacy of 2% ATE of different cultivars of black tea, viz orthodox, CTC and dust were tested in Ehrlich Ascites (EA) tumor bearing mice. The preventive effects of ATE were observed in terms of increased life span (ILS). All the cultivars of tea showed more than 25% increase in life span of the animals. Cytotoxic effect of various doses of all three cultivars of black tea was also observed \%in vitro \%on EA cells.

Health promoting activities and corresponding mechanism of(–)-epicatechin-3-gallate

(–)-Epicatechin-3-gallate(ECG),a bioactive polyphenolic compound,has contributed a lot to the health benefits of green tea.Great attention has been focused on(–)-epigallocatechin-3-gallate(EGCG),but limited research has been performed towards ECG.Like EGCG,ECG also possesses various pharmacological and physiological properties,such as mediation of antioxidant activities,anti-inflammation response,regulation of cell proliferation and apoptosis,as well as anticancer properties during angiogenesis,invasion and metastasis stages.Nontoxic ECG has various molecular targets within the cells,including CYP enzymes,phaseⅡdetoxification and antioxidant enzymes,as well as pro-inflammatory mediators.The antineoplastic mechanism contains inhibition of phase 1 CYP enzymes,induction of phaseⅡdetoxification and antioxidant enzymes,high anti-inflammatory efficacy,arrest of cell cycle progression,regulation of apoptosis,as well as mediation of metastasis processes.In particular,the gallate moiety of ECG is critical for mediating inhibitory effects towards cancer cells.Besides regulation of intracellular signaling pathways,ECG also inhibits RNase A and matrix metalloproteinase enzymatic activity via chelating metals(copper and zinc)in cancer cells.This review has summarized recent studies on pharmacological properties of ECG,and discussed corresponding mechanism on modulation of cellular signaling events by ECG,hoping to broaden its multiple usage.

The effect of folic acid on the development of stomach and other gastrointestinal cancers

OBJECTIVE: To evaluate the roles of folic acid and beta-carotene in the chemoprevention of gastric and other gastrointestinal (GI) cancers. METHODS: In a randomized, double-blind, placebo-controlled trial, a total of 216 patients with atrophic gastritis were randomly assigned to one of the four groups: (1) folate (FA, 20 mg per day plus vitamin B(12) 1 mg, intramuscularly, per month for one year, then 20 mg two times a week plus 1 mg per three months for the next year); (2) natural beta-carotene (N-betaC, 30 mg per day for first year, then 30 mg two times a week for the next); (3) synthetic beta-carotene (S-betaC, administered as in N-betaC); and (4) placebo. Follow-ups continued from 1994 to 2001. RESULTS: A total of 7 new cases of gastrointestinal cancers were diagnosed with 3 stomach, 1 colon and 1 esophageal cancers occurring in the placebo group; 1 stomach cancer in both of the N-betaC and S-betaC groups, and no cancer occurring in FA group. In terms of GI cancers, there was a significant reduction in the FA group, compared with the placebo group (P = 0.04). A similar trend was observed in both N-betaC and S-betaC groups (P = 0.07 - 0.08). Taken together, the three intervention groups displayed a highly significant decrease in occurrence (P = 0.004, vs placebo), and a lower risk for GI cancers (OR = 0.12; 95% confidence interval, 0.03 - 0.51). For development of gastric cancer, any one of the three active-treated groups did not reach statistically significant reduction. The FA group showed obvious improvement of the gastric mucosal lesions with more patients displaying lesions reversed or stable atrophy and inflammation (P = 0.04), reversed intestinal metaplasia (P = 0.06) at the end of follow-up, and reversed displasia (P = 0.017) at 12 months. Two cases of false jaundice were found in beta-carotene groups with no influence on administration, and no side-effects were reported in FA group. CONCLUSIONS: This trial revealed the interventional effect of folic acid on the development of GI cancers, a similar effect of beta-carotene was also detected. Also, folic acid may be of use to treat atrophic gastritis by preventing or reversing the precancerous lesions.