tannins and Stomach-Neoplasms

Topics: Animals; Breast Neoplasms; Carcinogens, Environmental; Colonic Neoplasms; Diet; Dietary Fats; Esophageal Neoplasms; Humans; Liver Neoplasms; Lung Neoplasms; Mammary Neoplasms, Experimental; Neoplasms; Pancreatic Neoplasms; Stomach Neoplasms; Tannins; Urinary Bladder Neoplasms

Seaweeds are one of the largest producers of biomass in the marine environment and a source of multiple bioactive metabolites with valuable health benefits. Among these, phlorotannins have been widely recognized for their promising bioactive properties. The potential antitumor capacity of

Topics: Apoptosis; Caco-2 Cells; Cell Line, Tumor; Chromatography, High Pressure Liquid; Colorectal Neoplasms; Flow Cytometry; Fucus; Gastrointestinal Tract; Humans; Plant Extracts; Seaweed; Signal Transduction; Stomach Neoplasms; Tannins

Tannic acid inhibits the mutagenicity of several polycyclic aromatic hydrocarbons (PAHs) and their bay-region diol-epoxides. Our prior studies have shown that when applied topically to Sencar mice, tannic acid caused substantial inhibition of epidermal PAH metabolism, subsequent PAH-DNA adduct formation, and PAH-induced skin tumorigenesis (H. Mukhtar et al., Cancer Res., 48:2361-2365, 1988, and references therein). In this study the effects of tannic acid supplementation in the diet (1%, w/w, in AIN-76 diet) of Sencar mice on benzo(a)pyrene (BP) metabolism and its subsequent DNA binding and tumorigenesis in lung and forestomach were evaluated. Animals receiving a tannic acid-containing diet showed diminished aryl hydrocarbon hydroxylase and 7-ethoxy-resorufin O-deethylase activities in the forestomach and lung. Elevated glutathione S-transferase and NAD(P)H:quinone reductase activities were observed in these tissues. Maximum effects occurred after 45 days of feeding. Administration of [3H]BP p.o. to animals resulted in lower covalent binding to DNA in forestomach and lung of animals receiving tannic acid-containing diet as compared to animals receiving AIN-76 control diet. Tumor induction studies in forestomach and lung revealed significant protection against BP-induced tumorigenesis in animals fed tannic acid-supplemented diet as compared to animals fed control diet. The mice fed tannic acid-supplemented diet developed 3.3 forestomach tumors/mouse compared to 5.2 tumors/mouse in animals receiving control diet. The numbers of pulmonary tumors per mouse in animals fed tannic acid-supplemented diet and control diet were 1.6 and 3.1, respectively. Topical application of 7,12-dimethylbenz(a)anthracene to animals fed tannic acid-supplemented diet did not result in significant protection against skin tumorigenesis. However, a slight delay in the onset of skin tumor formation occurred in tannic acid-fed animals when compared to animals receiving control diet. Our data suggest that dietary supplementation with tannic acid affords protection against BP-induced forestomach and lung tumorigenesis in rodents.

Topics: 9,10-Dimethyl-1,2-benzanthracene; Animals; Aryl Hydrocarbon Hydroxylases; Benzo(a)pyrene; Cytosol; Diet; DNA; DNA Adducts; Female; Gastric Mucosa; Hydrolyzable Tannins; Lung; Lung Neoplasms; Mice; Microsomes; Skin; Skin Neoplasms; Stomach; Stomach Neoplasms; Tannins

Topics: 2-Acetylaminofluorene; Carcinogenesis; Fluoresceins; Humans; Stomach Neoplasms; Tannins