title: Tomato and garlic can modulate azoxymethane-induced colon carcinogenesis in rats.
abstract: Tomato (Lycopersicon esculentum) and garlic (Allium cepa) are important constituents of the human diet. Compounds like diallyl sulfides, diallyl disulfides and quercetin, which are active components of garlic, have known anti-inflammatory, antimutagenic activities. Similarly, active components in tomato, such as kaempferol and chlorogenic acid, have antimutagenic activities and lycopene is the most active oxygen quencher with potential chemopreventive activities. In view of this, an endeavour was made to evaluate the anticarcinogenic effect, if any, of tomato and garlic consumption individually and in combination on azoxymethane-induced colonic precancerous lesion, the aberrant crypt foci in animal model. Sprague-Dawley rats (4-5 weeks old) were injected with azoxymethane (15 mg/kg b.w.) and orally administered with 2% (w/v) of tomato, garlic and a combination of both. After 12 weeks of first azoxymethane injection, colons were assessed for aberrant crypt foci and compared with the carcinogen control group. Lipid peroxidation level and glutathione-S-transferase (GST) activity were assessed in liver as well as in colon. Furthermore, in situ cell proliferation and apoptosis were estimated using the Brdu incorporation method and TUNEL method respectively. It was observed that aberrant crypt foci were reduced in all treated groups (by 32.11% in garlic, by 76.14% in tomato and by 55.96% in the combination group). Among treated groups, GST activity was found to be induced in both liver and colon, whereas considerable reduction in lipid peroxidation level was observed in liver as well as in colon with respect to the carcinogen control group. Significant reduction in Brdu labelling index and increase in apoptotic index in colon was noted in the treated groups. These results suggest that tomato and garlic suspensions have a protective effect on colon carcinogenesis, which is mediated by modulation of different biological pathways during carcinogenesis.
authors.affiliation: Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute 37, Kolkata, India. archanadi1@rediffmail.com
authors.forename: A
authors.initials: A
authors.lastname: Sengupta
authors.forename: S
authors.initials: S
authors.lastname: Ghosh
authors.forename: S
authors.initials: S
authors.lastname: Das
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D001397:Azoxymethane / Q000008:administration & dosage / Q000633:toxicity*; D015197:Carcinogenicity Tests; D002273:Carcinogens / Q000008:administration & dosage / Q000633:toxicity*; D002455:Cell Division / Q000187:drug effects; D003106:Colon / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D003110:Colonic Neoplasms / Q000139:chemically induced* / Q000178:diet therapy* / Q000378:metabolism; D004195:Disease Models, Animal; D005737:Garlic; D005982:Glutathione Transferase / Q000187:drug effects; D007279:Injections, Subcutaneous; D015227:Lipid Peroxidation / Q000187:drug effects; D018551:Solanum lycopersicum; D019697:Onions; D008517:Phytotherapy; D011230:Precancerous Conditions / Q000139:chemically induced / Q000178:diet therapy / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016588:Anticarcinogenic Agents; D002273:Carcinogens; D005982:Glutathione Transferase; D001397:Azoxymethane