Maté attenuates DNA damage and carcinogenesis induced by diethylnitrosamine and thermal injury in rat esophagus

• Published in: Food and chemical toxicology 2009-07, Vol.47 (7), p.1521-1529
• Main Authors: Silva, Juliana Ferreira da, Bidinotto, Lucas Tadeu, Furtado, Kelly Silva, Salvadori, Daisy Maria Fávero, Rivelli, Diogo Pineda, Barros, Silvia Berlanga de Moraes, Rodrigues, Maria Aparecida Marchesan, Barbisan, Luis Fernando
• Format: Article
• Language: English
• Subjects: animal models; Animals; Anticarcinogenic Agents; Aquifoliaceae - chemistry; Aspartate Aminotransferases - blood; Beverages; Biological and medical sciences; Body Weight - drug effects; burns (injuries); Burns - complications; Burns - pathology; Caffeine - pharmacology; carcinogenesis; Carcinogenesis, carcinogens and anticarcinogens; Chemical agents; Comet Assay; diethylnitrosamine; Diethylnitrosamine - antagonists & inhibitors; Diethylnitrosamine - toxicity; Diethylnitrosamine-induced esophageal and liver lesions; DNA Damage; esophageal neoplasms; Esophageal Neoplasms - pathology; Esophageal Neoplasms - prevention & control; esophagus; Esophagus - injuries; Glutathione Peroxidase - metabolism; human diseases; Ilex paraguariensis; Immunohistochemistry; leukocytes; Leukocytes - drug effects; Leukocytes - pathology; Leukocytes - ultrastructure; liver; liver neoplasms; Male; Maté; Medical sciences; nitrosamines; Organ Size - drug effects; pathogenesis; Proliferating Cell Nuclear Antigen - analysis; Protective Agents; protective effect; Rats; Rats, Wistar; risk assessment; risk factors; stimulant plants; Tea; tea (beverage); toxicity; Toxicology; traditional foods; Tumors; yerba mate
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2009.03.040

Drinking hot maté has been associated with risk for esophageal cancer in South America. Thus, the aims of this study were to evaluate the modifying effects of maté intake on DNA damage and esophageal carcinogenesis induced by diethylnitrosamine (DEN) and thermal injury (TI) in male Wistar rats. At the initiation phase of carcinogenesis, rats were treated with DEN (8 × 80 mg/kg) and submitted to TI (water at 65 °C, 1 ml/rat, instilled into the esophagus). Concomitantly, the animals received maté (2.0% w/v) for 8 weeks. Samples of peripheral blood were collected 4 h after the last DEN application for DNA damage analysis. At weeks 8 and 20, samples from esophagus and liver were also collected for histological and immunohistochemical analysis. Maté significantly decreased DNA damage in leukocytes, cell proliferation rates in both esophagus and liver and the number of preneoplastic liver lesions from DEN/TI-treated animals at week 8. A significant lower incidence of esophageal papillomas and liver adenomas and tumor multiplicity was observed in the animals previously treated with maté at week 20. Thus, maté presented protective effects against DNA damage and esophageal and liver carcinogenesis induced by DEN.