Abstract
Abstract Background: It is well known that a daily consumption of foods that are rich in antioxidants prevents the oxidative damage caused by reactive species (ROS), including DNA damage, and can reduce the risk of cancer, atherosclerosis and other degenerative diseases. The pulp of Caryocar brasiliense Camb, most known as pequi, is a Brazilian fruit that has high levels of antoxidants properties, such as vitamin C, carotenoids, phenolic compounds like flavonoids, saponins and tannins, and essential oils. The aim of this study was to evaluate the action of the pequi oil in the DNA damage in experimental model of lung cancer induced by the urethane. Material and Methods: Male BALB/c mice (n=14) received by gavage 0,5μL/mg/day of pequi oil (CBC oil) during 75 days. After 15 days of the beginning of the gavage, 10 of these animals received two doses of 1,5g/kg intraperitoneal of urethane (Urethane + CBC oil). Urethane animals (n=4) were only submitted to two doses of 1,5g/kg intraperitoneal of urethane (urethane group). After these 75 days, lung tissues were submitted to histological and biochemical analysis by comet assay method to evaluated the DNA damage. The DNA damage was quantificate by image analysis. Results: The lung parenchyma from the urethane groups without oil and with oil showed neoplasic formations induced by the chemical carcinogenesis in contrast with oil control group. The image analysis of the comet assay showed a statistical significant diminish of the DNA damage cells in the urethane oil group when compared with urethane control group (p=0.001). The decreased DNA damage was very similar that we obtained in the oil control group. Conclusion: We conclude that the different antioxidant components found in the pequi oil diminish the DNA damage in the mouse lung after chemical carcinogenesis, suggesting that this type of strategies may have a greater impact in lung cancer treatment. Financial Support: FAPESP, CNPq Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1604. doi:1538-7445.AM2012-1604
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