Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats
- Authors
- No, Ha-Na; Kwon, Hoonjeong; Park, You-Gyoung; Cheon, Choong-Ill; Park, Jong-Sug; Park, Taesun; Aruoma, Okezie I.; Sung, Mi-Kyung
- Issue Date
- Oct-2007
- Publisher
- PERGAMON-ELSEVIER SCIENCE LTD
- Keywords
- quercetin; oxidative DNA damage; colon cancer; antioxidants; 1,2-dimethylhydrazine; colon-aberrant crypts; rats
- Citation
- NUTRITION RESEARCH, v.27, no.10, pp 659 - 664
- Pages
- 6
- Journal Title
- NUTRITION RESEARCH
- Volume
- 27
- Number
- 10
- Start Page
- 659
- End Page
- 664
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14626
- DOI
- 10.1016/j.nutres.2007.08.001
- ISSN
- 0271-5317
- Abstract
- Quercetin is a potent free radical-scavenging antioxidant exerting chemopreventive activity by reducing oxidative stresses. However, oxidized quercetin behaves as a prooxidant, which can lead to paradoxical effects. This study was conducted to investigate the effects of quercetin supplementation on 1,2-dimethylhydrazine (DMH)-induced oxidative DNA damage and precancerous lesion formation in the colon. Mate Sprague-Dawley rats were randomized into 5 groups. The rats in groups 3, 4, and 5 were treated with DMH (30 mg/kg body weight IP), twice on weeks 2 and 3. The experimental diets were as follows: control diet (group 1), 2% quercetin diet (group 2), control diet (group 3), 0.2% quercetin diet (group 4), and 2% quercetin diet (group 5). The DMH-induced oxidative tissue damage was examined 24 hours after the first DMH injection, and the aberrant crypt foci formation was measured at week 12. The results show the following: (1) that DMH significantly increased the level of 8-hydroxyguanine (8-OH-Gua) in the liver, where the metabolic conversion of DMH occurs, but did not significantly change the level of 8-OH-Gua in the colon; (2) that both the 0.2% and 2% quercetin supplementation suppressed the extent of 8-OH-Gua formation in the liver; (3) that dietary quercetin did not affect the formation of aberrant crypt foci; and (4) that 2% quercetin supplementation only slightly increased the liver oxidative damage without statistical significance. These results indicate that quercetin may not be an effective anticarcinogen against DMH-induced colon cancer, where oxidative tissue damage is not a primary event in the formation of a precancerous region. The context of quercetin as a hepatoprotective agent, however, must be emphasized. (C) 2007 Elsevier Inc. All rights reserved.
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