Dietary quercetin inhibits 1,2-dimethylhydrazine–induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats
- 作者：Ha-Na No ; Hoonjeong Kwon ; You-Gyoung Park ; Choong-Ill Cheon ; Jong-Sug Park ; Taesun Park ; Okezie I. Aruoma ; Mi-Kyung Sung
- 关键词：Quercetin ; Oxidative DNA damage ; Colon cancer ; Antioxidants ; 1 ; 2-Dimethylhydrazine ; Colon-aberrant crypts ; Rats
- 刊名：Nutrition Research
- 出版年：2007
- 期刊代码：123_02715317
- 类别：bio
- 出版时间：October 2007
- 卷：27
- 期：10
- 页码：659-664
- 文件大小：214 K
摘要
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. Male 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.