Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats

Ha Na No, Hoonjeong Kwon, You Gyoung Park, Choong Ill Cheon, Jong Sug Park, Taesun Park, Okezie I. Aruoma, Mi Kyung Sung

Research output: Contribution to journalArticle

14 Citations (Scopus)

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. 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.

Original languageEnglish
Pages (from-to)659-664
Number of pages6
JournalNutrition Research
Volume27
Issue number10
DOIs
Publication statusPublished - 2007 Oct 1

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1,2-Dimethylhydrazine
Quercetin
DNA Damage
Colon
Dimethylhydrazines
Liver
Diet
Aberrant Crypt Foci
Anticarcinogenic Agents
Control Groups
Colonic Neoplasms
Free Radicals
Sprague Dawley Rats
Oxidative Stress

All Science Journal Classification (ASJC) codes

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

No, Ha Na ; Kwon, Hoonjeong ; Park, You Gyoung ; Cheon, Choong Ill ; Park, Jong Sug ; Park, Taesun ; Aruoma, Okezie I. ; Sung, Mi Kyung. / Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats. In: Nutrition Research. 2007 ; Vol. 27, No. 10. pp. 659-664.
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title = "Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats",
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. 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.",
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Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats. / No, Ha Na; Kwon, Hoonjeong; Park, You Gyoung; Cheon, Choong Ill; Park, Jong Sug; Park, Taesun; Aruoma, Okezie I.; Sung, Mi Kyung.

In: Nutrition Research, Vol. 27, No. 10, 01.10.2007, p. 659-664.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Dietary quercetin inhibits 1,2-dimethylhydrazine-induced liver DNA damage without altering colon DNA damage or precancerous lesion formation in rats

AU - No, Ha Na

AU - Kwon, Hoonjeong

AU - Park, You Gyoung

AU - Cheon, Choong Ill

AU - Park, Jong Sug

AU - Park, Taesun

AU - Aruoma, Okezie I.

AU - Sung, Mi Kyung

PY - 2007/10/1

Y1 - 2007/10/1

N2 - 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.

AB - 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.

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