Format

Send to

Choose Destination
Mutagenesis. 2009 Sep;24(5):405-11. doi: 10.1093/mutage/gep016. Epub 2009 Jun 24.

Flavonoids inhibit the genotoxicity of hydrogen peroxide (H(2)O(2)) and of the food mutagen 2-amino-3-methylimadazo[4,5-f]-quinoline (IQ) in lymphocytes from patients with inflammatory bowel disease (IBD).

Author information

1
Division of Biomedical Sciences, University of Bradford, Bradford BD7 1DP, UK.

Abstract

Inflammatory bowel disease (IBD) including Crohn's disease (CD) and ulcerative colitis (UC) is a chronic inflammatory gastrointestinal autoimmune condition with an inappropriate immune response. We investigated DNA damage induced in vitro in lymphocytes from IBD patients caused by oxidative stress through H(2)O(2) and 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and whether the plant flavonoids, quercetin and epicatechin, found in fruits, tea and soybeans could effectively reduce such stress. Lymphocytes from IBD patients and healthy volunteers were treated with 50 microg/ml H(2)O(2) or IQ in the presence of quercetin (0-250 microg/ml) or epicatechin (0-100 microg/ml). Flavonoid supplementation (250 microM quercetin or 100 microM epicatechin) caused an overall significant decrease of induced DNA damage resulting in a 48.6% (P < 0.001) reduction of H(2)O(2)-induced and a 43% (P < 0.001) reduction of IQ-induced DNA damage within the patient groups; for the control groups, reductions in DNA damage were 35.2 and 57.1%, respectively (both, P < 0.001). There was less induced DNA damage within lymphocytes from UC patients compared to CD patients for both series of experiments (H(2)O(2) and quercetin, IQ and epicatechin). In conclusion, flavonoids dramatically reduced oxidative stress in vitro in lymphocytes from IBD patients and healthy individuals. Thus, flavonoids could be very effective in the treatment of oxidative stress and encouraged in the diet of IBD patients.

PMID:
19553277
DOI:
10.1093/mutage/gep016
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Silverchair Information Systems
Loading ...
Support Center