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Probiotic mixture decreases DNA adduct formation in colonic epithelium induced by the food mutagen 2-amino-9H-pyrido[2,3-b]indole in a human-flora associated mouse model

 

作者: H Horie,   M Zeisig,   K Hirayama,   T Midtvedt,   L Möller,   J Rafter,  

 

期刊: European Journal of Cancer Prevention  (OVID Available online 2003)
卷期: Volume 12, issue 2  

页码: 101-107

 

ISSN:0959-8278

 

年代: 2003

 

出版商: OVID

 

关键词: 2-Amino-9H-pyrido[2;3-b]indole (2-amino-alpha-carboline);DNA adduct;colon cancer;heterocyclic amine;32P-high-performance liquid chromatography;probiotics

 

数据来源: OVID

 

摘要:

Consumption of probiotic bacteria such as bifidobacteria has been shown to reduce the risk of colon cancer in animal models. However, the composition and metabolic activities of the intestinal flora of experimental animals are significantly different from those of humans. The aim of the study was to examine whether the probiotic mixture, which consisted ofStreptococcus faecalis,Clostridium butyricumandBacillus mesentericus, could decrease DNA adduct formation induced by 2-amino-9H-pyrido[2,3-b]indole (2-amino-alpha-carboline; AAC) in the colonic epithelium of a human-flora-associated (HFA) mouse model. Ten HFA mice were divided into a control group (n=4) and a probiotic group (n=6). The control group was administered AAC for 3 days and sacrificed 24 h after the last dose. The probiotic group was administered the probiotic mixture for 2 weeks prior to the administration of AAC. Analysis of DNA adducts with the32P-high-performance liquid chromatography method was performed on stomach, jejunum and colonic epithelium, representing direct exposure sites of AAC, and colon wall, liver and kidney, representing indirect exposure sites. The mean level of the DNA adducts in the colonic epithelium of the probiotic group was significantly lower than that of control group, while the mean levels at the other sites did not differ significantly between the groups. The results indicated that the probiotic mixture could decrease the DNA adduct formation in the colonic epithelium induced by AAC.

 

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