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©2009 The WJG Press and Baishideng.
World J Gastroenterol. Jul 21, 2009; 15(27): 3329-3340
Published online Jul 21, 2009. doi: 10.3748/wjg.15.3329
Published online Jul 21, 2009. doi: 10.3748/wjg.15.3329
Cells/tissues | Bile acids that induce DNA damage | Assay for damage | Ref. |
Cultured SV40-transformed, squamous esophageal epithelial cells (HET1-A) and Barrett’s associated adenocarcinoma cells (FLO-1) | DCA; also cocktail containing GCA, TCA, TCDCA | Comet assay1 for strand breaks | [18] |
Cultured SV40-transformed, squamous esophageal epithelial cells (HET1-A) | DCA | Comet assay for strand breaks; evidence for oxidative mechanism involving nitric oxide | [19] |
Cultured human adenocarcinoma cells (OE33) | DCA | Micronuclei assay; induction of micronuclei by DCA, reduced by antioxidants | [1520] |
Biopsies from human Barrett’s esophageal metaplastic tissue | Cocktail containing DCA, GCA, TCA, GDCA, GCDCA | 8-OHdG, an oxidized form of the DNA base guanine; assayed by IHC | [14] |
Mouse model of esophagitis and Barrett’s esophagus | DCA (as dietary supplement; also zinc deficiency) | 8-OHdG assayed by IHC | [17] |
- Citation: Bernstein H, Bernstein C, Payne CM, Dvorak K. Bile acids as endogenous etiologic agents in gastrointestinal cancer. World J Gastroenterol 2009; 15(27): 3329-3340
- URL: https://www.wjgnet.com/1007-9327/full/v15/i27/3329.htm
- DOI: https://dx.doi.org/10.3748/wjg.15.3329