We are analyzing https://link.springer.com/article/10.1007/s00394-008-0725-8.

Title:
Genotoxic effect of bile acids on human normal and tumour colon cells and protection by dietary antioxidants and butyrate | European Journal of Nutrition
Description:
Background Colorectal cancer is the second cause of death for tumour worldwide. Among the risk factors for this disease the dietary habits seem to have a pivotal role. An elevated intake of fats causes a high release in the gut lumen of bile acids that are positively correlated with colorectal cancer, since they act as detergents and proliferation promoters. Recently, it was evidenced that bile acids can also be able to induce DNA damage. Aim of the study In this study the genotoxicity of deoxycholic acid (DCA) and chenodeoxycholic acid CDCA) has been evaluated in human normal colonocytes derived from 60 colon biopsies and in tumour cells. The involvement of reactive oxygen species (ROS) and the oxidative DNA damage was assessed. In addition, the protective effect exerted by both two well-known antioxidants commonly present in the diet, β-carotene and α-tocopherol, and butyrate which is known to be involved in the regulation of several cellular functions, has also been tested. Methods The DNA damage was evaluated by the “comet assay” or single cell gel electrophoresis (SCGE) both in its conventional use and by the Endonuclease III modified method, which allow to detect the presence of oxidized pyrimidines. Results Bile acids (CDA and CDCA) resulted genotoxic on both normal and tumour human colon cells. The inclusion of the endonuclease III digestion step in the comet assay demonstrated that bile acids induced an oxidative DNA damage. In addition, treatment of colonocytes with bile acids in the presence of the antioxidants (β-carotene, α-tocopherol) and Na-butyrate caused a reduction of DNA damage. Conclusion Our results suggest that bile acids may be involved in the tumour initiation by inducing a DNA oxidative damage, and so add further evidences to the preventive properties of antioxidants present in the Mediterranean diet.
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Topics {✒️}

phorbol-ester-type tumor promoters month download article/chapter stress-response proteins poly glutathione s-transferases genes n-methyl-n-nitroguanidine glutathione s-transferase p1 na-butyrate caused oxidative dna damage dna oxidative damage anaerobic bacterial metabolism bile salt-induced apoptosis induce dna damage related subjects p53-independent differentiation bile acids induced article european journal dna adducts isolated human colonocytes full article pdf colonic mucosal dna human lymphocytes dna privacy choices/manage cookies dna strand breaks wild-type p53 bile acids reduce tumour colon cells normal rat colon detachment-induced apoptosis dietary cholic acid check access instant access colorectal cancer tissue dna damage european economic area ht29 tumour cells chenodeoxycholic acid cdca oxidative damage human colon cells cox-2 promoter activity antioxidants commonly present human gastrointestinal cancers human sigmoid colon la rue jm colorectal cancer risk docosahexaenoic acids reduce reddy bs bile acid human colon adenoma favourably modulating expression colonic luminal components

Questions {❓}

Booth LA, Gilmore IT, Bilton RF (1997) Secondary bile acid induced DNA damage in HT29 cells: are free radicals involved?
Davidovic M (1999) Genetic stability: the key to longevity?
Sengupta S, Muir JG, Gibson BR (2006) Does butyrate protect from colorectal cancer?

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         description:Colorectal cancer is the second cause of death for tumour worldwide. Among the risk factors for this disease the dietary habits seem to have a pivotal role. An elevated intake of fats causes a high release in the gut lumen of bile acids that are positively correlated with colorectal cancer, since they act as detergents and proliferation promoters. Recently, it was evidenced that bile acids can also be able to induce DNA damage. In this study the genotoxicity of deoxycholic acid (DCA) and chenodeoxycholic acid CDCA) has been evaluated in human normal colonocytes derived from 60 colon biopsies and in tumour cells. The involvement of reactive oxygen species (ROS) and the oxidative DNA damage was assessed. In addition, the protective effect exerted by both two well-known antioxidants commonly present in the diet, β-carotene and α-tocopherol, and butyrate which is known to be involved in the regulation of several cellular functions, has also been tested. The DNA damage was evaluated by the “comet assay” or single cell gel electrophoresis (SCGE) both in its conventional use and by the Endonuclease III modified method, which allow to detect the presence of oxidized pyrimidines. Bile acids (CDA and CDCA) resulted genotoxic on both normal and tumour human colon cells. The inclusion of the endonuclease III digestion step in the comet assay demonstrated that bile acids induced an oxidative DNA damage. In addition, treatment of colonocytes with bile acids in the presence of the antioxidants (β-carotene, α-tocopherol) and Na-butyrate caused a reduction of DNA damage. Our results suggest that bile acids may be involved in the tumour initiation by inducing a DNA oxidative damage, and so add further evidences to the preventive properties of antioxidants present in the Mediterranean diet.
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