Dextran sulfate enhances the level of an oxidative DNA damage biomarker, 8-oxo-7,8-dihydro-2′-deoxyguanosine, in rat colonic mucosa

Tardieu, Didier; Jaeg, Jean-Philippe; Cadet, Jean; Embvani, E.; Corpet, Denis E.; Petit, Claude

doi:10.1016/s0304-3835(98)00228-6

Cited by 37 publications

(31 citation statements)

References 22 publications

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“…An oxidized form of guanine is 8-oxodG that is generated by ROS and is widely used as a marker of oxidative DNA damage [27,62]. DSS treatment enhances ROS levels [63] and free radicals induce oxidative DNA damage in colonic mucosa [64]. Our results show that DSS increased the lipid peroxidation level, measured as MDA and oxidized DNA (as ratio 8-oxodG/dG).…”

Section: Discussionmentioning

confidence: 59%

Polyphenol metabolites from colonic microbiota exert anti‐inflammatory activity on different inflammation models

Larrosa

Luceri

Vivoli

et al. 2009

Molecular Nutrition Food Res

224

191

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The polyphenols in fruits and vegetables may be partly responsible for the health-promoting effects attributed to fruit and vegetable intake. Although their properties have been relatively well studied, the activity of their metabolites, produced after ingestion, has been poorly investigated. Thus, the aim of this work was to study the potential anti-inflammatory effect of 18 polyphenol metabolites, derived from colon microbiota. They were screened by measuring prostaglandin E(2) (PGE(2)) production by CCD-18 colon fibroblast cells stimulated with IL-1beta. Metabolites that inhibited more than 50% PGE(2) production were hydrocaffeic (HCAF), dihydroxyphenyl acetic (dOHPA), and hydroferulic acid (HFER), that subsequently were tested with the writhing and paw pressure test in rodents where all three compounds showed an anti-inflammatory effect. The effect of HCAF administered orally (50 mg/kg) was also tested in the dextran sodium sulfate (DSS)-induced colitis model. Weight loss and fecal water content were more pronounced in DSS rats than in DSS-HCAF treated rats. HCAF treatment diminished the expression of the cytokines IL-1beta, IL-8, and TNF-alpha, reduced malonyldialdehyde (MDA) levels and oxidative DNA damage (measured as 8-oxo-2'-deoxyguanosine levels) in distal colon mucosa. These results indicate that HCAF, dOHPA, and HFER have anti-inflammatory activity in vitro and in vivo.

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Section: Discussionmentioning

confidence: 59%

Polyphenol metabolites from colonic microbiota exert anti‐inflammatory activity on different inflammation models

Larrosa

Luceri

Vivoli

et al. 2009

Molecular Nutrition Food Res

224

191

View full text Add to dashboard Cite

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“…It is possible that c-Rel compensates for loss of RelA in basal expression of some antiapoptotic NF-Btarget genes such as cFLIP, XIAP, and survivin. Further work is required to determine whether, under the significant stress of elevated cytokine production and DNA damage associated with experimental murine colitis (62,63), the ability of c-Rel to provide some measure of antiapoptotic gene expression is surpassed, resulting in widespread epithelial cell death.…”

Section: Discussionmentioning

confidence: 99%

Loss of Epithelial RelA Results in Deregulated Intestinal Proliferative/Apoptotic Homeostasis and Susceptibility to Inflammation

Steinbrecher

Harmel‐Laws

Sitcheran

et al. 2008

The Journal of Immunology

151

140

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NF-κB plays a central, proinflammatory role in chronic intestinal inflammation, yet recent work suggests a predominantly protective function for this transcription factor group in some cell types of the intestine. We herein describe the conditional deletion of the NF-κB RelA gene in murine intestinal epithelia and determine its function in homeostatic control of enterocyte proliferation/apoptosis and susceptibility to colonic inflammation. Mice lacking RelA in ileal and colonic enterocytes were born in expected Mendelian ratios, and RelA-null epithelia differentiated normally. Spontaneous intestinal disease and death occurred with low penetrance in neonates lacking epithelial RelA. IκBα and IκBβ were significantly diminished in RelA-null epithelia, and endotoxin challenge revealed elevated p50 and c-Rel DNA binding activity as compared with controls. Deletion of RelA resulted in diminished expression of antimicrobial (defensin-related cryptdin 4, defensin-related cryptdin 5, RegIIIγ) and antiapoptotic, prorestitution genes (Bcl-xL, RegIV, IL-11, IL-18), and basal rates of epithelial apoptosis and proliferation were elevated. Mice lacking colonic RelA were sensitive to dextran sodium sulfate-induced colitis. Although experimental colitis enhanced proliferation in cells lacking RelA, sustained epithelial cell apoptosis precluded mucosal healing and decreased animal survival. We conclude that activation of RelA is required for homeostatic regulation of cell death and division in intestinal epithelia, as well as for protection from development of severe, acute inflammation of the intestine.

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“…39) Indeed, measures of oxidative stress, including 8-oxoguanine and 4-hydroxy-2-nonenal-modified proteins, were increased in colonic mucosa of IBD patients [40][41][42] and inflamed colonic tissue of rodents treated with DSS. 43,44) An ongoing study in our laboratory will clarify the contribution of oxidative stress to colon carcinogenesis in our model.…”

Section: Discussionmentioning

confidence: 99%

Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

et al. 2004

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Previously, we proposed a novel mouse model for colitis-related colon carcinogenesis using azoxymethane (AOM) and dextran sodium sulfate (DSS) (Cancer Sci 2003; 94: 965-73). In the current study, sequential analysis of pathological alterations during carcinogenesis in our model was conducted to establish the influence of inflammation caused by DSS on colon carcinogenesis in this model. Male ICR mice were given a single intraperitoneal injection of AOM (10 mg/kg body weight) and given 2% (w/v) DSS in the drinking water for 7 days, starting 1 week after the AOM injection. They were sequentially sacrificed at weeks 2, 3, 4, 5, 6, 9, 12, and 14 for histopathological and immunohistochemical examinations. Colonic adenomas were found in 2 (40% incidence and 0.40 ± ± ± ±0.49 multiplicity) of 5 mice at week 3 and colon carcinomas developed in 2 (40% incidence and 2.00 ± ± ± ±3.52 multiplicity) of 5 mice at week 4. Their incidence gradually increased with time and reached 100% (6.20 ± ± ± ±2.48 multiplicity) at week 6. At week 14, the multiplicity of adenocarcinoma was 9.75 ± ± ± ±2.49 (100% incidence). In addition, colonic dysplasia was noted at all time-points. The scores of colonic inflammation and nitrotyrosine immunohistochemistry were extremely high at early time-points and were well correlated. Our results suggest that combined treatment of mice with AOM and DSS generates neoplasms in the colonic mucosa via dysplastic lesions induced by nitrosative stress. (Cancer Sci 2004; 95: 721-727) n the developed countries, colorectal cancer (CRC) is one of the commonest non-smoking related causes of cancer deaths. Remarkable differences in the incidence worldwide have led to the hypothesis that this variation could be explained largely by environmental influences. 1)The occurrence of inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is affected by several factors, including race and geography.2, 3) Life style, particularly intake of high amount of animal fat, is involved in the occurrence of IBD. 4) Over recent decades the incidence of IBD has been rising throughout the world, including Japan, as it has been in the last 50 years in Europe and North America.5) This increase may be caused by increased intake of animal fat. 6) CRC is one of the most serious complications of IBD, especially UC and CD. The risk of CRC becomes greater with increasing extent and duration of the disease. A recent meta-analysis has estimated the incidence rate at 7 per 1000 person-years duration and 12 per 1000 persons per year duration in the second and third decades of UC, respectively.7) The risk for CRC development in CD patients is also high.8) The highest risk of CRC in CD patients was reported to be 26.6 (standardized incidence ratio), although the estimate applied only to patients younger than 21 years of age. 9) Gillen et al. 10)compared the CRC risk in patients with UC and CD and found an 18-fold increase in the risk of developing CRC in extensive CD and a 19-fold increase in risk in extensive...

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Dextran sulfate enhances the level of an oxidative DNA damage biomarker, 8-oxo-7,8-dihydro-2′-deoxyguanosine, in rat colonic mucosa

Cited by 37 publications

References 22 publications

Polyphenol metabolites from colonic microbiota exert anti‐inflammatory activity on different inflammation models

Polyphenol metabolites from colonic microbiota exert anti‐inflammatory activity on different inflammation models

Loss of Epithelial RelA Results in Deregulated Intestinal Proliferative/Apoptotic Homeostasis and Susceptibility to Inflammation

Sequential observations on the occurrence of preneoplastic and neoplastic lesions in mouse colon treated with azoxymethane and dextran sodium sulfate

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