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dc.contributor.authorKawanishi, Shosuke
dc.contributor.authorHiraku, Yusuke
dc.contributor.authorPinlaor, Somchai
dc.contributor.authorMa, Ning
dc.date.accessioned2009-04-03T07:35:32Z
dc.date.available2009-04-03T07:35:32Z
dc.date.issued2006-04
dc.identifier.citationBiol. Chem. 2006, 387 (4):365-372en
dc.identifier.issn1431-6730
dc.identifier.pmid16606333
dc.identifier.doi10.1515/BC.2006.049
dc.identifier.urihttp://hdl.handle.net/10146/59293
dc.descriptionKEYWORDS CLASSIFICATION: analogs & derivatives;Animals;complications;Cholangiocarcinoma;Colonic Neoplasms;DNA Damage;etiology;Guanine;Helicobacter pylori;Humans;immunology;Infection;Inflammation;Inflammatory Bowel Diseases;Japan;Liver Neoplasms;metabolism;microbiology;mechanisms of carcinogenesis;Mice;Mouth Neoplasms;Neoplasms;Oxidative Stress;physiopathology.en
dc.description.abstractInfection and chronic inflammation are proposed to contribute to carcinogenesis through inflammation-related mechanisms. Infection with hepatitis C virus, Helicobacter pylori and the liver fluke, Opisthorchis viverrini (OV), are important risk factors for hepatocellular carcinoma (HCC), gastric cancer and cholangiocarcinoma, respectively. Inflammatory bowel diseases (IBDs) and oral diseases, such as oral lichen planus (OLP) and leukoplakia, are associated with colon carcinogenesis and oral squamous cell carcinoma (OSCC), respectively. We performed a double immunofluorescence labeling study and found that nitrative and oxidative DNA lesion products, 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), were formed and inducible nitric oxide synthase (iNOS) was expressed in epithelial cells and inflammatory cells at the site of carcinogenesis in humans and animal models. Antibacterial, antiviral and antiparasitic drugs dramatically diminished the formation of these DNA lesion markers and iNOS expression. These results suggest that oxidative and nitrative DNA damage occurs at the sites of carcinogenesis, regardless of etiology. Therefore, it is considered that excessive amounts of reactive nitrogen species produced via iNOS during chronic inflammation may play a key role in carcinogenesis by causing DNA damage. On the basis of our results, we propose that 8-nitroguanine is a promising biomarker to evaluate the potential risk of inflammation-mediated carcinogenesis.
dc.language.isoenen
dc.relation.urlhttp://www.reference-global.com/doi/abs/10.1515/BC.2006.049en
dc.subjectCarcinogenesisen
dc.subjectDNA damageen
dc.subjectInducible nitric oxide synthaseen
dc.subjectInflammationen
dc.subject8-nitroguanineen
dc.subject8-oxo-7,8-dihydro-2'-deoxyguanosineen
dc.subject.meshAnimals
dc.subject.meshCholangiocarcinoma
dc.subject.meshColonic Neoplasms
dc.subject.meshDNA Damage
dc.subject.meshGuanine
dc.subject.meshHumans
dc.subject.meshInfection
dc.subject.meshInflammation
dc.subject.meshInflammatory Bowel Diseases
dc.subject.meshLiver Neoplasms
dc.subject.meshMice
dc.subject.meshMouth Neoplasms
dc.subject.meshNeoplasms
dc.subject.meshOxidative Stress
dc.titleOxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis.en
dc.typeArticleen
dc.identifier.journalBiological chemistryen
html.description.abstractInfection and chronic inflammation are proposed to contribute to carcinogenesis through inflammation-related mechanisms. Infection with hepatitis C virus, Helicobacter pylori and the liver fluke, Opisthorchis viverrini (OV), are important risk factors for hepatocellular carcinoma (HCC), gastric cancer and cholangiocarcinoma, respectively. Inflammatory bowel diseases (IBDs) and oral diseases, such as oral lichen planus (OLP) and leukoplakia, are associated with colon carcinogenesis and oral squamous cell carcinoma (OSCC), respectively. We performed a double immunofluorescence labeling study and found that nitrative and oxidative DNA lesion products, 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), were formed and inducible nitric oxide synthase (iNOS) was expressed in epithelial cells and inflammatory cells at the site of carcinogenesis in humans and animal models. Antibacterial, antiviral and antiparasitic drugs dramatically diminished the formation of these DNA lesion markers and iNOS expression. These results suggest that oxidative and nitrative DNA damage occurs at the sites of carcinogenesis, regardless of etiology. Therefore, it is considered that excessive amounts of reactive nitrogen species produced via iNOS during chronic inflammation may play a key role in carcinogenesis by causing DNA damage. On the basis of our results, we propose that 8-nitroguanine is a promising biomarker to evaluate the potential risk of inflammation-mediated carcinogenesis.


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