Oxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis.

2.50
Hdl Handle:
http://hdl.handle.net/10146/59293
Title:
Oxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis.
Authors:
Kawanishi, Shosuke; Hiraku, Yusuke; Pinlaor, Somchai; Ma, Ning
Abstract:
Infection 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.
Citation:
Biol. Chem. 2006, 387 (4):365-372
Journal:
Biological chemistry
Issue Date:
Apr-2006
URI:
http://hdl.handle.net/10146/59293
DOI:
10.1515/BC.2006.049
PubMed ID:
16606333
Additional Links:
http://www.reference-global.com/doi/abs/10.1515/BC.2006.049
Type:
Article
Language:
en
Description:
KEYWORDS 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.
ISSN:
1431-6730
Appears in Collections:
Articles with annotation

Full metadata record

DC FieldValue Language
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.en
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

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