Modulation of oxidative DNA damage repair by the diet, inflammation and neoplastic transformation.

2.50
Hdl Handle:
http://hdl.handle.net/10146/28007
Title:
Modulation of oxidative DNA damage repair by the diet, inflammation and neoplastic transformation.
Authors:
Tudek, B.; Swoboda, M.; Kowalczyk, P.; Olinski, R.
Abstract:
Oxidative DNA damage and DNA repair may mediate several cellular processes, like replication and transcription, mutagenesis and apoptosis and thus may be important for the organism development as well as its pathogenesis, including cancer. Activity of DNA repair enzymes can depend on many factors, such as gene polymorphism, mRNA and protein level, as well as enzymes activation and inhibition. Modulation of base excision repair pathway eliminating from DNA oxidatively formed lesions may be caused by the diet, inflammation and neoplastic transformation. Reactive oxygen species and some diet components induce transcription of several Base Excision Repair enzymes, e.g. major human AP-endonuclease, (APE1) and 8-oxoG-DNA glycosylase (OGG1). The carcinogenic process in human lung decreases repair activity for 8-oxoGin transcription independent manner, but increases repair activity of epsilon A and epsilon C, as measured in tumors and unchanged lung tissues of lung cancer patients. Thus, modulation of repair enzymes activities may be a cell response on their way to differentiation ot neoplastic transformation.
Citation:
J. Physiol. Pharmacol. 2006, 57 Suppl 7:33-49
Journal:
Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
Issue Date:
Nov-2006
URI:
http://hdl.handle.net/10146/28007
PubMed ID:
17228095
Additional Links:
http://www.jpp.krakow.pl/
Type:
Article
Language:
en
ISSN:
1899-1505
Sponsors:
This work was supported by Ministry of Scientific Research and Information Technology, grants No PBZ-KBN-093/P06/2003, 3 P05A 019. RO. was partly supported by ECNIS (European Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: “Food Quality and Safety” (Contract No 513943) and by a Foundation for Polish Science fellowship.
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorTudek, B.-
dc.contributor.authorSwoboda, M.-
dc.contributor.authorKowalczyk, P.-
dc.contributor.authorOlinski, R.-
dc.date.accessioned2008-05-26T11:39:03Z-
dc.date.available2008-05-26T11:39:03Z-
dc.date.issued2006-11-
dc.identifier.citationJ. Physiol. Pharmacol. 2006, 57 Suppl 7:33-49en
dc.identifier.issn1899-1505-
dc.identifier.pmid17228095-
dc.identifier.urihttp://hdl.handle.net/10146/28007-
dc.description.abstractOxidative DNA damage and DNA repair may mediate several cellular processes, like replication and transcription, mutagenesis and apoptosis and thus may be important for the organism development as well as its pathogenesis, including cancer. Activity of DNA repair enzymes can depend on many factors, such as gene polymorphism, mRNA and protein level, as well as enzymes activation and inhibition. Modulation of base excision repair pathway eliminating from DNA oxidatively formed lesions may be caused by the diet, inflammation and neoplastic transformation. Reactive oxygen species and some diet components induce transcription of several Base Excision Repair enzymes, e.g. major human AP-endonuclease, (APE1) and 8-oxoG-DNA glycosylase (OGG1). The carcinogenic process in human lung decreases repair activity for 8-oxoGin transcription independent manner, but increases repair activity of epsilon A and epsilon C, as measured in tumors and unchanged lung tissues of lung cancer patients. Thus, modulation of repair enzymes activities may be a cell response on their way to differentiation ot neoplastic transformation.en
dc.description.sponsorshipThis work was supported by Ministry of Scientific Research and Information Technology, grants No PBZ-KBN-093/P06/2003, 3 P05A 019. RO. was partly supported by ECNIS (European Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5: “Food Quality and Safety” (Contract No 513943) and by a Foundation for Polish Science fellowship.en
dc.language.isoenen
dc.relation.urlhttp://www.jpp.krakow.pl/en
dc.subject8-oxoguanineen
dc.subject1,N6-ethenoadenineen
dc.subject3, N4-ethenocytosineen
dc.subjectDNA repairen
dc.subjectOGG1 polymorphismen
dc.subjectgene expressionen
dc.subjectlung canceren
dc.subject.meshAnimals-
dc.subject.meshCell Transformation, Neoplastic-
dc.subject.meshDNA Damage-
dc.subject.meshDNA Repair-
dc.subject.meshDiet-
dc.subject.meshHumans-
dc.subject.meshInflammation-
dc.subject.meshLung Neoplasms-
dc.subject.meshOxidative Stress-
dc.titleModulation of oxidative DNA damage repair by the diet, inflammation and neoplastic transformation.en
dc.typeArticleen
dc.identifier.journalJournal of physiology and pharmacology : an official journal of the Polish Physiological Societyen

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