Role of GSTT1 deletion in DNA oxidative damage by exposure to polycyclic aromatic hydrocarbons in humans.

2.50
Hdl Handle:
http://hdl.handle.net/10146/24121
Title:
Role of GSTT1 deletion in DNA oxidative damage by exposure to polycyclic aromatic hydrocarbons in humans.
Authors:
Garte, Seymour; Taioli, Emanuela; Popov, Todor; Kalina, Ivan; Sram, Radim; Farmer, Peter
Abstract:
A useful approach for studies on the mechanisms of genetic variation in cancer susceptibility is to use intermediary biochemical endpoints with mechanistic relevance to the genes under study. We examined the effects of individual genotype at seven metabolic gene loci on a marker of oxidative DNA damage, 8-oxo-7,8-dihydro-2-deoxyguanosine, in people exposed to polycyclic aromatic hydrocarbons (PAH) from three Central European cities. The GSTT1 homozygous deletion variant was associated with a significant protective effect for exposure to total PAHs and to eight specific PAHs, although the magnitude and significance of the effect varied among these compounds. Categorical sensitivity analysis was used to determine that the frequency of the GSTT1 deletion was significantly higher in people who proved to be more resistant to the DNA damaging effects of PAH exposure than in people who were the most sensitive. There is a growing literature on the protective effect of GSTT1 deletion in both disease and intermediary endpoints related to environmental carcinogenesis. The mechanism for this effect might be related to specific PAH substrate specificities, or could be related to other functions of GSTT1 gene in oxidative stress induced damage pathways.
Citation:
Int. J. Cancer 2007, 120 (11):2499-2503
Journal:
International Journal of Cancer. Journal international du cancer
Issue Date:
1-Jun-2007
URI:
http://hdl.handle.net/10146/24121
DOI:
10.1002/ijc.22477
PubMed ID:
17330842
Additional Links:
http://www3.interscience.wiley.com/cgi-bin/abstract/114131920/ABSTRACT?CRETRY=1&SRETRY=0
Type:
Article
Language:
en
ISSN:
0020-7136
Sponsors:
Grant sponsor: European Commission (Quality of life and management of living resources program); Grant number: QLK4-CT-2000-00091; Grant sponsor: ECNIS project; Grant number: EU Contract 513943.
Appears in Collections:
Articles

Full metadata record

DC FieldValue Language
dc.contributor.authorGarte, Seymour-
dc.contributor.authorTaioli, Emanuela-
dc.contributor.authorPopov, Todor-
dc.contributor.authorKalina, Ivan-
dc.contributor.authorSram, Radim-
dc.contributor.authorFarmer, Peter-
dc.date.accessioned2008-04-24T11:40:59Z-
dc.date.available2008-04-24T11:40:59Z-
dc.date.issued2007-06-01-
dc.identifier.citationInt. J. Cancer 2007, 120 (11):2499-2503en
dc.identifier.issn0020-7136-
dc.identifier.pmid17330842-
dc.identifier.doi10.1002/ijc.22477-
dc.identifier.urihttp://hdl.handle.net/10146/24121-
dc.description.abstractA useful approach for studies on the mechanisms of genetic variation in cancer susceptibility is to use intermediary biochemical endpoints with mechanistic relevance to the genes under study. We examined the effects of individual genotype at seven metabolic gene loci on a marker of oxidative DNA damage, 8-oxo-7,8-dihydro-2-deoxyguanosine, in people exposed to polycyclic aromatic hydrocarbons (PAH) from three Central European cities. The GSTT1 homozygous deletion variant was associated with a significant protective effect for exposure to total PAHs and to eight specific PAHs, although the magnitude and significance of the effect varied among these compounds. Categorical sensitivity analysis was used to determine that the frequency of the GSTT1 deletion was significantly higher in people who proved to be more resistant to the DNA damaging effects of PAH exposure than in people who were the most sensitive. There is a growing literature on the protective effect of GSTT1 deletion in both disease and intermediary endpoints related to environmental carcinogenesis. The mechanism for this effect might be related to specific PAH substrate specificities, or could be related to other functions of GSTT1 gene in oxidative stress induced damage pathways.en
dc.description.sponsorshipGrant sponsor: European Commission (Quality of life and management of living resources program); Grant number: QLK4-CT-2000-00091; Grant sponsor: ECNIS project; Grant number: EU Contract 513943.en
dc.language.isoenen
dc.relation.urlhttp://www3.interscience.wiley.com/cgi-bin/abstract/114131920/ABSTRACT?CRETRY=1&SRETRY=0en
dc.subjectbiological markersen
dc.subjectsusceptibilityen
dc.subjectcohort studyen
dc.subject.meshDNA Damage-
dc.subject.meshGlutathione Transferase-
dc.subject.meshHumans-
dc.subject.meshOxidative Stress-
dc.subject.meshPolycyclic Compounds-
dc.titleRole of GSTT1 deletion in DNA oxidative damage by exposure to polycyclic aromatic hydrocarbons in humans.en
dc.typeArticleen
dc.identifier.journalInternational Journal of Cancer. Journal international du canceren

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