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Verfasst von:Nair, Jagadeesan [VerfasserIn]   i
 Fürstenberger, Gerhard [VerfasserIn]   i
 Bürger, Friederike [VerfasserIn]   i
 Marks, Friedrich [VerfasserIn]   i
 Bartsch, Helmut [VerfasserIn]   i
Titel:Promutagenic etheno−DNA adducts in multistage mouse skin carcinogenesis
Titelzusatz:Correlation with Lipoxygenase-Catalyzed Arachidonic Acid Metabolism
Verf.angabe:Jagadeesan Nair, Gerhard Fürstenberger, Friederike Bürger, Friedrich Marks, and Helmut Bartsch
E-Jahr:2000
Jahr:July 8, 2000
Umfang:7 S.
Fussnoten:Gesehen am 28.01.2021
Titel Quelle:Enthalten in: Chemical research in toxicology
Ort Quelle:New York, NY : ACS Publ., 1988
Jahr Quelle:2000
Band/Heft Quelle:13(2000), 8, Seite 703-709
ISSN Quelle:1520-5010
Abstract:Formation of the lipoxygenase-catalyzed metabolites of arachidonic acid, 8-hydroxyeicosatetraenoic acid (8-HETE) and 12-hydroxyeicosatetraenoic acid (12-HETE), and of the exocyclic DNA adducts 1,N6-ethenodeoxyadenosine (εdA) and 3,N4-ethenodeoxycytidine (εdC) was investigated in NMRI mouse skin carcinogenesis induced by 7,12-dimethylbenz[a]anthracene (DMBA) and promoted by 12-O-tetradecanoylphorbol-13-acetate (TPA). In reversible papillomas obtained after 20 weeks of TPA treatment, 15- and 68-fold higher contents of 8-HETE and 12-HETE, respectively, were observed, which were paralleled by 12- and 9-fold increased amounts of εdA and εdC, respectively. When compared to the level in vehicle-treated control skin, these elevations were statistically significant. In irreversible papillomas harvested 20 weeks after the last TPA treatment, the levels of HETEs and etheno−DNA adducts were found to be slightly reduced, as compared to those in reversible papillomas, but were still increased over control levels in age-matched mice. Comparison of mean group values by simple regression analysis showed a close positive correlation between HETE and etheno−DNA adduct levels. Consistent with the miscoding properties of εdA causing mainly A → T transversions, its increased formation in papillomas could thus contribute to this type of mutation in codon 61 of cHa-ras, shown to be a hallmark of DMBA-initiated and TPA-promoted mouse skin carcinogenesis. Although direct evidence that etheno adducts are derived from lipoxygenase-catalyzed metabolites of arachidonic acid is missing, our results implicate DNA damage by oxidative stress and lipid peroxidation as a cause of genetic instability observed at late stages of tumor promotion in mouse skin carcinogenesis.
DOI:doi:10.1021/tx000045d
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1021/tx000045d
 Volltext: https://pubs.acs.org/doi/10.1021/tx000045d
 DOI: https://doi.org/10.1021/tx000045d
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1745926577
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