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Titolo:
Evidence that a burst of DNA depurination in SENCAR mouse skin induces error-prone repair and forms mutations in the H-ras gene
Autore:
Chakravarti, D; Mailander, PC; Li, KM; Higginbotham, S; Zhang, HL; Gross, ML; Meza, JL; Cavalieri, EL; Rogan, EG;
Indirizzi:
Univ Nebraska, Med Ctr 986805, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA Univ Nebraska Omaha NE USA 68198 s Canc & Allied Dis, Omaha, NE 68198 USA Univ Nebraska, Med Ctr 986805, Dept Prevent & Societal Med, Omaha, NE 68198 USA Univ Nebraska Omaha NE USA 68198 vent & Societal Med, Omaha, NE 68198 USA Washington Univ, Dept Chem, St Louis, MO 63130 USA Washington Univ St Louis MO USA 63130 , Dept Chem, St Louis, MO 63130 USA
Titolo Testata:
ONCOGENE
fascicolo: 55, volume: 20, anno: 2001,
pagine: 7945 - 7953
SICI:
0950-9232(20011129)20:55<7945:ETABOD>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
BASE EXCISION-REPAIR; HAMSTER OVARY CELLS; DEOXYRIBONUCLEIC ACID; TUMOR INITIATION; IN-VITRO; ADDUCTS; GLYCOSYLASE; SITES; OVEREXPRESSION; IDENTIFICATION;
Keywords:
estradiol-3,4-quinone; depurinating adducts; abasic sites; DNA repair; mismatched heteroduplex; H-ras mutation in SENCAR mouse skin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Chakravarti, D Univ Nebraska, Med Ctr 986805, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA Univ Nebraska Omaha NE USA 68198 Dis, Omaha, NE 68198 USA
Citazione:
D. Chakravarti et al., "Evidence that a burst of DNA depurination in SENCAR mouse skin induces error-prone repair and forms mutations in the H-ras gene", ONCOGENE, 20(55), 2001, pp. 7945-7953

Abstract

Treatment of SENCAR mouse skin with dibenzo[a,l]pyrene results in abundantformation of abasic sites that undergo error-prone excision repair, forming oncogenic H-ras mutations in the early preneoplastic period. To examine whether the abundance of abasic sites causes repair infidelity, we treated SENCAR mouse skin with estradiol-3,4-quinone (E-2-3,4-Q) and determined adduct levels I h after treatment, as well as mutation spectra in the H-ras gene between 6 h and 3 days after treatment. E-2-3,4-Q formed predominantly (greater than or equal to 99%) the rapidly-depurinating 4-hydroxy estradiol (4-OHE2)-1-N3Ade adduct and the slower-depurinating 4-OHE2-1-N7Gua adduct. Between 6 h and 3 days, E-2-3,4-Q induced abundant A to G mutations in H-rasDNA, frequently in the context of a 3'-G residue. Using a T.G-DNA glycosylase (TDG)-PCR assay, we determined that the early A to G mutations (6 and 12 h) were in the form of G.T heteroduplexes, suggesting misrepair at A-specific depurination sites. Since G-specific mutations were infrequent in the spectra, it appears that the slow rate of depurination of the N7Gua adductsduring active repair may not generate a threshold level of G-specific abasic sites to affect repair fidelity. These results also suggest that E-2-3,4-Q, a suspected endogenous carcinogen, is a genotoxic compound and could cause mutations.

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Documento generato il 25/11/20 alle ore 18:53:07