Deficient DNA repair exacerbates ethanol-initiated DNA oxidation and embryopathies in ogg1 knockout mice: gender risk and protection by a free radical spin trapping agent

Reactive oxygen species (ROS) have been implicated in the teratogenicity of alcohol (ethanol, EtOH). To determine the involvement of embryonic oxidative DNA damage, DNA repair-deficient oxoguanine glycosylase 1 ( ogg1 ) knockout embryos were exposed in culture to EtOH (2 or 4 mg/ml), with or without...

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Veröffentlicht in:Archives of toxicology 2016-02, Vol.90 (2), p.415-425
Hauptverfasser: Miller-Pinsler, Lutfiya, Wells, Peter G.
Format: Artikel
Sprache:eng
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Zusammenfassung:Reactive oxygen species (ROS) have been implicated in the teratogenicity of alcohol (ethanol, EtOH). To determine the involvement of embryonic oxidative DNA damage, DNA repair-deficient oxoguanine glycosylase 1 ( ogg1 ) knockout embryos were exposed in culture to EtOH (2 or 4 mg/ml), with or without pretreatment with the free radical spin trap phenylbutylnitrone (PBN) (0.125 mM). Visceral yolk sacs were used to genotype embryos for DNA repair status and gender. EtOH caused a concentration-dependent decrease in anterior neuropore closure (ANPC), somite development, turning, crown–rump length (CRL), yolk sac diameter (YSD) and head length (HL) ( p  
ISSN:0340-5761
1432-0738
DOI:10.1007/s00204-014-1397-1