(Journal Article): Antisense evidence for nuclear factor-kappaB-dependent embryopathies initiated by phenytoin-enhanced oxidative stress.
 
Kennedy JC, Memet S, Wells PG (Faculty of Pharmacy, University of Toronto, 19 Russell St., Toronto, Ontario, Canada M5S 2S2.)
 
IN: Mol Pharmacol 2004; 66:404-412
Impact Factor(s) of Mol Pharmacol: 5.8 (2004), 5.65 (2003), 5.48 (2002), 5.297 (2001)

ABSTRACT: Endogenous and xenobiotic-enhanced oxidative stress may initiate embryonic death and birth defects via reactive oxygen species (ROS) signaling pathways involving nuclear transcription factor-kappaB (NF-kappaB). Using embryo culture and a transgenic mouse engineered with a NF-kappaB-dependent beta-galactosidase reporter gene, we employed NF-kappaB antisense oligonucleotide therapy to determine whether NF-kappaB signaling contributes to the embryopathic effects of the ROS-initiating teratogen phenytoin. Phenytoin selectively increased NF-kappaB activity in target tissues and caused embryopathies, both of which were blocked by NF-kappaB antisense oligonucleotides but not by sense and nonsense oligonucleotide controls. NF-kappaB signaling may therefore contribute to the mechanism of ROS-mediated embryopathies.

TYPE OF PUBLICATION: Original article

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