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Antisense evidence for nuclear factor-kappaB-dependent embryopathies initiated by phenytoin-enhanced oxidative stress.

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.