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Piorczynski TB, Lapehn S, Ringer KP, et al. NRF2 activation inhibits valproic acid-induced neural tube defects in mice. Neurotoxicol Teratol. 2021;89:107039doi: 10.1016/j.ntt.2021.107039.
Piorczynski, T. B., Lapehn, S., Ringer, K. P., Allen, S. A., Johnson, G. A., Call, K., Lucas, S. M., Harris, C., & Hansen, J. M. (2021). NRF2 activation inhibits valproic acid-induced neural tube defects in mice. Neurotoxicology and teratology, 89107039. https://doi.org/10.1016/j.ntt.2021.107039
Piorczynski, Ted B, et al. "NRF2 activation inhibits valproic acid-induced neural tube defects in mice." Neurotoxicology and teratology vol. 89 (2021): 107039. doi: https://doi.org/10.1016/j.ntt.2021.107039
Piorczynski TB, Lapehn S, Ringer KP, Allen SA, Johnson GA, Call K, Lucas SM, Harris C, Hansen JM. NRF2 activation inhibits valproic acid-induced neural tube defects in mice. Neurotoxicol Teratol. 2021 Oct 29;89:107039. doi: 10.1016/j.ntt.2021.107039. Epub 2021 Oct 29. PMID: 34737154.
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Neurotoxicol Teratol. 2021 Oct 29;89:107039. doi: 10.1016/j.ntt.2021.107039. Epub 2021 Oct 29.

NRF2 activation inhibits valproic acid-induced neural tube defects in mice.

Neurotoxicology and teratology

Ted B Piorczynski, Samantha Lapehn, Kelsey P Ringer, Spencer A Allen, Garett A Johnson, Krista Call, S Marc Lucas, Craig Harris, Jason M Hansen

Affiliations

  1. Department of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
  2. Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109, USA.
  3. Department of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA. Electronic address: [email protected].

PMID: 34737154 DOI: 10.1016/j.ntt.2021.107039

Abstract

Valproic acid (VPA) is a widely prescribed medication that has traditionally been used to treat epilepsy, yet embryonic exposure to VPA increases the risk of the fetus developing neural tube defects (NTDs). While the mechanism by which VPA causes NTDs is unknown, we hypothesize that VPA causes dysmorphogenesis through the disruption of redox-sensitive signaling pathways that are critical for proper embryonic development, and that protection from the redox disruption may decrease the prevalence of NTDs. Time-bred CD-1 mice were treated with 3H-1,2-dithiole-3-thione (D3T), an inducer of nuclear factor erythroid 2-related factor 2 (NRF2)-a transcription factor that activates the intracellular antioxidant response to prevent redox disruptions. Embryos were then collected for whole embryo culture and subsequently treated with VPA in vitro. The glutathione (GSH)/glutathione disulfide (GSSG) redox potential (E

Copyright © 2021 Elsevier Inc. All rights reserved.

Keywords: Embryogenesis; Glutathione; NRF2; Neural tube defects; Valproic acid

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