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Lipid Remodeling in Mouse SR-B1-Deficient Embryos with Oxidative Stress-Associated Neural Tube Defects.

Alonso Quiroz1, Nicolás Santander2, Greene D E Nicolás3

  • 1Ph.D. Program in Medical Science, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago 8331150, Chile.

Antioxidants (Basel, Switzerland)
|May 27, 2026
PubMed
Summary

Maternal vitamin E supplementation prevents neural tube defects in mice lacking Scavenger Receptor Class B Type 1. This study links embryonic oxidative stress and altered lipid metabolism, particularly phospholipid remodeling, to these defects.

Keywords:
SR-B1lipidomicsneural tube defectsoxidative stresstranscriptomics

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Area of Science:

  • Developmental Biology
  • Biochemistry
  • Nutritional Science

Background:

  • Neural tube defects (NTD) are congenital malformations impacting brain and spine development.
  • Scavenger Receptor Class B Type 1 (SR-B1) deficient mouse embryos show increased NTD incidence, linked to vitamin E deficiency and oxidative stress.

Purpose of the Study:

  • To investigate the link between oxidative stress, lipid metabolism, and NTD in SR-B1 deficient embryos.
  • To explore the role of phospholipid remodeling in NTD susceptibility.

Main Methods:

  • Shotgun lipidomics to analyze fatty acid distribution and lipid species.
  • Transcriptomic analysis to identify gene expression changes.
  • Assessment of lipoperoxidative damage markers in embryos.

Main Results:

  • SR-B1 KO embryos exhibit elevated lipoperoxidative damage markers.
  • Significant alterations in fatty acid composition, phospholipid levels (reduced phosphatidylcholine, increased lysophosphatidylcholine), and triacylglyceride storage were observed.
  • Upregulation of genes involved in phospholipid synthesis and remodeling was identified.

Conclusions:

  • Oxidative stress contributes to NTD in SR-B1 KO embryos.
  • Disruptions in embryonic lipid metabolism, specifically phospholipid remodeling, are linked to NTD susceptibility.
  • Maternal vitamin E supplementation ameliorates NTD by normalizing oxidative stress and lipid homeostasis.