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Related Concept Videos

Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

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Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

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Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
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Assessing Teratogenic Changes in a Zebrafish Model of Fetal Alcohol Exposure
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Epigenetic modifications in valproic acid-induced teratogenesis.

Emily W Y Tung1, Louise M Winn

  • 1Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario K7L3N6, Canada.

Toxicology and Applied Pharmacology
|August 14, 2010
PubMed
Summary

Maternal exposure to valproic acid (VPA) causes epigenetic changes in mouse embryos, including altered histone acetylation and methylation. These molecular alterations may explain how VPA leads to neural tube defects (NTDs) and congenital malformations.

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Area of Science:

  • Developmental biology
  • Epigenetics
  • Toxicology

Background:

  • In utero exposure to valproic acid (VPA), an anticonvulsant, increases the risk of neural tube defects (NTDs).
  • VPA is a known histone deacetylase inhibitor, suggesting potential epigenetic mechanisms underlying its teratogenic effects.
  • The precise molecular pathways linking VPA exposure to embryonic malformations remain largely unknown.

Purpose of the Study:

  • To investigate whether maternal VPA exposure induces epigenetic alterations in mouse embryos.
  • To determine if these epigenetic changes correlate with the teratogenic effects of VPA.

Main Methods:

  • Pregnant mice were administered a teratogenic dose of VPA on gestation day 9.0.
  • Embryos were collected at various time points (1, 3, 6, 24 hours post-injection).
  • Histone acetylation, histone methylation (H3K4, H3K9), and DNA methylation were assessed using Western blotting, immunohistochemistry, and cytosine extension assays.

Main Results:

  • VPA exposure significantly increased embryonic histone acetylation and altered histone methylation patterns (increased H3K4me, decreased H3K9me).
  • Immunohistochemistry confirmed increased histone acetylation and altered H3K9me/H3K4me in specific embryonic tissues like the neuroepithelium.
  • No significant changes in global or CpG island DNA methylation were detected.

Conclusions:

  • Maternal VPA exposure induces significant epigenetic modifications in early mouse embryos.
  • These VPA-induced epigenetic changes, particularly in histone acetylation and methylation, are potential contributors to VPA-associated teratogenesis and congenital malformations.