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Effect of developmental dioxin exposure on methylation and expression of specific imprinted genes in mice

Emmanuel Somm1, Christelle Stouder, Ariane Paoloni-Giacobino

  • 1Division of Development and Growth, Department of Paediatrics, University of Geneva Medical School, 1211 Geneva 14, Switzerland. Emmanuel.Somm@unige.ch

Reproductive Toxicology (Elmsford, N.Y.)
|November 13, 2012
PubMed

Insights

Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) during pregnancy impacts male offspring. TCDD altered imprinted gene expression in sperm, muscle, and liver, but not always via DNA methylation changes.

Area of Science:

  • Environmental Toxicology
  • Reproductive Biology
  • Epigenetics

Background:

  • 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent endocrine disruptor.
  • TCDD exposure is linked to adverse effects on the human reproductive system.

Purpose of the Study:

  • To investigate the impact of prenatal TCDD exposure on imprinted gene expression and DNA methylation in male offspring.
  • To analyze the effects on Snrpn, Peg3, and Igf2r genes in sperm, skeletal muscle, and liver.

Main Methods:

  • Pregnant mice were administered TCDD at doses of 2-10 ng/kg/day.
  • Analysis of DNA methylation and mRNA expression of specific imprinted genes (Snrpn, Peg3, Igf2r) and Air ncRNA.
  • Tissues analyzed included sperm, skeletal muscle, and liver.

Main Results:

  • TCDD (10 ng/kg/day) reduced sperm count in male offspring.
  • Prenatal TCDD exposure increased mRNA expression of Snrpn, Peg3, Igf2r, and Air ncRNA in sperm without altering methylation.
  • In muscle and liver, TCDD (10 ng/kg/day) increased methylation and decreased Igf2r mRNA expression.

Conclusions:

  • TCDD robustly affects imprinted gene mRNA expression in sperm, muscle, and liver.
  • These gene expression changes are not consistently mediated by alterations in DNA methylation.
  • TCDD poses a significant risk to reproductive health and epigenetic regulation in offspring.

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