Long-term consequences of prenatal exposure to lead on brain development in rats

Neurosci Behav Physiol. 2008 Feb;38(2):145-9. doi: 10.1007/s11055-008-0021-3.

Abstract

Administration of singe doses of lead citrate (200 mg/kg) to pregnant rats (on day 18 of pregnancy) was followed by the appearance of destructive changes in brains at age 40 days, with cysts, foci of gliocyte proliferation, pyknotic neurons, and decreases in NADH and NADPH diaphorase activities in neocortical and hippocampal neurons. Decreases in the density of neurons in the cortex and decreases in cortical thickness were also observed. The intensity of free-radical oxidation in the cortex increased three-fold, along with a 3.9-fold increase in the concentration of lipid peroxides, providing evidence of oxidative stress. The possible mechanisms by which these alterations develop are analyzed.

MeSH terms

  • Animals
  • Brain / growth & development*
  • Brain / pathology*
  • Cell Proliferation / drug effects
  • Female
  • Free Radicals / metabolism
  • Hippocampus / growth & development
  • Hippocampus / pathology
  • Lead Poisoning, Nervous System / pathology*
  • Lipid Peroxides / metabolism
  • Luminescence
  • NADH, NADPH Oxidoreductases / metabolism
  • Neocortex / growth & development
  • Neocortex / pathology
  • Neurons / metabolism
  • Organ Size / physiology
  • Oxidative Stress / physiology
  • Pregnancy
  • Prenatal Exposure Delayed Effects / pathology*
  • RNA / biosynthesis
  • RNA / genetics
  • Rats

Substances

  • Free Radicals
  • Lipid Peroxides
  • RNA
  • NADH, NADPH Oxidoreductases