Primary and secondary zinc deficiency as factors contributing to abnormal central nervous system development

Carl L Keen, M. W. Taubeneck, G. P. Daston, M. Eric Gershwin, A. Ansari, J. M. Rogers

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Zinc deficiency is a recognized reproductive hazard. The most common cause of embryonic zinc deficiency is low maternal plasma concentrations of the element, which can occur via numerous routes including the following: inadequate dietary zinc intake, genetic abnormalities in zinc metabolism, disease and drug-induced changes in zinc uptake and excretion, and cytokine-induced changes in zinc metabolism. Evidence is presented that tumor necrosis factor-α is a cytokine whose teratogenicity may be attributed, in part, to its effect on zinc metabolism. The concept that cytokine-induced changes in zinc metabolism represents a common mechanism underlying the developmental toxicity of several diverse toxicants is discussed.

Original languageEnglish (US)
Pages (from-to)79-89
Number of pages11
JournalDevelopmental Brain Dysfunction
Volume8
Issue number2-3
StatePublished - 1995

Keywords

  • α-Hederin
  • Ethanol
  • Metallothionein
  • Pregnancy
  • Tumor necrosis factor-α
  • Urethane
  • Zinc

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

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