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 language||English (US)|
|Number of pages||11|
|Journal||Developmental Brain Dysfunction|
|State||Published - 1995|
- Tumor necrosis factor-α
ASJC Scopus subject areas
- Clinical Neurology