Abstract
The essentiality of zinc for humans was recognized in 1963. It is now evident that nutritional deficiency of zinc in human populations throughout the developing world is common. The major factor responsible for this deficiency is the consumption of mainly cereal proteins rich in phytate. The clinical manifestations of zinc deficiency include growth retardation and male hypogonadism in the adolescents, rough skin, poor appetite, mental lethargy, delayed wound healing, cell‐mediated immune dysfunctions, and abnormal neurosensory disorders. A conditioned deficiency of zinc has been observed in many diseased states. In this work I have summarized our current knowledge concerning the molecular mechanisms of zinc action on T helper cells. Our studies showed that in zinc‐deficient HUT‐78 cells, phosphorylated IκB and Iκk, ubiquitinated IκB, and binding of nuclear factor (NF)‐κB to DNA were significantly decreased. Zinc increased the translocation of NF‐κB from cytosol to nucleus. These data show that zinc plays an important role in the activation of NF‐κB in HUT‐78 cells. We showed a significant effect of zinc on gene expression of interleukin (IL)‐2 and IL‐2 receptors α and β. We also showed that a decrease in gene expression of IL‐2 and its receptors in zinc‐deficient HUT‐78 cells may be the result of decreased activation of NF‐κB in zinc‐deficient cells. J. Trace Elem. Exp. Med. 16:139–163, 2003. © 2003 Wiley‐Liss, Inc.