Abstract
Zinc is essential for human health, and its deficiency in human beings results in growth failure, immune disorders affecting Th1 functions, decreased interleukin-2 (IL-2) production, and cognitive impairment. Nearly 2000 transcription factors require zinc for their structural integrity; however, it is not known whether cellular zinc deficiency results in any change in activation of any of the transcription factors. Inasmuch as NF-κB binds to the promoter enhancer area of IL-2 and IL-2Rα genes, we investigated the effect of zinc deficiency on activation of NF-κB and its binding to DNA in HUT-78, a Th0 malignant human lymphoblastoid cell line. We show here for the first time that in zinc-deficient HUT-78 cells, phosphorylated IκB, and IKK, ubiquitinated IκB and binding of NF-κB to DNA were all significantly decreased. Zinc increased the translocation of NF-κB from cytosol to nucleus. We also demonstrate that the binding of recombinant NF-κB (p50)2 to DNA in HUT-78 cells was zinc specific. We conclude that zinc plays an important role in the activation of NF-κB in HUT-78 cells. (J Lab Clin Med 2001;138:250-6)
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