Zinc: an overview

Abstract

Zn deficiency in humans is widespread throughout the world. It is more prevalent in areas where the population subsists on cereal proteins. Conditioned Zn deficiency is seen in many disease states. Its deficiency during growth periods results in growth failure and lack of gonadal development in males. Other effects of Zn deficiency include skin changes, poor appetite, mental lethargy, delayed wound healing, neurosensory disorders, and cell-mediated immune disorders. Severe Zn deficiency, as seen in acrodermatitis enteropathica (a genetic disorder), is fatal if Zn is not administered to these patients. A clinical diagnosis of marginal Zn deficiency in humans remains problematic. Assays of Zn in granulocytes and lymphocytes provide better diagnostic criteria for marginal Zn deficiency than plasma Zn. Approximately 300 enzymes are known to require Zn for their activities. Zn is required for DNA synthesis, cell division, and protein synthesis. Recently, we learned that Zn-finger proteins are involved in genetic expression of various growth factors and steroid receptors. We suspect that several hundred Zn-containing nucleoproteins are probably involved in gene expression of various proteins. Zn deficiency adversely affects lymphocyte proliferation. This may be related to the enzymatic role of Zn in DNA synthesis and cell division. Thymulin, a thymic hormone involved in T-lymphocyte maturation, is known to be Zn dependent and is adversely affected by Zn deficiency. Thus, an adverse effect of Zn deficiency may also be in lymphocyte differentiation and maturity. Zn deficiency is known to decrease interleukin 2 production by helper T lymphocytes, and abnormalities in T-lymphocyte subpopulations have been observed in Zn-deficient humans.(ABSTRACT TRUNCATED AT 250 WORDS)