The role of zinc in wound healing. Adv Wound Care

Geriatric and Long Term Care Services, Ross Products Division, Abbott Laboratories, Columbus, OH, USA.
Advances in wound care: the journal for prevention and healing 05/1999; 12(3):137-8.
Source: PubMed


Zinc deficiency has been associated with delayed wound healing. Because zinc deficiency may be common in the United States, foods rich in zinc, as well as all other essential nutrients, should be promoted in the diet of patients who are malnourished or at risk for malnutrition.

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    • "Zinc is an essential trace element that is involved in numerous cellular enzymatic reactions and gene regulation through the modulation of several transcription factors [1]. Zinc deficiency is associated with diverse disorders, such as impaired immunity [2], retarded growth, brain development disorders and delayed wound healing [3] [4]. In adults, zinc deficiency has been associated with retarded skeletal development and development of osteoporosis [5] [6]. "
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    ABSTRACT: Changes in extracellular zinc concentration participate in modulating fundamental cellular processes such as proliferation, secretion, and ion transport in a mechanism that is not well understood. Here, we show that a micromolar concentration of extracellular zinc triggers a massive release of calcium from thapsigargin-sensitive intracellular pools in the colonocytic cell line HT29. Calcium release was blocked by a phospholipase-C inhibitor, indicating that formation of inositol 1,4,5-triphosphate is required for zinc-dependent calcium release. Zinc influx was not observed, indicating that extracellular zinc triggered the release. The Ca(i)2+ release was zinc specific and could not be triggered by other heavy metals. Furthermore, zinc failed to activate the Ca(2+)-sensing receptor heterologously expressed in HEK293 cells. The zinc-induced Ca(i)2+ rise stimulated the activity of the Na(+)/H(+) exchanger in HT29 cells. Our results indicate that a previously uncharacterized extracellular, G protein-coupled, Zn(2+)-sensing receptor is functional in colonocytes. Because Ca(i)2+ rise is known to regulate key cellular and signal-transduction processes, the zinc-sensing receptor may provide the missing link between extracellular zinc concentration changes and the regulation of cellular processes.
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