Apoptosis may underlie the pathology of zinc-deficient skin

Wilson, Dallas, Varigos, George and Ackland, Leigh 2006, Apoptosis may underlie the pathology of zinc-deficient skin, Immunology and cell biology, vol. 84, pp. 28-37, doi: 10.1111/j.1440-1711.2005.01391.x.

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Title Apoptosis may underlie the pathology of zinc-deficient skin
Author(s) Wilson, Dallas
Varigos, George
Ackland, LeighORCID iD for Ackland, Leigh orcid.org/0000-0002-7474-6556
Journal name Immunology and cell biology
Volume number 84
Start page 28
End page 37
Publisher University of Adelaide
Place of publication Adelaide, S.Aust.
Publication date 2006
ISSN 0818-9641
Keyword(s) apoptosis
zinc deficiency
Summary The trace element zinc is essential for the survival and function of all cells. Zinc deficiency, whether nutritional or genetic, is fatal if left untreated. The effects of zinc deficiency are particularly obvious in the skin, seen as an erythematous rash, scaly plaques, and ulcers. Electron microscopy reveals degenerative changes within keratinocytes. Despite the well-documented association between zinc deficiency and skin pathology, it is not clear which cellular processes are most sensitive to zinc deficiency and could account for the typical pathological features. We used the cultured HaCaT keratinocyte line to obtain insight into the cellular effects of zinc deficiency, as these cells show many characteristics of normal skin keratinocytes. Zinc deficiency was induced by growing cells in the presence of the zinc chelator, TPEN, or by growth in zinc-deficient medium. Growth of cells in zinc-deficient medium resulted in a 44% reduction of intracellular zinc levels and a 75% reduction in the activity of the zinc-dependent enzyme, 5'-nucleotidase, relative to the control cells. Over a period of 7 days of exposure to zinc-deficient conditions, no changes in cell viability and growth, or in the cytoskeletal and cell adhesion systems, were found in HaCaT cells. At 7 days, however, induction of apoptosis was indicated by the presence of DNA fragmentation and expression of active caspase-3 in cells. These results demonstrate that apoptosis is the earliest detectable cellular change induced by zinc deficiency in HaCaT keratinocytes. Our observations account for many of the features of zinc deficiency, including the presence of degenerate nuclei, chromatin aggregates and abnormal organization of keratin, that may represent the later stages of apoptosis. In summary, a major causal role for apoptosis in the pathology of zinc deficiency in the skin is proposed. This role is consistent with the previously unexplained diverse range of degenerative cellular changes seen at the ultrastructural level in zinc-deficient keratinocytes.
Notes Published online 19 December 2005
Language eng
DOI 10.1111/j.1440-1711.2005.01391.x
Field of Research 060405 Gene Expression (incl Microarray and other genome-wide approaches)
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2006, Australasian Society for Immunology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30003974

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