Zinc homeostasis in aging: two elusive faces of the same metal





E. Mocchegiani, L. Costarelli, R. Giacconi, C. Cipriano, E. Muti, M. Malavolta

Immunology Ctr. (Section: Nutrition, Immunity, Ageing) Res. Dept. INRCA, via Birarelli 8, 60121 Ancona, Italy.



Zinc is required for the catalytic, structural and regulatory functions of > 300 enzymes, including representatives from all six major functional classes. Moreover, zinc is also a structural cofactor for many proteins and transcription factors, including the ubiquitous zinc finger DNA binding proteins.

The relevance of proteins involved in zinc homeostasis has been particularly studied since the discovery of the zinc binding proteins called metallothioneins (MT). Despite the great interest aroused around these proteins, an unequivocally established biological function for MT has not yet been defined. What is firm is that MT bound zinc with high affinity but, at the same time, release free Zn ions in response to oxidative stress, suggesting an intriguing role for zinc, similar to that found for calcium as signal transducer. In other words zinc signals tells the cells to express "shield" and "protection" genes such as chaperones and MT and trigger the activation of intracellular "weapons", such as the CuZn-superoxide dismutase (SOD) enzyme, to fight oxidative stress. For instance, zinc deficiency prejudices immune functions, impairs cognitive performance and brain functions. Moreover, zinc deficiency is a common event in aging due to a reduced intake of this trace element and perhaps to the persistent stress induced overexpression of zinc-binding proteins such as MT. In contrast, zinc excess causes also detrimental effects probably due to the binding of zinc to metalloproteins that require other metals for their biological activities and to a massive activation of some zinc dependent enzymes, which, in turn, depletes intracellular energy stores. The influx of toxic amounts of zinc into degenerating neurons seems to be mainly responsible for the neurodegenerative process in transient forebrain ischemia, seizures and traumatic brain injury, and excessive amount of zinc may have a role in Alzheimer pathology. Therefore, it is not surprising that the cell uses sophisticated mechanisms to control the intracellular levels and movements of zinc. The age-related alteration of these mechanisms have been just begun to be studied and constitute a growing field of research in order to search for anti-aging targets. However, before developing these therapies it is necessary to better clarify the biology and biochemical features of these mechanisms with particular attention to aging, taking also carefully into account that what is of benefits during young/adult age may be detrimental in aging. New insight into the functionality of zinc homeostasis in aging may be acquired soon, with the application in aging research of specific fluorescent "zinc sensors", which localize into different intracellular compartments and stain specifically the amount of free plus "loosely bound" zinc.




Key words: zinc, zinc homeostasis, aging, metallothioneins







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