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Biogerontology. 2006 Oct-Dec;7(5-6):307-14.

Oxidative stress and brain aging: is zinc the link?

Author information

1
Department of Neurology, Molecular Neurology Unit, CeSI-Center for Excellence on Aging, University G. d'Annunzio, Chieti, 66013, Italy.

Abstract

Zn(2+) dyshomeostasis has been strongly linked to neuronal injury in many neurological conditions. Toxic accumulation of intracellular free Zn(2+) ([Zn(2+)](i)) may result from either flux of the cation through glutamate receptor-associated channels, voltage-sensitive calcium channels, or Zn(2+)-sensitive membrane transporters. Injurious [Zn(2+)](i) rises can also result from release of the cation from intracellular sites such as metallothioneins (MTs) and mitochondria. Chronic inflammation and oxidative stress are hallmarks of aging. Zn(2+) homeostasis is affected by oxidative stress, which is a potent trigger for detrimental Zn(2+) release from MTs. Interestingly, Zn(2+) itself is a strong inducer of oxidative stress by promoting mitochondrial and extra-mitochondrial production of reactive oxygen species. In this review, we examine how Zn(2+) dyshomeostasis and oxidative stress might act synergistically to promote aging-related neurodegeneration.

PMID:
17028932
DOI:
10.1007/s10522-006-9045-7
[Indexed for MEDLINE]

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