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Mol Med. 2007 Jul-Aug;13(7-8):350-5.

Intracellular zinc release, 12-lipoxygenase activation and MAPK dependent neuronal and oligodendroglial death.

Author information

1
Department of Anatomy, Physiology and Genetics and Program in Neuroscience, Uniformed Services University of the Health Sciences, Bethesda, Maryland 20814, USA. yzhang@usuhs.mil

Abstract

Zinc translocation from presynaptic nerve terminals to postsynaptic neurons has generally been considered the critical step leading to the accumulation of intracellular free zinc and subsequent neuronal injury. Recent evidence, however, strongly suggests that the liberation of zinc from intracellular stores upon oxidative and nitrative stimulation contributes significantly to the toxicity of this metal not only to neurons, but also to oligodendrocytes. The exact cell death signaling pathways triggered by zinc are beginning to be deciphered. In this review, we describe how the activation of 12-lipoxygenase and mitogen-activated protein kinase (MAPK) contribute to the toxicity of liberated zinc to neurons and oligodendrocytes.

PMID:
17622306
PMCID:
PMC1952666
DOI:
10.2119/2007–00042.Zhang
[Indexed for MEDLINE]
Free PMC Article

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