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Neuroprotection of zinc against apoptotic cell death in model of anoxia in vitro
Author(s) -
Nagańska E.,
Matyja E.,
Zielińska M.,
Gębarowska J.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.27.x
Subject(s) - neuroprotection , hippocampal formation , programmed cell death , apoptosis , neuroscience , in vitro , hippocampus , cell damage , biology , pharmacology , chemistry , microbiology and biotechnology , biochemistry
Zinc is the trace element considered the one of the etiological agents involved in nerve cell damage in certain human neurodegenerative disorders. Growing evidence indicates the diverse effect of zinc ions, associated with its neuroprotective and neurotoxic abilities. We examined the effect of zinc on the evolution of anoxia‐induced neuronal injury in the organotypic cultures of rat hippocampus. The cultures had been pretreated with ZnCl 2 (25–500 μ m ) 30 min prior anoxia. The ultrastructural findings documented dose‐dependent ability of Zn to reduce anoxia‐induced neuronal changes in hippocampal neurones in vitro . The significant neuroprotection involved the development of late apoptotic changes, whereas the early necrotic anoxia‐induced neuronal injury was not significantly reduced. However, the quite‐well preserved pyramidal neurones displayed the mitochondrial abnormalities, reflecting the combined neuroprotective and neurotoxic Zn properties.