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Zn 2+ , mitochondria and neuronal injury
Author(s) -
Sensi S. L.
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.s2.10_4.x
Subject(s) - mitochondrion , cytosol , homeostasis , microbiology and biotechnology , chemistry , membrane potential , biophysics , apoptosis , neuroscience , biology , biochemistry , enzyme
Zn 2+ critically contributes to the neural injury observed in epilepsy and transient global ischaemia. Mechanisms by which Zn 2+ exerts its potent neurotoxic effects are still largely unknown. We have recently suggested that an important factor could be Zn 2+ dependent disruption of mitochondrial function. As in the case of Ca 2+ , neuronal mitochondria take up Zn 2+ to restore Zn 2+ i homeostasis. However, mitochondrial Zn 2+ sequestration leads to potent mitochondrial dysfunction with prolonged loss of mitochondrial membrane potential and free radicals generation. Intriguingly, in direct comparison to Ca 2+ , Zn 2+ seems to induce these effects with a considerably greater degree of potency. These injurious, and likely necrotic, effects are particularly evident upon large (micromolar) Zn 2+ i rises. Conversely, submicromolar [Zn 2+ ] i increases promote release of pro‐apoptotic factors, suggesting that different degrees of cytosolic [Zn 2+ ] i rises might activate distinct injurious pathways.