Chelation of mitochondrial iron prevents seizure-induced mitochondrial
dysfunction and neuronal injury.
liang LP, Jarrett SG, Patel M
J Neurosci 2008 Nov 5; 28(45):11550-6.
Chelatable iron is an im****tant catalyst for the initiation and
propagation of free radical reactions and implicated in the
pathogenesis of diverse neuronal disorders. Studies in our laboratory
have shown that mitochondria are the principal source of reactive
oxygen species production after status epilepticus (SE).
We asked whether SE modulates mitochondrial iron levels by two
independent methods and whether consequent mitochondrial dysfunction
and neuronal injury could be ameliorated with a cell-permeable iron
chelator.
Kainate-induced SE resulted in a time-dependent increase in chelatable
iron in mitochondrial but not cytosolic fractions of the rat
hippocampus.
Systemically administered N,N'-bis (2-hydroxybenzyl) ethylenediamine-
N,N'-diacetic acid (HBED), a synthetic iron chelator, ameliorated SE-
induced changes in chelatable iron, mitochondrial oxidative stress (8-
hydroxy-2' deoxyguanosine and glutathione depletion), mitochondrial
DNA integrity and hippocampal cell loss. Measurement of brain HBED
levels after systemic administration confirmed its penetration in
hippocampal mitochondria.
These results suggest a role for mitochondrial iron in the
pathogenesis of SE-induced brain damage and subcellular iron chelation
as a novel therapeutic approach for its management.
The Journal of neuroscience : the official journal of the Society for
Neuroscience [J Neurosci]
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