delocalization of iron / seizures / status epilepticus

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doe - 11 Nov 2004 18:16 GMT

This study give even more credence to the fact .. iron .. free iron .. causes
.. epilepsy ..

Evidenced in animals in which iron is introduced to induce an animal model of
epilepsy ..

J Appl Toxicol. 2001 Dec;21 Suppl 1:S87-94. Related Articles, Links

Soman-induced seizures: limbic activity, oxidative stress and neuroprotective
proteins.

Pazdernik TL, Emerson MR, Cross R, Nelson SR, Samson FE.

Ralph L. Smith Research Center, University of Kansas Medical Center, Kansas
City, KS 66160, USA. tpazdern@kumc.edu

Soman, a potent acetylcholinesterase inhibitor, induces status epilepticus in
rats followed by conspicuous neuropathology, most prominent in piriform cortex
and the CA3 region of the hippocampus. Cholinergic seizures originate in
striatal-nigral pathways and with fast-acting agents (soman) rapidly spread to
limbic related areas and finally culminate in a full-blown status epilepticus.
This leads to neurochemical changes, some of which may be neuroprotective
whereas others may cause brain damage. Pretreatment with lithium sensitizes the
brain to cholinergic seizures. Likewise, other agents that increase limbic
hyperactivity may sensitize the brain to cholinergic agents. The hyperactivity
associated with the seizure state leads to an increase in intracellular
calcium, cellular edema and metal delocalization producing an oxidative stress.
These changes induce the synthesis of stress-related proteins such as heat
shock proteins, metallothioneins and heme oxygenases. We show that
soman-induced seizures cause a depletion in tissue glutathione and an increase
in tissue 'catalytic' iron, metallothioneins and heme oxygenase-1. The
oxidative stress induces the synthesis of stress-related proteins, which are
indicators of 'stress' and possibly provide neuroprotection. These findings
suggest that delocalization of iron may catalyze Fenton-like reactions, causing
progressive cellular damage via free radical products. Copyright 2001 John
Wiley & Sons, Ltd.

PMID: 11920927 [PubMed - indexed for MEDLINE]

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markd@toad-net.com - 11 Nov 2004 19:11 GMT

"This study give even more credence to the fact .. iron .. free iron ..
causes
.. epilepsy .."

No, it illustrates but another blow against the iron causes all disease
thesis. What it shows is that free iron is caused by seasures, it it is
an end product, is a dynamic interaction and a case of chicken and egg; it
says nothing about the "cause" of this disorder, only it's effects. Why
don't all people with "iron" have this disorder? Here is the core of the
process; note that free iron comes in as the tail, not the dog:

"The hyperactivity associated with the seizure state leads to an
increase in intracellular calcium, cellular edema and metal
delocalization producing an oxidative stress. These changes induce the
synthesis of stress-related proteins such as heat shock proteins,
metallothioneins and heme oxygenases. We show that soman-induced
seizures cause a depletion in tissue glutathione and an increase in
tissue 'catalytic' iron, metallothioneins and heme oxygenase-1. The
oxidative stress induces the synthesis of stress-related proteins,
which aresuggest that delocalization of iron may catalyze Fenton-like
reactions, causing progressive cellular damage via free radical
products."

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