Lipoic acid and acetyl-carnitine reverse iron-induced oxidative stress

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Offline Andy Battaglia

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Pat Girondi sent this article out today, along with a reminder to buy his CDs at cdbaby.com. The proceeds from every CD sold go to fund a cure for orphan diseases, especially thalassemia. http://www.cdbaby.com/cd/patg3#

The article is attached as a pdf file. pdf files can be read with the free Adobe Acrobat Reader. This can be safely downloaded at
http://get.adobe.com/reader/

The conclusion of the article.

Quote
These results suggest that LA (Lipoic acid) is a potent antioxidant in
the presence of excess iron, and its effect is further
enhanced by the addition of ALCAR (acetyl-carnitine). Antioxidant treatment
with these compounds may reduce oxidation of
biomolecules and produce clinical benefits in patients

with iron overload.

I want to also point out that iron is NOT the ONLY cause of oxidative stress in the body and that antioxidants are important for numerous reasons. The hemolysis itself which takes place in thalassemia, is another major source of oxidative stresses.
Andy

All we are saying is give thals a chance.

Re: Lipoic acid and acetyl-carnitine reverse iron-induced oxidative stress
« Reply #1 on: January 03, 2010, 05:19:28 AM »
The hemolysis itself which takes place in thalassemia, is another major source of oxidative stresses.

Could lipoic acid BE preventing this hemolysis since it is an iron chelator ?

Intraerythrocytic Iron Chelation: A New Therapy for Thalassemia?
Mark D. Scott a
a Center for Immunology and Microbial Disease,
Albany Medical College, Albany, NY
Hematology, Volume 6, Issue 1 July 2001 , pages 73 - 89
Subject: Hematology;


Abstract
Thalassemic red blood cells (RBC) are characterized by
alterations in globin chain stability that result in
the release of redox-active iron within the RBC.
This iron, via a self-propagating and self-amplifying
reaction, destabilizes additional hemoglobin (hence,
releasing more iron) and causes significant oxidant
damage to other cellular components.
To attenuate this iron-mediated damage pharmacologically,
an intraerythrocytic iron chelation shuttle system is
proposed.
The iron shuttle system consists of low affinity, RBC
permeable, iron-binding agents which enter the cell, bind
iron, diffuse out, and hand-off the iron to a high affinity,
RBC-impermeable, high molecular weight starch derivative of
desferrioxamine (S-DFO).
It is proposed that interruption of the iron-dependent damage
via intraerythrocytic iron chelation results in improved RBC
survival and may obviate the need for the initiation of
transfusion therapy in some patients.
Putative shuttle agents include 2,2'-bipyridyl,
2,3-dihydroxybenzoic acid (2,3-DHB),
N,N-bis(2-hydroxybenzyl)ethylene-diamine-N,N-diacetic acid,
and pyridoxal isonico-tinoyl hydrazone.
The proposed nonpermeable terminal chelator is a high molecular
weight starch derivative of desferrioxamine that exhibits
prolonged vascular survival (up to 7 days) and very
significantly reduced toxicity relative to unmodified
desferrioxamine.
As is discussed, in vitro data demonstrate that a two component
iron shuttle system effectively slows iron-driven oxidative
damage improving the viability of model thalassemic RBC.
Further in vivo studies may prove that the intraerythrocytic
iron chelation shuttle system may have therapeutic potential
in the treatment of thalassemia.
Keywords: Thalassemia; red blood cell; iron; chelator

 

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