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Subject: MD/chelator/iron
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Med Hypotheses 13: 153-60 (1984)[84190712]
Proposed treatment of Duchenne muscular dystrophy with desferrioxamine.
I. A. Clark
The primary disturbance in Duchenne muscular dystrophy (DMD) appears
to affect membrane function, and changes characteristic of
oxidant-induced damage occur in skeletal muscle and erythrocytes.
There is recent evidence that DMD is a functional tocopherol
deficiency, with reduced levels of the lipoprotein required to carry
tocopherol to tissues. This may explain the parallels between DMD and
dietary tocopherol deficiency. Thus DMD should follow the usual
experience of other examples of oxidative pathology, where the balance
between tocopherol, the main antioxidant in membrane lipids, and non
protein-bound iron, an important catalyst of reactions which produce
oxidizing free radicals, largely determines whether or not tissue
damage occurs. Desferrioxamine prevents oxidant damage in vitro and in
vivo by removing this iron, and may therefore be able to reverse the
muscle damage of DMD. Recent experience with this drug in long term
dialysis patients is consistent with this suggestion.
MeSH Terms:
* Animal
* Deferoxamine/therapeutic use
* Genes, Recessive
* Human
* Iron/metabolism
* Linkage (Genetics)
* Membrane Lipids/metabolism
* Muscles/metabolism
* Muscular Dystrophy/drug therapy
* Muscular Dystrophy/etiology
* Muscular Dystrophy/genetics
* Muscular Dystrophy, Animal/metabolism
* Oxidation-Reduction
* Support, Non-U.S. Gov't
* Vitamin E/metabolism
* Vitamin E Deficiency/complications
Substances:
* Iron
* Vitamin E
* Membrane Lipids
* Deferoxamine
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