Effects of iron complexes on brain calcium homeostasis
Identifieur interne : 004C82 ( Main/Merge ); précédent : 004C81; suivant : 004C83Effects of iron complexes on brain calcium homeostasis
Auteurs : L. J. Anghileri [France] ; P. Thouvenot [France] ; A. Bertrand [France]Source :
- Annals of clinical and laboratory science [ 0091-7370 ] ; 1997.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Calcium.
English descriptors
- KwdEn :
Abstract
The effects of two physiological low molecular weight iron complexes, ferric lactate and ferric adenosine triphosphate (ATP) on brain Ca2+ homeostasis modification, have been studied in vitro and in vivo. In vitro ferric ATP complex shows a higher efficiency as modifier of Ca2+ homeostasis. This higher reactivity and the in vivo observed effect of increased brain uptake of iron from ferric lactate provoked by the presence of ATP, corroborate in vitro results showing an iron transfer from ferric lactate to ATP, as well as the mediator role of ATP in the iron-induced cellular Ca2+ homeostasis modification process. The possible role of this process in Parkinson's disease is discussed.
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Pascal:97-0299238Le document en format XML
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<term>Calcium</term>
<term>Cell culture</term>
<term>In vitro</term>
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<term>Iron complex</term>
<term>Mouse</term>
<term>Parkinson disease</term>
<term>Pathogenesis</term>
<term>Phosphocalcic homeostasis</term>
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<term>Homéostasie phosphocalcique</term>
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<front><div type="abstract" xml:lang="en">The effects of two physiological low molecular weight iron complexes, ferric lactate and ferric adenosine triphosphate (ATP) on brain Ca<sup>2+</sup>
homeostasis modification, have been studied in vitro and in vivo. In vitro ferric ATP complex shows a higher efficiency as modifier of Ca<sup>2+</sup>
homeostasis. This higher reactivity and the in vivo observed effect of increased brain uptake of iron from ferric lactate provoked by the presence of ATP, corroborate in vitro results showing an iron transfer from ferric lactate to ATP, as well as the mediator role of ATP in the iron-induced cellular Ca<sup>2+</sup>
homeostasis modification process. The possible role of this process in Parkinson's disease is discussed.</div>
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