Serveur d'exploration Chloroquine

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Effect of chronic chloroquine administration on iron loading in the liver and reticuloendothelial system and on oxidative responses by the alveolar macrophages

Identifieur interne : 002675 ( Main/Exploration ); précédent : 002674; suivant : 002676

Effect of chronic chloroquine administration on iron loading in the liver and reticuloendothelial system and on oxidative responses by the alveolar macrophages

Auteurs : Rachida Legssyer [Belgique] ; Roberta J. Ward [Belgique] ; Robert R. Crichton [Belgique] ; Johan R. Boelaert [Belgique]

Source :

RBID : ISTEX:E442511253432CBB73B48DF3FA13AECC2585AC0E

Descripteurs français

English descriptors

Abstract

Abstract: The ability of chloroquine to alter iron loading in the liver, spleen, and alveolar macrophages was investigated in iron-loaded or -depleted rats. Chloroquine significantly reduced incorporation of iron into the liver, spleen, and alveolar macrophages of animals loaded in vivo with iron dextran. The ability of these macrophages to respond to oxidative stress was assayed by their capacity to release reactive nitrogen intermediates after lipopolysaccharide (LPS) stimulation. A significant reduction in nitrite release was observed in primary cultures of macrophages isolated from chloroquine/iron dextran-administered rats in comparison to macrophages lavaged from rats iron-loaded alone. Macrophages isolated from iron-deficient rats showed a significant increase in nitrite after LPS stimulation, whereas nitrite release in the macrophages lavaged from the rats which had also received chloroquine during the iron depletion regime was much lower. These results indicate that the use of agents which decrease the iron content and diminish the oxidative response of the cell to altered iron status may be of therapeutic value in patients with iron loading, particularly of the reticuloendothelial system.

Url:
DOI: 10.1016/S0006-2952(98)00368-2


Affiliations:


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Le document en format XML

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<term>Chloroquine</term>
<term>Digestive system</term>
<term>Free radical</term>
<term>Human</term>
<term>In vitro</term>
<term>Iron</term>
<term>Lipopolysaccharide</term>
<term>Liver</term>
<term>Macrophage</term>
<term>Nitrogen</term>
<term>Parasiticid</term>
<term>Pulmonary alveolus</term>
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<term>Respiratory system</term>
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<term>Antiparasitaire</term>
<term>Appareil digestif</term>
<term>Appareil respiratoire</term>
<term>Azote</term>
<term>Chloroquine</term>
<term>Fer</term>
<term>Foie</term>
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<term>In vitro</term>
<term>Lipopolyoside</term>
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<term>Chloroquine</term>
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<term>Iron depletion</term>
<term>Iron dextran</term>
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<term>Iron status</term>
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<term>Nitrite release</term>
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<term>Primary cultures</term>
<term>Rat</term>
<term>Reactive nitrogen intermediates</term>
<term>Receptor</term>
<term>Respiratory burst</term>
<term>Reticuloendothelial system</term>
<term>Rheumatoid arthritis</term>
<term>Significant increase</term>
<term>Significant reduction</term>
<term>Spleen</term>
<term>Tissue iron</term>
<term>Universite catholique</term>
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<div type="abstract" xml:lang="en">Abstract: The ability of chloroquine to alter iron loading in the liver, spleen, and alveolar macrophages was investigated in iron-loaded or -depleted rats. Chloroquine significantly reduced incorporation of iron into the liver, spleen, and alveolar macrophages of animals loaded in vivo with iron dextran. The ability of these macrophages to respond to oxidative stress was assayed by their capacity to release reactive nitrogen intermediates after lipopolysaccharide (LPS) stimulation. A significant reduction in nitrite release was observed in primary cultures of macrophages isolated from chloroquine/iron dextran-administered rats in comparison to macrophages lavaged from rats iron-loaded alone. Macrophages isolated from iron-deficient rats showed a significant increase in nitrite after LPS stimulation, whereas nitrite release in the macrophages lavaged from the rats which had also received chloroquine during the iron depletion regime was much lower. These results indicate that the use of agents which decrease the iron content and diminish the oxidative response of the cell to altered iron status may be of therapeutic value in patients with iron loading, particularly of the reticuloendothelial system.</div>
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