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 : 002676Effect 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 :
- Biochemical Pharmacology [ 0006-2952 ] ; 1999.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Animal, Antimalarial, Chloroquine, Digestive system, Free radical, Human, In vitro, Iron, Lipopolysaccharide, Liver, Macrophage, Nitrogen, Parasiticid, Pulmonary alveolus, Rat, Respiratory system, Reticuloendothelial system, Spleen, Superoxide dismutase, iron loading, iron depletion, chloroquine, alveolar macrophages.
- Teeft :
- Acidic organelles, Alveolar macrophages, Antimicrob agents chemother, Biochem pharmacol, Boelaert, Bronchoalveolar macrophages, Chloroquine, Chloroquine administration, Chronic chloroquine administration, Clin, Comparable changes, Control rats, Cryptococcus neoformans infection, Dextran, Elsevier science, Haematological parameters, Histoplasma capsulatum, Hydrogen peroxide, Inos expression, Intracellular, Intracellular multiplication, Intracellular pathogens, Intracellular trafficking, Iron content, Iron depletion, Iron dextran, Iron loading, Iron metabolism, Iron overload, Iron status, Iron uptake, Legionella pneumophila, Macrophage, Macrophages lavaged, Murine macrophages, Murine model, Nitric, Nitric oxide, Nitric oxide synthase activity, Nitrite release, Oxidative stress, Pathway, Phagocytic cells, Present study, Primary cultures, Rat, Reactive nitrogen intermediates, Receptor, Respiratory burst, Reticuloendothelial system, Rheumatoid arthritis, Significant increase, Significant reduction, Spleen, Tissue iron, Universite catholique, Vifor pharmaceuticals, Vivo stimulation, Vivo studies.
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:
- Belgique
- Province du Brabant wallon, Région wallonne
- Louvain-la-Neuve
- Université catholique de Louvain
Links toward previous steps (curation, corpus...)
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Le document en format XML
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<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>
<term>Rat</term>
<term>Respiratory system</term>
<term>Reticuloendothelial system</term>
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<term>Appareil respiratoire</term>
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<term>Chloroquine</term>
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<term>Macrophage</term>
<term>Radical libre</term>
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<term>Système réticuloendothélial</term>
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<term>Chloroquine</term>
<term>Chloroquine administration</term>
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<term>Iron status</term>
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<front><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>
</front>
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