Inhibition of the growth of Plasmodium falciparum in vitro by covalent modification of hemoglobin
Identifieur interne : 003635 ( Main/Exploration ); précédent : 003634; suivant : 003636Inhibition of the growth of Plasmodium falciparum in vitro by covalent modification of hemoglobin
Auteurs : Timothy G. Geary [États-Unis] ; Edward J. Delaney [États-Unis] ; Irving M. Klotz [États-Unis] ; James B. Jensen [États-Unis]Source :
- Molecular & Biochemical Parasitology [ 0166-6851 ] ; 1983.
English descriptors
- Teeft :
- Acetaminophen, Acetylsalicylic acid, Antimalarial, Antimalarial activity, Antimalarial effects, Aspirin, Cathepsin, Chloroquine, Continuous exposure, Covalent, Covalent modification, Dbnf, Derivative, Dibromoaspirin, Diester, Diesters, Erythrocyte, Erythrocyte membrane, Erythrocytes pretreated, Falciparum, Final parasitemia, Fumarate, Hemoglobin, Human serum, Ibuprofen, Indomethacin, Initial exposure, Klotz, Malaria, Malaria parasites, Modification, Other experiments, Parasite, Parasite development, Parasite protease, Parasite proteases, Parasite survival, Parasitemia, Parasitol, Phenylbutazone, Plasmodium, Plasmodium falciparum, Plasmodiumfalciparum, Pretreated, Pretreated erythrocytes, Protease, Ring stage, Ring stage parasites, Rpmi, Schizonts, Succinate, Trophozoite.
Abstract
Abstract: Antimalarial effects might be expected from compounds that modify hemoglobin. Dibromoaspirin and bis(dibromosalicyl) diesters decrease gelation of hemoglobin by specific covalent modification (acetylation and crosslinking) of this protein but do not interfere with oxygen transport. These compounds were toxic to malaria parasites when continuously present in culture, as were drugs with similar pharmacological effects such as indomethacin, ibuprofen, and phenylbutazone. Aspirin and acetaminophen were much less effective. When erythrocytes were pretreated with these compounds prior to parasite exposure, only dibromoaspirin and dibromosalicyl diesters prevented parasite development. The modified hemoglobin was highly resistant to digestion by cathepsin D and parasite proteases, suggesting that covalent modifications of hemoglobin that do not disrupt normal hemoglobin function have antimalarial effects.
Url:
DOI: 10.1016/0166-6851(83)90057-9
Affiliations:
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Le document en format XML
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<term>Antimalarial effects</term>
<term>Aspirin</term>
<term>Cathepsin</term>
<term>Chloroquine</term>
<term>Continuous exposure</term>
<term>Covalent</term>
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<term>Malaria</term>
<term>Malaria parasites</term>
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<term>Other experiments</term>
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<term>Parasite development</term>
<term>Parasite protease</term>
<term>Parasite proteases</term>
<term>Parasite survival</term>
<term>Parasitemia</term>
<term>Parasitol</term>
<term>Phenylbutazone</term>
<term>Plasmodium</term>
<term>Plasmodium falciparum</term>
<term>Plasmodiumfalciparum</term>
<term>Pretreated</term>
<term>Pretreated erythrocytes</term>
<term>Protease</term>
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<front><div type="abstract" xml:lang="en">Abstract: Antimalarial effects might be expected from compounds that modify hemoglobin. Dibromoaspirin and bis(dibromosalicyl) diesters decrease gelation of hemoglobin by specific covalent modification (acetylation and crosslinking) of this protein but do not interfere with oxygen transport. These compounds were toxic to malaria parasites when continuously present in culture, as were drugs with similar pharmacological effects such as indomethacin, ibuprofen, and phenylbutazone. Aspirin and acetaminophen were much less effective. When erythrocytes were pretreated with these compounds prior to parasite exposure, only dibromoaspirin and dibromosalicyl diesters prevented parasite development. The modified hemoglobin was highly resistant to digestion by cathepsin D and parasite proteases, suggesting that covalent modifications of hemoglobin that do not disrupt normal hemoglobin function have antimalarial effects.</div>
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