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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2009-8-27
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pubmed:abstractText |
Antiretroviral protease inhibitors significantly potentiated the sensitivity of chloroquine-resistant malaria parasites to the antimalarial drug in vitro and in vivo. Ritonavir was found to be potent in potentiating CQ antimalarial activities in both -resistant and -sensitive lines. The mechanism by which the APIs modulate the CQ resistance in malaria parasites was further investigated. CQ-resistant parasites showed increased intracellular glutathione levels in comparison with the CQ-sensitive parasites. Treatment with APIs significantly reduced the levels of GSH and glutathione S-transferase activities in CQ-resistant parasites. Ritonavir also decreased glutathione reductase activities and glutathione peroxidase activities in CQ-resistant parasite line. Taken together, these results demonstrate that parasite GSH and GST may play an important role in CQ resistance and APIs are able to enhance the sensitivity of CQ-resistant malaria parasite to the drug by influencing the levels of GSH and the activities of the related enzymes.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Retroviral Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antimalarials,
http://linkedlifedata.com/resource/pubmed/chemical/Chloroquine,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Reductase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Transferase,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Protease Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Nelfinavir,
http://linkedlifedata.com/resource/pubmed/chemical/Ritonavir,
http://linkedlifedata.com/resource/pubmed/chemical/Saquinavir
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1090-2449
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
123
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
122-7
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pubmed:meshHeading |
pubmed-meshheading:19538959-Animals,
pubmed-meshheading:19538959-Anti-Retroviral Agents,
pubmed-meshheading:19538959-Antimalarials,
pubmed-meshheading:19538959-Chloroquine,
pubmed-meshheading:19538959-Drug Resistance,
pubmed-meshheading:19538959-Drug Synergism,
pubmed-meshheading:19538959-Female,
pubmed-meshheading:19538959-Glutathione,
pubmed-meshheading:19538959-Glutathione Peroxidase,
pubmed-meshheading:19538959-Glutathione Reductase,
pubmed-meshheading:19538959-Glutathione Transferase,
pubmed-meshheading:19538959-HIV Protease Inhibitors,
pubmed-meshheading:19538959-Inhibitory Concentration 50,
pubmed-meshheading:19538959-Malaria,
pubmed-meshheading:19538959-Mice,
pubmed-meshheading:19538959-Nelfinavir,
pubmed-meshheading:19538959-Plasmodium chabaudi,
pubmed-meshheading:19538959-Plasmodium falciparum,
pubmed-meshheading:19538959-Ritonavir,
pubmed-meshheading:19538959-Saquinavir
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pubmed:year |
2009
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pubmed:articleTitle |
Antiretroviral protease inhibitors potentiate chloroquine antimalarial activity in malaria parasites by regulating intracellular glutathione metabolism.
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pubmed:affiliation |
Center for Infection and Immunity, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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