Open AccessEffect of calmodulin inhibitors on viability and mitochondrial potential of Plasmodium falciparum in culture
Author(s) -
Timothy G. Geary,
Alan A. Divo,
James B. Jensen
Publication year - 1986
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.30.5.785
Subject(s) - calmodulin , trifluoperazine , hypoxanthine , plasmodium falciparum , protozoa , rhodamine 123 , biology , biochemistry , mitochondrion , chlorpromazine , promethazine , microbiology and biotechnology , pharmacology , malaria , antibiotics , enzyme , immunology , multiple drug resistance
Calmodulin inhibitors are toxic for a variety of protozoa. Chlorpromazine, calmidazolium, and trifluoperazine inhibited the incorporation of [3H]hypoxanthine and [3H]phenylalanine into Plasmodium falciparum organisms in cultures with 50% inhibitory concentrations varying from 5.1 microM (with calmidazolium) to 48 microM (with chlorpromazine), the former being more sensitive than the latter. However, these concentrations also immediately dissipated rhodamine 123 from the parasite mitochondrion. Similar concentrations inhibit other protozoa, as well as mammalian cells, and the possibility that mitochondrial function rather than that of calmodulin is the target of these drugs should be considered.