
ABSTRACT Here the mechanism by which perifosine induced cell death in Leishmania donovani and Leishmania amazonensis is described. The drug reduced Leishmania mitochondrial membrane potential and decreased cellular ATP levels while increasing phosphatidylserine externalization. Perifosine did not increase membrane permeabilization. We also found that the drug inhibited the phosphorylation of Akt in the parasites. These results highlight the potential use of perifosine as an alternative to miltefosine against Leishmania .
Membrane Potential, Mitochondrial, Phosphorylcholine, Leishmania mexicana, Antiprotozoal Agents, Protozoan Proteins, Gene Expression, Apoptosis, Phosphatidylserines, Mitochondria, Inhibitory Concentration 50, Adenosine Triphosphate, Phosphorylation, Proto-Oncogene Proteins c-akt, Leishmania donovani
Membrane Potential, Mitochondrial, Phosphorylcholine, Leishmania mexicana, Antiprotozoal Agents, Protozoan Proteins, Gene Expression, Apoptosis, Phosphatidylserines, Mitochondria, Inhibitory Concentration 50, Adenosine Triphosphate, Phosphorylation, Proto-Oncogene Proteins c-akt, Leishmania donovani
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