Volume 15, Issue 3 (vol-3 2009)                   Intern Med Today 2009, 15(3): 13-20 | Back to browse issues page

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1- , khademvatan@ajums.ac.ir
Abstract:   (13645 Views)
Abstract Background and Aim: Discovering the drug mechanisms in visceral leishmaniasis is very important to confirm treatment methods. The direct effect on the cell membrane and induction of necrosis are the causes of side-effects in conventional drugs like Glucantime. Therefore, if a drug induces apoptosis but not necrosis in leishmania, we could conclude that the drug is more effective. The aim of this study was the assessment of miltefosine on cell death mechanisms and the apoptosis of standard strain of lishmania infantum in Iran. Materials and Methods: The cytotoxic effect of miltefosine was studied with colorimetric assay (MTT) and the promastigotes apoptosis was studied with flow cytometry. In summary, 105 leishmania infantum promastigotes treated with IC50 dose of miltefosine, and control cells were added to binding buffer with FITC conjugate, annexin V and propidum iodide (PI). The cells were studied with flowcytometry and the results were analyzed with cell quest program. Morphology and cell size of promastigote were studied. Results: IC50 of Miltefosine were calculated 7-8 μmol. After a 24-hour incubation of treated cells with miltefosine, 22% were annexin-V FITC positive but only 2% of control cells were annexin-V FITC positive. After 48 hours the percent of apoptotic cells increased (80% annexin-V FITC) whereas no change was detected in control group. Conclusion: Initially, it was assumed that apoptosis emerged with metazoan. Recently, several studies have demonstrated that a process of apoptosis also operates in eukaryotic organisms including various species of leishmania. Studying the precise mechanism of cell death pathway and induction of death in leishmania treated with miltefosine is very important for planning effective treatment strategies.
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Type of Study: Original | Subject: Internal Medicine
Received: 2010/02/14 | Published: 2009/10/15

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