ArticleAntimicrobial agents and chemotherapy2002
Proinflammatory and cytotoxic effects of hexadecylphosphocholine (miltefosine) against drug-resistant strains of Trypanosoma cruzi.
Article in Antimicrobial agents and chemotherapy, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
- Miltefosine and Benznidazole Combination Improve Anti-Frontiers in cellular and infection microbiology · 2022Article
- A functional genomic screen in Saccharomyces cerevisiae reveals divergent mechanisms of resistance to different alkylphosphocholine chemotherapeutic agents.G3 (Bethesda, Md.) · 2021Article
- Identification ofMicroorganisms · 2021Article
- Nano-Medicines a Hope for Chagas Disease!Frontiers in molecular biosciences · 2021Review
- Nanotechnological interventions for treatment of trypanosomiasis in humans and animals.Drug delivery and translational research · 2020Article
- Reviewing the Effects of Miltefosine and Suggesting It for the Treatment of Coronavirus Disease (COVID-19).Infectious diseases · 2020Review
- P-type transport ATPases in Leishmania and Trypanosoma.Parasite (Paris, France) · 2019Review
- Experimental and Clinical Treatment of Chagas Disease: A Review.The American journal of tropical medicine and hygiene · 2017Review
- In vitro drug susceptibility of two strains of the wildlife trypanosome, Trypanosoma copemani: A comparison with Trypanosoma cruzi.International journal for parasitology. Drugs and drug resistance · 2017Article
- Evaluation of the effect of miltefosine on Trichomonas vaginalis.Parasitology research · 2014Article
- Bioactivity of miltefosine against aquatic stages of Schistosoma mansoni, Schistosoma haematobium and their snail hosts, supported by scanning electron microscopy.Parasites & vectors · 2011Article
- Disruption of cellular cholesterol transport and homeostasis as a novel mechanism of action of membrane-targeted alkylphospholipid analogues.British journal of pharmacology · 2010Article
- Alterations in the homeostasis of phospholipids and cholesterol by antitumor alkylphospholipids.Lipids in health and disease · 2010Article
- Effect of therapeutic chemical agents in vitro and on experimental meningoencephalitis due to Naegleria fowleri.Antimicrobial agents and chemotherapy · 2008Article
- The toxic effects of piperine against Trypanosoma cruzi: ultrastructural alterations and reversible blockage of cytokinesis in epimastigote forms.Parasitology research · 2008Article
- Ultrastructural analysis of edelfosine-treated trypomastigotes and amastigotes of Trypanosoma cruzi.Parasitology research · 2006Article
- Characterization of the inositol phosphorylceramide synthase activity from Trypanosoma cruzi.The Biochemical journal · 2005Article
- Possible mechanism of miltefosine-mediated death of Leishmania donovani.Antimicrobial agents and chemotherapy · 2004Article
- Miltefosine induces apoptosis-like death in Leishmania donovani promastigotes.Antimicrobial agents and chemotherapy · 2004Article
- Molecular and functional characterization of the ceramide synthase from Trypanosoma cruzi.Molecular and biochemical parasitologyArticle
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The increased resistance of the protozoan parasite Trypanosoma cruzi to nitro derivatives is one of the major problems for the successful treatment of Chagas' disease. In the present study, we have tested the effects of 1-O-hexadecylphosphocholine (miltefosine) against strains of T. cruzi that are partially resistant (strain Y) and highly resistant (strain Colombiana) to the drugs in clinical use. As expected, epimastigotes of strain Colombiana showed higher levels of resistance to benznidazole than those of strain Y. However, the level of resistance to miltefosine was the same for both strains. This alkylphospholipid was also extremely toxic against intracellular amastigotes of both strains. This ether-lipid analogue induced in a dose-dependent manner the production of tumor necrosis factor alpha and nitric oxide (NO) radicals by infected and noninfected macrophages, suggesting that miltefosine may activate macrophages in vitro. Nevertheless, the cytotoxic effect of miltefosine against intracellular amastigotes was independent of the amount of NO produced by the infected macrophages since the same dose-response curves for miltefosine were observed when the NO production was blocked by the NO synthase inhibitor N(G)-monomethyl-L-arginine monoacetate. Preliminary in vivo studies with BALB/c mice infected with strain Y indicated that oral miltefosine promoted survival and reduced the parasitemia to levels comparable to those observed when benznidazole was used. Four months after treatment, no parasites were detected in the blood or spleen tissue sections maintained in culture. Together, these results support the hypothesis that miltefosine may be used for the treatment of Chagas' disease, including cases caused by resistant strains of T. cruzi.
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