Amphotericin B-induced damage of Trypanosoma cruzi epimastigotes

Amphotericin B (AmB) autoxidation resulted in oxygen consumption, superoxide anion formation and production of thiobarbituric acid (TBA)-reactive material (malondialdehyde). Malondialdehyde formation increased after incubation of the drug with ascorbate-ADP-FeCl 3. Growth of Trypanosoma cruzi epimas...

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Veröffentlicht in:	Chemico-biological interactions 1989, Vol.71 (1), p.91-103
Hauptverfasser:	Haido, Rosa Maria T., Barreto-Bergter, Eliana
Format:	Artikel
Sprache:	eng
Schlagworte:	Amphotericin B Amphotericin B - pharmacology Animals Antibiotics. Antiinfectious agents. Antiparasitic agents Antiparasitic agents Biological and medical sciences Fatty acids Fatty Acids - metabolism Malondialdehyde - metabolism Medical sciences Oxidation-Reduction Pharmacology. Drug treatments Sterols - metabolism Superoxide anion Superoxides - metabolism Trypanosoma cruzi Trypanosoma cruzi - drug effects Trypanosoma cruzi - growth & development Trypanosoma cruzi - metabolism
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Zusammenfassung:	Amphotericin B (AmB) autoxidation resulted in oxygen consumption, superoxide anion formation and production of thiobarbituric acid (TBA)-reactive material (malondialdehyde). Malondialdehyde formation increased after incubation of the drug with ascorbate-ADP-FeCl 3. Growth of Trypanosoma cruzi epimastigotes in the presence of AmB induced a decrease in the free fatty acid content of the cells (57% in control cells vs. 7% in AmB-treated cells), and in the proportion of unsaturated fatty acids as well as cell killing. No changes were detected on sterol content. No evidence was found for lipid peroxidation as a mechanism of cell injury by this antibiotic.
ISSN:	0009-2797 1872-7786
DOI:	10.1016/0009-2797(89)90092-6