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-FeCl3. 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.
Haido
R M
RM
Departamento de Microbiologia Geral, Universidade Federal do Rio de Janeiro, Brazil.
Barreto-Bergter
E
E
D000666:Amphotericin B / Q000494:pharmacology*; D000818:Animals; D005227:Fatty Acids / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D010084:Oxidation-Reduction; D013261:Sterols / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D014349:Trypanosoma cruzi / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism
D005227:Fatty Acids; D013261:Sterols; D013481:Superoxides; D008315:Malondialdehyde; D000666:Amphotericin B