amphotericin-b and desertomycin

In Saccharomyces uvarum cultures, subinhibitory doses of amphotericin B and desertomycin induced alterations in the plasma membrane phospholipid composition. Amphotericin B increased the lipid content in the plasma membrane. It showed a pronounced effect on fatty acyl constituents by raising the amounts of mono- and polyunsaturated derivatives in phospholipids. On the other hand, desertomycin had no apparent effect on fatty acid synthesis but altered the relative composition of phospholipids in the membrane. Phosphatidyl choline and phosphatidyl ethanolamine contents decreased, while their precursors, phosphatidyl serine and phosphatidic acid, increased. On the other hand, the rates of phosphatidyl inositol were not significantly affected by the action of either antifungal agent.

Topics: Amphotericin B; Anti-Bacterial Agents; Cell Membrane; Dose-Response Relationship, Drug; Fatty Acids; In Vitro Techniques; Macrolides; Membrane Lipids; Phospholipids; Saccharomyces

A metabolite with antifungal activity, of non polyenic macrolide structure, was extracted and purified from the culture supernatant of a soil-isolated Streptomyces spectabilis strain, BT 352. This product was found to be related to (or being) desertomycin. Six yeast and five filamentous fungus strains were used to determine minimum concentration of the metabolite that inhibits growth by 80% (IMC); it was established at 50 micrograms/mL for the fungi and at 100 micrograms/mL or more for the yeasts tested. Short-term genotoxicity tests showed no antifungal effect on the bacterial genome, and desertomycin at concentration levels of 100 micrograms/mL or more affected protein synthesis. The antifungal metabolite had no immediate inhibiting effect upon yeast respiration, even at high concentrations; however, the respiration activity of cells grown in the presence of subinhibiting doses and collected during their growth phase was reduced by as much as 40%. Saccharomyces uvarum spheroplast regeneration in a liquid medium containing desertomycin was inhibited at doses fivefold weaker than the IMC determined with intact cells. Contrary to amphotericin B, desertomycin subinhibiting doses do not modify, and if so lightly, the yeast latent phase or the spheroplast wall regeneration phase, thus indicating a fungicidal action. Moreover, following a 30-min contact with desertomycin subinhibiting and inhibiting doses, yeasts liberated potassium in large amounts, indicating that plasma membranes were affected.

Topics: Amphotericin B; Anti-Bacterial Agents; Antifungal Agents; Cycloheximide; Fungal Proteins; Fungi; Genes, Bacterial; Lipids; Macrolides; Mutagenicity Tests; Oxygen Consumption; Potassium; Saccharomyces; Soil Microbiology; SOS Response, Genetics; Spheroplasts; Streptomyces; Tunicamycin; Yeasts