The activity of amphotericin B against Candida albicans is not directly associated with extracellular calcium concentration

Phillip Rogers, Robert E. Kramer, Janice K. Crews, Russell E. Lewis

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The ability of amphotericin B to increase intracellular calcium concentrations in human cells is associated with the toxicity of this antifungal agent. The present study was performed to determine whether amphotericin B affects the influx or efflux of calcium in Candida albicans, and whether the antifungal activity of amphotericin B is dependent upon extracellular calcium concentrations. Concentration-response studies demonstrated that the addition of up to 1 mM EGTA to standard growth medium, with a more than 4000-fold decrease in extracellular calcium concentration, had no effect on the activity of amphotericin B against C. albicans. Amphotericin B did affect the kinetics of calcium influx acutely (≤10 min), but had no net effect on long-term (1-24 h) calcium accumulation. Calcium efflux was also not affected by amphotericin B. These results indicate that, unlike its effects on mammalian cells, the toxicity of amphotericin B against C. albicans is not dependent upon increased movement of calcium across the cell membrane or the presence of extracellular calcium.

Original languageEnglish (US)
Pages (from-to)305-312
Number of pages8
JournalJournal of Antimicrobial Chemotherapy
Volume51
Issue number2
DOIs
StatePublished - Feb 1 2003

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Amphotericin B
Candida albicans
Calcium
Antifungal Agents
Egtazic Acid
Cell Membrane
Growth

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Microbiology (medical)
  • Infectious Diseases
  • Pharmacology (medical)

Cite this

The activity of amphotericin B against Candida albicans is not directly associated with extracellular calcium concentration. / Rogers, Phillip; Kramer, Robert E.; Crews, Janice K.; Lewis, Russell E.

In: Journal of Antimicrobial Chemotherapy, Vol. 51, No. 2, 01.02.2003, p. 305-312.

Research output: Contribution to journalArticle

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