Role of cell defense against oxidative damage in the resistance of Candida albicans to the killing effect of amphotericin B

M. Sokol-Anderson, J. E. Sligh, S. Elberg, J. Brajtburg, G. S. Kobayashi, G. Medoff

Research output: Contribution to journalArticle

75 Scopus citations


A laboratory-derived mutant of Candida albicans B311 (L) and a clinical isolate (C) of C. albicans, both lacking membrane ergosterol, were less susceptible to amphotericin B (AmB)-induced cell membrane permeability to K+ and lethality than was the wild-type laboratory strain (B311) which contained ergosterol. The resistance of L and C to AmB-induced killing was much greater than the level of resistance to AmB-induced cell membrane permeability. L and C were also less susceptible to killing by H2O2 than was B311, an when treated with menadione, they each produced less H2O2 than did B311. In addition, their levels of catalase activity were 3.8-fold (L) and 2-fold (C) higher than that of B311. The ergosterol deficiency in L and C probably impaired AmB binding to the cells, thereby lowering AmB effectiveness as measured by both cell membrane permeability and killing. Resistance of strains L and C to oxidation-dependent damage likely contributed to a diminished response to AmB-induced lethality.

Original languageEnglish (US)
Pages (from-to)702-705
Number of pages4
JournalAntimicrobial Agents and Chemotherapy
Issue number5
StatePublished - Jan 1 1988
Externally publishedYes


ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)
  • Infectious Diseases

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