Open AccessRole of cell defense against oxidative damage in the resistance of Candida albicans to the killing effect of amphotericin B
Author(s) -
Marcia L. Sokol-Anderson,
James E. Sligh,
S Elberg,
J Brajtburg,
George S. Kobayashi,
Gerald Medoff
Publication year - 1988
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.32.5.702
Subject(s) - candida albicans , ergosterol , menadione , microbiology and biotechnology , catalase , biology , corpus albicans , membrane permeability , amphotericin b , cell membrane , cell , oxidative stress , biochemistry , membrane , antifungal
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, and 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.