Resistance of Candida parapsilosis to drugs.
Several strains of Candida parapsilosis, isolated independently in our laboratory, had their resistance compared to a series of inhibitors which act either at the level of mitochondrial ribosomes (chloramphenicol, erythromycin, paromomycin) or at the level of mitochondrial respiration and oxidative phosphorylation (oligomycin, antimycin A, diuron, carbonylcyanide m-chlorophenylhydrazone). Cells were grown on glycerol media supplemented with one of these inhibitors, and it was demonstrated that the resistance of these yeasts to a large spectrum of antibiotics was due to several features: a resistance to oligomycin was found at the permeation level; the resistance to the other drugs was correlated to the relative insensitivity of cytochrome biosynthesis to the drugs; the cells developed, at the same time, two types of alternative pathways: the one branched at the ubiquinone level which drove electrons from Krebs cycle substrates to oxygen, and the other, antimycin A-insensitive but inhibited by amytal, salicylhydroxamic acid and high cyanide concentrations. This secondary mitochondrial pathway, driving reducing equivalents from cytoplasmic NADH to cytochrome c and then to cytochrome aa3 or to alternate oxidase, allowed the growth of Candida parapsilosis on a non fermentescible medium, supplemented with these drugs.
D000968:Antimycin A / Q000494:pharmacology; D002175:Candida / Q000187:drug effects* / Q000235:genetics; D002701:Chloramphenicol / Q000494:pharmacology; D003580:Cytochromes / Q000378:metabolism; D004272:DNA, Mitochondrial / Q000235:genetics; D004237:Diuron / Q000494:pharmacology; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D005656:Fungal Proteins / Q000235:genetics; D010101:Oxygen Consumption / Q000187:drug effects; D013045:Species Specificity
D003580:Cytochromes; D004272:DNA, Mitochondrial; D005656:Fungal Proteins; D004917:Erythromycin; D000968:Antimycin A; D002701:Chloramphenicol; D004237:Diuron