Chemiluminescence of superoxide generated byCandida albicans: differential effects of the superoxide generator paraquat on a wild-type strain and a respiratory mutant
| Autor: | K. Takeo, Valerio Vidotto, S. Aoki, K. Nakamura, S. Ito-Kuwa, Y. Nakamura |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Paraquat
Cytochrome Mutant Respiratory chain Cell Count Antimycin A chemistry.chemical_compound Oxygen Consumption Superoxides Candida albicans biology Strain (chemistry) Superoxide Imidazoles General Medicine biology.organism_classification Molecular biology Infectious Diseases chemistry Biochemistry Pyrazines Luminescent Measurements Mutation biology.protein |
| Zdroj: | Medical Mycology. 40:13-19 |
| ISSN: | 1460-2709 1369-3786 |
| DOI: | 10.1080/mmy.40.1.13.19 |
| Popis: | We previously reported that a respiration-competent parent strain (K) of Candida albicans was more susceptible to the intracellular superoxide radical (O2-) generator paraquat (PQ) than was a respiration-deficient mutant (KRD-19), although both showed a similar sensitivity to extracellularly generated O2-. To clarify the cause of the differential PQ lethality, we developed a chemiluminescence method for measuring O2- generated by C. albicans cells by using the probe methyl-Cypridina-luciferin analogue (MCLA), and examined the effects of PQ on O2- generation in both parent and mutant strains. Endogenous O2- generation without stimulation by PQ was unexpectedly low in both strains. PQ-induced O2- generation in the parent strain was maximal in logarithmic phase cells and lowered in stationary phase cells. In contrast, O2- generation in the mutant remained low throughout the growth phase, even when stimulated by PQ. The extent of PQ-induced O2- generation in the parent strain depended on the carbon source added to the assay mixture; in decreasing order, glucose, glycerol, no carbon source. The inhibitor of the cytochrome respiratory chain, antimycin A, suppressed almost completely the PQ-induced O2- generation in the parent strain. It has been established that PQ is converted to its radical form (PQ+) by receiving a single electron in cells. PQ+ then reduces molecular oxygen to O2- by redox cycling. Thus, the high tolerance to PQ of the respiration-deficient mutant can be explained by minimal PQ+/O2- production due to the limited supply of electrons from the impaired respiratory system. |
| Databáze: | OpenAIRE |
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