Toxicity of nalidixic acid on Candida albicans, Saccharomyces cerevisiae, and Kluyveromyces lactis
Sobieski, Rodney J.
Brewer, Alan R.
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Sobieski RJ, Brewer AR. Toxicity of nalidixic acid on candida albicans, Saccharomyces cerevisiae, and Kluyveromyces lactis. Antimicrob Agents Chemother. 1976;9(3):485-92.
The antibacterial drug nalidixic acid (Nal) can suppress the growth of Candida albicans at levels of the drug normally found in urine. Growth suppression increases as drug levels are increased, and Nal also causes a similar proportional inhibition of the synthesis of all cellular macromolecules. However, growth temperature (25 versus 37C) and the divalent cations Mg2+ and Mn2+ can increase C. albicans resistance to Nal. Also, nitrogen depletion of Candida shows that Nal treated and untreated cells exhibit no difference in leucine uptake during readaptation to nitrogen. In Nal treated, nitrogen starved cells, ribonucleic acid and deoxyribonucleic acid (DNA) biosynthesis are less affected than in unstarved Nal treted cells, but of the two nucleic acids DNA synthesis is the most affected. Nal resistant strains of C. albicans exhibit a slight toxicity for macromolecular synthesis. Nal treatment of a synchronized population of Saccharomyces cerevisiae results in an increase in the culture mean doubling time of, at most, 20%, but Nal causes the loss of synchronous cell vision. With a synchronized population of Kluyveromyces lactis, Nal causes an increase in the mean doubling time of upwards of 300%, with synchrony of cell division being maintained. It is known that S. cerevisiae asynchronously synthesizes mitochondrial DNA during the cell cycle, whereas with K. lactis it is synchronous. Thus, with C. albicans Nal toxicity is dependent both on the dose and the physiological state of the cell. Furthermore, Nal inhibits growth of yeast with synchronous mitochondrial DNA synthesis more adversely than yeast with asynchronous mitochondrial DNA synthesis.
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