Abstract
The mechanism by which propiolic acid (β-naphthyl) methyl ester (PNE) caused an antifungal action on Candida albicans was studied. PNE inhibited the growth of C. albicans, and minimum inhibitory concentration and minimum fungicidal concentration were 6.25μg/ml and 12.5μg/ml, respectively. PNE at concentrations causing an antifungal action strongly inhibited the endogenous respiration, the exogenous respiration utilizing glucose, succinate, citrate and pyruvate, the uptakes of [3H] leucine and [3H] adenine into cells, the incorporation of [3H] leucine into trichloroacetic acid-precipitated fraction and the incorpporation of [3H] adenine into HClO4-precipitated fractions. However, the inhibitory actions of PNE were not observed in cell free system. During the incubation ofC. albicanswith PNE (12.5-25μg/ml), 20-30% of intracellular K+ was leaked, but leakages of protein and 260nm-absorbing materials were not observed. On the electromicroscopic observations, the surface of C. albicans was smooth and, 1 h after the treatment with PNE (12.5μg/ml), that was changed to be rough. After 24 h, big depressiens were found in almost fungi. These results suggcsted that PNE caused a damage in cell membrane ofC.albicansand that, as the results, the leakage of intracellular K+ and decrease in various metabolic functions of C.albicans occurred.
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