The primary effects of nystatin, a polyene antibiotic, on the yeast Saccharomyces cerevisiae were investigated. Though K+ leakage was observed shortly after the addition of nystatin, Ca2+ leakage was delayed 2-3 h after its application and it occurred only at an acidic pH and in the absence of K+, Na+ or Mg2+ from the medium. However, within 4 min after application nystatin induced a passive influx of Ca2+ into the cells even at a concentration of 1 microM in the medium. These results led to the conclusion that the primary membranal lesion induced by nystatin is not restricted to monovalent cations but is also manifested by increased permeability to Ca2+. The delayed leakage of Ca2+ is explained by the assumption that the bulk of cellular calcium is sequestered so that the concentration of free Ca2+ in the cytoplasm is very low. The sequestered calcium may be liberated 2-3 h after the addition of nystatin as a consequence of secondary damage to the cells such as intracellular acidification and loss of cations.
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