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Efflux of ions and ATP depletion induced by pediocin PA‐1 are concomitant with cell death in Listeria monocytogenes Scott A
Author(s) -
Chen Y.,
Montville T. J.
Publication year - 1995
Publication title -
journal of applied bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 0021-8847
DOI - 10.1111/j.1365-2672.1995.tb00955.x
Subject(s) - efflux , listeria monocytogenes , intracellular , pediococcus acidilactici , chemiosmosis , pi , chemistry , dithiothreitol , biochemistry , biology , atp synthase , bacteria , enzyme , lactic acid , genetics , lactobacillus plantarum
The bacteriocin pediocin PA‐1 (80 AU ml −1 ), which is produced by Pediococcus acidilactici PAC 1.0, reduced Listeria monocytogenes Scott A viability by 4.6 log. Concomitant with the cell death, pediocin PA‐1 induced irreversible K + and Pi efflux and ATP depletion in concentration‐dependent and time‐dependent fashions. The maximum amount of intracellular K + and Pi loss was 520 and 44.6 nmol mg −1 CDW, respectively. Intracellular ATP levels decreased from 2.8 to 0‐029 nmol mg −1 CDW, corresponding to 98.9% depletion. Less than 0.1% ATP efflux was found with pediocin concentrations up to 200 AU ml −1 . Approximately 10, 40 and 60 min were required for maximum K + efflux, ATP depletion and Pi efflux, respectively. Moreover, pediocin PA‐1 depleted 90% of cytoplasmic ATP when only 25% Pi efflux took place. These results suggest that loss of ATP is due to attempts by the cell to maintain proton‐motive force rather than the inability of the cell to produce ATP due to the loss of Pi. Dithiothreitol‐treated PA‐1 no longer inhibited the growth of L. monocytogenes cells, and caused neither concentration‐dependent ion efflux nor ATP depletion.