Abstract

Inactivation of Listeria monocytogenes (10 8 CFU/ml) by high hydrostatic pressure (HHP) from 400 to 600 MPa at 25 °C for 10 min was investigated with various concentrations of sodium chloride, sucrose, and sodium phosphate buffer solutions. Sodium chloride significantly inhibited HHP-induced inactivation of L. monocytogenes at concentrations higher than 2.6 M. A low concentration of sodium chloride within 1.7 M had no effect on HHP-induced inactivation. Almost complete inactivation at relatively low sodium chloride concentration solution was observed with treatments above 500 MPa. Sucrose also significantly inhibited HHP-induced inactivation of L. monocytogenes when greater than 1.2 M sucrose solutions were used. HHP-treatment at 400 MPa reduced the number of L. monocytogenes in 1.2 M, 1.5 M, and 1.8 M sucrose solutions by 4.8, 2.0, and 0.7 log cycles, respectively. Higher pressure did not yield significant reductions. Sodium phosphate buffer significantly inhibited HHP-induced inactivation of L. monocytogenes. In particular, 1 M phosphate buffer completely inhibited HHP-induced inactivation even at 600 MPa. HHP-treatment at 400 MPa reduced the number of L. monocytogenes in 0.1 M, 0.25 M, and 0.5 M phosphate buffer solutions by 5.6, 4.1, and 3.2 log cycles, respectively. The effect of HHP-induced inactivation of L. monocytogenes in the three kinds of solution was evaluated by adjusting water activity ( a w). However, the baroprotective effect differed depending on the kind of solute even at the same a w. This result showed no consistent correlation between a w and solute concentration in terms of the baroprotective effect. As an alternative approach, saturation of suspension solution was used for evaluating the effect of HHP-induced inactivation of L. monocytogenes. As the saturation of suspension media increased, the effect of HHP-induced inactivation of L. monocytogenes decreased regardless of the kinds of solute. The saturation of solution would be an alternative parameter of inhibition in terms of HHP-induced inactivation of bacteria.

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