Induction of Oxidative Stress by High Hydrostatic Pressure in <i>Escherichia coli</i>

  • Abram Aertsen
    Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Leuven, Belgium
  • Philipp De Spiegeleer
    Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Leuven, Belgium
  • Kristof Vanoirbeek
    Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Leuven, Belgium
  • Maria Lavilla
    Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Leuven, Belgium
  • Chris W. Michiels
    Laboratory of Food Microbiology, Katholieke Universiteit Leuven, Leuven, Belgium

抄録

<jats:title>ABSTRACT</jats:title> <jats:p> Using leaderless alkaline phosphatase as a probe, it was demonstrated that pressure treatment induces endogenous intracellular oxidative stress in <jats:italic>Escherichia coli</jats:italic> MG1655. In stationary-phase cells, this oxidative stress increased with the applied pressure at least up to 400 MPa, which is well beyond the pressure at which the cells started to become inactivated (200 MPa). In exponential-phase cells, in contrast, oxidative stress increased with pressure treatment up to 150 MPa and then decreased again, together with the cell counts. Anaerobic incubation after pressure treatment significantly supported the recovery of MG1655, while mutants with increased intrinsic sensitivity toward oxidative stress ( <jats:italic>katE</jats:italic> , <jats:italic>katF</jats:italic> , <jats:italic>oxyR</jats:italic> , <jats:italic>sodAB</jats:italic> , and <jats:italic>soxS</jats:italic> ) were found to be more pressure sensitive than wild-type MG1655. Furthermore, mild pressure treatment strongly sensitized <jats:italic>E. coli</jats:italic> toward <jats:italic>t-</jats:italic> butylhydroperoxide and the superoxide generator plumbagin. Finally, previously described pressure-resistant mutants of <jats:italic>E. coli</jats:italic> MG1655 displayed enhanced resistance toward plumbagin. In one of these mutants, the induction of endogenous oxidative stress upon high hydrostatic pressure treatment was also investigated and found to be much lower than in MG1655. These results suggest that, at least under some conditions, the inactivation of <jats:italic>E. coli</jats:italic> by high hydrostatic pressure treatment is the consequence of a suicide mechanism involving the induction of an endogenous oxidative burst. </jats:p>

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