Phenylphosphonate transport by Helicobacter pylori


Background: Helicobacter pylori can utilize phenylphosphonate as a sole source of phosphorus, and it is able to transport the phosphonate N-phosphonoacetyl-L-aspartate. However, H. pylori does not have any genes homologous to those of the known pathways for phosphonate degradation in bacteria, indicating that it must have novel pathways for the transport and metabolism of phosphonates.

Methods: Phenylphosphonate transport by H. pylori was studied in strains LC20, J99 and N6 by the centrifugation through oil method using [14C]-labeled phenylphosphonate.

Results: The Michaelis constants of transport Kt and Vmax for phenylphosphonate showed similar kinetics in the three strains. The Arrhenius plot for phenylphosphonate transport rates at permeant concentrations of 50 µmol/L was linear over the temperature range 10–40 °C with an activation energy of 3.5 kJ/mol, and a breakpoint between 5 and 10 °C. Transport rates increased with monovalent cation size. The effects of various inhibitors were investigated: iodoacetamide, amiloride, valinomycin, and nigericin reduced the rate of phenylphosphonate transport; sodium azide and sodium cyanide increased the transport rate; and monensin had no effect.

Conclusions: The kinetics and properties of H. pylori phenylphosphonate transport were characterized, and the data suggested a carrier-mediated transport mechanism.


peer-reviewed, helicobacter pylori, phosphonate metabolism, phosphonate transport, phenylphosphonate, centrifugation through oil

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