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Suicidal destruction of Helicobacter pylori: metabolic consequence of intracellular accumulation of ammonia.
  1. W D Neithercut,
  2. M A Greig,
  3. M Hossack,
  4. K E McColl
  1. University Department of Pathological Biochemistry, Western Infirmary, Glasgow.

    Abstract

    The role of pH, citrate buffer, and urea were investigated in the suicidal destruction of Helicobacter pylori, with particular reference to the organism's urea and ammonia metabolism. The median five minute survival of H pylori in the presence of 50 mmol/l urea in 0.2 M citrate buffer at pH 6.0 was only 14%, compared with 53% in the same solution at pH 7.0. The median amount of ammonium released into the incubating solution over five minutes was lower at pH 6.0 (9 mumol) than at pH 7.0 (18 mumol) despite similar uptake of urea. The median five minute survival of H pylori in 0.2 M citrate buffer, pH 6.0, decreased from 89% to 14% when the urea concentration was increased from 1 mmol/l to 50 mmol/l. Likewise, the recovery in the incubating solution of ammonia resulting from the hydrolysis of urea fell from 27% to 3% when the initial urea concentration was increased from 1 mmol/l to 50 mmol/l. Survival of H pylori in the presence of 30 mmol/l urea at pH 6.0 was compared in 0.2 M citrate, acetate, and phosphate buffers. The median five minute survival was less in the citrate buffer, at 29%, than in either the acetate buffer 80% or the phosphate buffer 100%. The percentage recovery of ammonia was similar in the three buffers. These findings indicate that the suicidal destruction of the bacterium may be explained by intracellular accumulation of ammonia due to production in excess of the rate of excretion.

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