Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.

無カタラーゼ血液症患者血液に対する2, 3細菌の作用について 第2編 菌の呼吸に対する赤血球の影響

河田 幹太郎 岡山大学医学部耳鼻咽喉科教室
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As previously reported in Part Ⅰ the author found that hemoglobin had tendency to show the production of MetHb and the decolorization remarkably when Streptococcus hemolyticus, Streptococcus viridans, and Diprococcus pneumoniae Ⅰ, Ⅱ and Ⅲ were cultured in the medium using the blood of acatalasemic patients. These changes clearly have indicated that the blood of these patients lacking in the catalase is unable to dispose of hydrogen peroxide (H(2)O(2)) produced by bacteria and subsequently Hb is oxidized to form MetHb and with progress of oxidation the constituents of the blood seem to turn to decolorization substances such as propentodyopent. This time with a view to clarify this point still further, the author studied action of still bacteria en erythrocytes of the normal and the patients, and from the results of this study arrived at the following conclusion. 1) Diprococcus pneumoniae Ⅱ, Ⅲ and Streptococcus viridans markedly accumulate H(2)O(2) during oxidation process of glucose. 2) When glucose is used as substrate loaded with acatalasemic erythrocytes and shaken, in the case of Diprococcus pnemoniae Ⅰ, Ⅱ, or Streptococcus viridans, a marked production of MetHb has bean observed, when normal erythrocytes are loaded, the production of MetHb has been extremely small as compared with each of these bacteria in the case of the acatalasemic erythrocytes. When pyruvate, succinate, or aspartate is used as substrate, the influences of each of these bacteria on erythrocytes are on the whole quite small. 3) Productivity of MetHb and decolorization by bacteria have a parallel relationship with the accumulation of H(2)O(2). 4) Using glucose as substrate, influences of Diprococcus pneumoniae Ⅱ on the respiration of erythrocytes are as follows. a. In the case where erythrocytes are not loaded (the control) O(2)-consumption decreases by 60-90 minutes. b. In the case where acatalasemic erythrocytes are loaded, so long as Hb exists, O(2)-consumption continues to rise. c. In the case where normal erythrocytes are loaded, up to 60 minutes O(2)-consumption is comparatively lower than that of the control but it does not fall even 120 minutes later. d. On examining H(2)O(2) in solution after these reactions, an extremely minutes quantity of it has been traced in the case of loading acatalasemic erythrocytes, while none can be traced in the case of loading normal erythrocytes. e. Thiourea and cysteine have been found to completely recompensate whatever influences exerted upon O(2)-comsumption of bacteria by acatalasemic blood. 5) After studying color changes of the erythrocytes to which H(2)O(2) of various concentrations had been adden, the results thus obtained were quite identical with those which erythrocytes had been influenced by respiring bacteria. 6) From these facts as far mentioned it may be assumed that the influences of respiring bacteria upon the acatalasemic erythrocytes are due to the action of H(2)O(2) produced by bacteria.