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Pyruvate kinase deficiency in dog and human erythrocytes: Effects of energy depletion on cation composition and cellular hydration
Author(s) -
MullerSoyano Aixa,
Platt Orah,
Glader Bertil E.
Publication year - 1986
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830230305
Subject(s) - reticulocyte , pyruvate kinase deficiency , hemolysis , oxidative phosphorylation , pyruvate kinase , potassium , glycolysis , mitochondrion , chemistry , biochemistry , red blood cell , dehydration , adenosine triphosphate , biology , metabolism , immunology , organic chemistry , messenger rna , gene
Pyruvate kinase‐ (PK) deficient human reticulocytes incubated 4 hr under conditions where mitochondrial oxidative phosphorylation is inhibited become ATP‐depleted. Concomitantly, these energy‐depeleted red blood cells (RBC) lose massive amounts of potassium and water. PK‐deficient reticulocyte‐rich RBC from a Basenji dog, incubated under the same conditions, also manifest ATP‐depletion and K‐loss. In contrast to the cation changes in human cells, however, K‐loss in PK‐deficient dog reticulocyte‐rich RBC is balanced by an equivalent Na gain, and consequently these canine erythrocytes do not undergo any change in cellular hydration, Potassium depletion and dehydration, which may be related to membrane injury in human RBC, do not appear to be involved in the hemolysis of PK‐deficient dog erythrocytes.