Studies on the mechanism of the erythrocyte enzyme abnormalities induced by chemotherapy.
With the aim of determining the possible mechanisms of the red cell enzyme deficiencies induced by chemotherapy, deficient red cell glucose-6-phosphate dehydrogenase (G-6-PD), pyruvate kinase (PK) and phosphofructokinase (PFK) from 17 patients were purified and characterized. In all cases G-6-PD showed normal kinetics, electrophoretic mobility and thermostability suggesting that a decreased enzyme synthesis was possible for the deficient enzyme activity. In each case studied, at least one of the PK properties was modified, either in affinity for phosphoenol pyruvate, thermal stability or electrophoretic mobility, indicating a primary or secondary molecular abnormality. In some patients PFK had significantly increased affinity for citrate inhibitor; however, neither the quantity nor quality of the M subunits seemed to be altered. Thus it appears that chemotherapy can induce qualitative as well as quantitative red cell enzyme abnormalities by different mechanisms. These are similar to those observed in spontaneous leukaemia and preleukaemic states. Such a similarity poses the question of whether or not the red cell enzyme abnormalities induced by chemotherapy could be considered as the first sign of secondary leukaemia due to treatment by oncostatic drugs.
D000970:Antineoplastic Agents / Q000009:adverse effects*; D004591:Electrophoresis, Polyacrylamide Gel; D004592:Electrophoresis, Starch Gel; D004912:Erythrocytes / Q000187:drug effects / Q000201:enzymology*; D005954:Glucosephosphate Dehydrogenase / Q000097:blood*; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000139:chemically induced; D006801:Humans; D007700:Kinetics; D010732:Phosphofructokinase-1 / Q000097:blood* / Q000172:deficiency; D011770:Pyruvate Kinase / Q000097:blood* / Q000172:deficiency
D000970:Antineoplastic Agents; D005954:Glucosephosphate Dehydrogenase; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase