Human spleen heme oxygenase and microsomal electron transport system component activity in normals and in patients with hemolytic anemia, idiopathic thrombocytopenic purpura, and lymphoproliferative disorders
Schacter, B.A.; Yoda, B.; Israels, L.G.
Journal of Laboratory and Clinical Medicine 93(5): 838-846
1979
ISSN/ISBN: 0022-2143 PMID: 107258 Document Number: 149526
Microsomal heme oxygenase [EC 1.14.99.3] and other microsomal electron transport system components (cytochrome P-450 and NADPH-cytochrome c reductase) were measured in 128 human spleens from normal subjects and patients with a variety of pathological conditions to determine the potential physiological role and adaptation of these enzymes to various conditions which might affect heme and Hb catabolism. Splenic heme oxygenase activity in normals was sufficient to provide for total normal Hb turnover. In states of chronic hemolysis, total splenic heme oxygenase activity increased an average of 7-fold by mechanisms including specific induction of the enzyme and increased splenic size. Some malignant states were also characterized by increased activity of spleen heme oxygenase (Hodgkin's disease, chronic lymphocytic leukemia, some patients with gastrointestinal tract cancer), whereas others were not associated with any significant change in activity (non-Hodgkin's lymphoma, chronic myelocytic leukemia). The specific activity of other microsomal electron transport system components were significantly increased only in chronic lymphocytic leukemia (NADPH-cytochrome c reductase) and Hodgkin's disease (cytochrome P-450). The role of spleen heme oxygenase in normal Hb catabolism was quantitated, and the nature of the functional adaptation of this enzyme in chronic hemolytic states was defined.