In a study of Co57B12 uptake by reticulocyte-rich erythrocytes, transfer from chronic myeloid leukemia (CML) serum was less efficient than from normal serum. Decreased transfer of Co57B12 was not due to excessive transfer of endogenous B12 (which is normally elevated in CML) but was associated with an α-globulin B12-binder (isolated from "baby" DEAE columns) unable to normally deliver B12 to erythrocytes. Delayed plasma clearance of intravenously injected B12 in CML may be due to this phenomenon.
B12-deficient serum delivered slightly more added Co57B12 to erythrocytes than did normal serum, possibly due to less interference by endogenous B12. α- and β-globulin B12 binders from B12-deficient serum transferred bound Co57B12 as efficiently as did normal serum α- and β-binders; the β-binders delivered more than the α-binders. CML β-binder delivered as well as did β- binder from pernicious anemia and normal serum. These findings suggest that the α-binder of CML serum is physiologically and therefore chemically different from the α-binder in normal and pernicious anemia serum.
Reticulocyte-rich, B12-deficient erythrocytes from pernicious anemia patients took up Co57B12 less well than did B12-sufficient reticulocyte-rich erythrocytes. This may partially explain delayed plasma clearance of B12 in B12 deficiency.
Rat liver homogenate uptake of Co57B12 was much greater when B12 was transferred from normal serum than from normal gastric juice or saline. Preliminary investigations showed that both α- and β-binders from normal serum transferred B12 to liver homogenate but CML α-binder transferred poorly.