Delivery of Co⁵⁷B₁₂ to Erythrocytes from α and β Globulin of Normal, B₁₂-Deficient, and Chronic Myeloid Leukemia Serum

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.