Summary. In‐vitro synthesis and release of a vitamin‐B12 binding protein by peripheral leucocytes derived from healthy subjects and patients with chronic myeloid leukaemia (CML), acute promyelocytic leukaemia (APL) and acute myeloblastic leukaemia (AML) were investigated.
Myeloid cells, incubated in a nutrient medium containing [3H]leucine, incorporated labelled amino‐acid into the vitamin‐B12 binding protein with an increase of the unsaturated vitamin‐B12 binding capacity (UBBC) of the cells.
The increase in the UBBC of the medium was due to the presence of the newly produced leucocyte binder which was released into the medium by the cells during incubation. On chromatography the newly synthesized binder was similar to transcobalamin I.
The incorporation of [3H]leucine into the leucocyte binder by mature granulo‐cytes and undifferentiated myeloblasts was very limited and reached a maximum after 60 min of incubation. Cells from CML and APL patients showed a higher rate of incorporation of the labelled amino‐acid which reached a plateau after 40 hr. The increase in the UBBC of the leucocyte binder was paralleled by the incorporation of [3H]leucine.
The percentage of immature myeloid cells in the incubation mixture (promyelocytes to stab forms) was correlated with both the incorporation of [3H]leucine and with the increase in UBBC.
Abstract. Sera from patients with viral hepatitis were examined for serum vitamin B12 concentration, unsaturated B12 binding capacity, total B12 binding capacity of whole serum and of separate transcobalamin‐I and transcobalamin‐II fractions. It was found that the high serum B12 concentrations observed were associated with an increase in the B12 binding of the transcobalamins. The B12 bound to transcobalamin‐I was found to be two to three times higher than that in normal subjects. The most striking difference was the finding of excessive amounts of B12 bound to transcobalamin‐II, as much as 30 to 40 times the normal. The unsaturated B12 binding capacity of hepatitis sera is usually very low. In addition to the B12 bound to transcobalamins, a considerable part of the elevated serum B12 in hepatitis was in a dialyzable form and was not bound to either transcobalamin‐I or transcobalamin‐II. This dialyzable B12 is apparently bound to a small peptide (M.W less than 10000) which permits its passage through dialysis membrane but makes the B12 molecule unavailable to the microorganism in the bioassay, unless it is released from the peptide complex by boiling.
The unsaturated BIZ binding capacity (UBBC) of the serum and the binding capacity of each of the 3 vitamin BIZ bindersthe transcobalamins (TC) I, I1 and 111 were determined in 21 patients with polycythaemia Vera (PV) during the course of the disease and following treatment, using the recently described charged cellulose filter technique. High serum UBBC due to elevated serum TCIII was found in all patients. TCI was moderately elevated in patients who had leucocytosis with a shift to the left. The changes in serum TCIII and UBBC correlated with the activity of the disease. Chemotherapy resulted in a decrease in TCIII and UBBC. The decrease in TCIII and UBBC folowing chemotherapy may be observed before a decrease in the haematocrit and the leucocyte count occurs. Activation of the disease may be assessed by the elevation of TCIII and UBBC. The onset of acute myeloblastic crisis in 1 patient was associated with a decrease in TCIII and TCI levels and a rise in serum TCII. The determination of TCIII and UBBC may be helpful in differentiating true from secondary polycythaemia.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.