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PubMed1991

Blood transcobalamin levels in malignant hepatoma.

Alpha-Fetoprotein (AFP) levels measured by RIA show a strong sensitivity for the biological diagnosis of malignant hepatoma (MH). However, this parameter lacks specificity. Previous observations of an alteration in vitamin B12 metabolism in the presence of hepatoma led us to study vitamin-B12-binding proteins. Vitamin B12, also called cobalamin, is transported in the blood by two proteins or transcobalamins: one is haptocorrin (HC), which is linked to most of the cobalamin, and the other is transcobalamin II, which is involved in tissue exchanges. In this work, the levels of AFP and transcobalamins were determined by RIA and radioisotope dilution assay, respectively. They were measured in patients with MH (group A) and in patients with other liver diseases (group B). Compared with group B, group A showed a significant increase in total serum HC (p less than 0.005). In conclusion, it was observed that MH is accompanied by increased levels of HC. The origin of these changes could be due to either an increase in HC synthesis or a catabolic defect.

Carcinoma, Hepatocellular↗
PubMed1992

FK 383 DS, a new silica gel for the determination of unsaturated haptocorrin and transcobalamin II in serum.

The ability of selective absorption of the polypeptide transcobalamin II by silica gel was used for the determination of the unsaturated cobalamin binding capacity of haptocorrin and transcobalamin II. Two different silica gels, QUSO G 761 and FK 383 DS, were compared by Sephacryl gel-filtration and by determination of unsaturated haptocorrin and transcobalamin II from forty different patient sera. It was found that the silica gels act identically for this purpose.

Chromatography, Gel↗
PubMed1982

Vitamin B12 binders (transcobalamins) in serum.

The measurement of plasma or serum vitamin B12 (B12) binders is important in the diagnosis of congenital megaloblastic anemias, the myeloproliferative disorders and perhaps in other malignancies. Two classes of binders circulate in plasma, Transcobalamin II (TC II) and R-binders. The latter have been divided by some authors into transcobalamin I (TC I) and transcobalamin III (TC III), and the validity of this division is discussed. R-binders and TC II differ in their apparent molecular weight on gel filtration chromatography, by which method they can be separated reliably. However, the technique is time-consuming and cumbersome and a variety of rapid separation methods have been described in the literature. These are discussed and compared to the standard gel filtration separation method. TC I and III are separable on the basis of their differing charges, and the methods which have been described for accomplishing this are compared and critically reviewed. There has been some controversy in the literature as to whether plasma or serum should be used to measure circulating B12 binders. Leukocytes, which contain R-binders, release these in vitro and this release is greatest when blood is allowed to clot and the serum separated. Consequently, the use of plasma, sometimes with agents added to prevent leukocytic release of binder, has been advocated. Yet, none of the agents used eliminates artifact totally, and this aspect, too, is reviewed. Lastly, several techniques for the purification of B12 binders have been described. Some techniques result in pure binder preparations, while others result in preparations which are free of other binders but contaminated with non-B12 binding proteins. Both approaches have advantages and disadvantages, and these are discussed.

Animals↗
PubMed2005

Elevation of serum transcobalamin II in patients with scrub typhus.

Serum transcobalamin II levels were measured in scrub typhus patients. Eighteen out of fifty-two patients admitted to Maharat Nakhon Ratchasima Hospital were diagnosed with scrub typhus infection. The serum unsaturated vitamin B12 binding protein (UBBC) and total vitamin B12 binding protein (TBBC) levels in these patients were significantly higher than in normal subjects (p < 0.001). The mean serum transcobalamin II level in the typhus patients was also significantly higher than in the normal subjects (p=0.004). There was a significant correlation between serum TCII levels and typhus IgM or IgG titers (p < 0.05), but not to total IgM levels. These findings indicate that patients with scrub typhus had stimulation of the recticuloendothelial system as a result of a considerable increase in transcobalamin II levels.

Adolescent↗
PubMed1990

Expression of transcobalamin II receptors by human leukemia K562 and HL-60 cells.

Plasma membrane receptors for the serum cobalamin-binding protein transcobalamin II (TCII) were identified on human leukemia K562 and HL-60 cells using immunoaffinity-purified human TCII labeled with [57Co]cyanocobalamin. The Bmax values for TCII receptors on proliferating K562 and HL-60 cells were 4,500 and 2,700 per cell, respectively. Corresponding dissociation constants (kd) were 8.0 x 10(-11) mol/L and 9.0 x 10(-11) mol/L. Rabbit TCII also bound to K562 and HL-60 cells but with slightly reduced affinities. Calcium was required for the binding of transcobalamin II to K562 cells. Brief treatment of these cells with trypsin resulted in almost total loss of surface binding activity. After removal of trypsin, surface receptors for TCII slowly reappeared, reaching pretrypsin treatment densities only after 24 hours. Reappearance of receptors was blocked by cycloheximide. TCII receptor densities on K562 and HL-60 cells correlated inversely with the concentration of cobalamin in the culture medium. This suggests that intracellular stores of cobalamin may affect the expression of transcobalamin receptors. Nonproliferating stationary-phase K562 cells had low TCII receptor densities (less than 1,200 receptors/cell). However, the density of TCII receptors increased substantially when cells were subcultured in fresh medium. Up-regulation of receptor expression coincided with increased 3H-thymidine incorporation, which preceded the resumption of cellular proliferation as measured by cell density. In the presence of cytosine arabinoside, which induces erythroid differentiation, K562 cells down-regulated expression of TCII receptors. When HL-60 cells were subcultured in fresh medium containing dimethysulfoxide to induce granulocytic differentiation, the up-regulation of TCII receptors was suppressed. This event occurred well before a diminution of 3H-thymidine incorporation and cessation of proliferation. Thus, changes in the regulation of expression of TCII receptors correlate with both the proliferative and differentiation status of cells.

Cell Division↗
PubMed1981

Stabilization of transcobalamins against heating on sephadex G-50.

The human serum stabilized on Sephadex G-50 did not show any changes in the distribution of radioactive vitamin B12 bound to transcobalamins during incubation at 56 degrees C (30 and 120 min.) and 80 degrees C (20 min.), whereas, in the non-stabilized serum, heating increased the vitamin 57CoB12 in transcobalamin I and III fraction and decreased or completely abolished the amount of radioactive vitamin B12 bound to transcobalamin II.

Blood Proteins↗
PubMed1984

Hereditary transcobalamin II deficiency with subnormal serum cobalamin levels.

An infant with transcobalamin II deficiency had the unusual feature of a low serum cobalamin level. Moreover, the level did not rise greatly with cobalamin therapy. Clinically, the features of the infant's illness were unexceptional other than the somewhat delayed onset of symptoms at 3 1/2 months of age. In addition, the patient's impaired antibody response to specific antigen challenge was not completely corrected following cobalamin therapy, and this result contrasts with the findings in the only previous examination of this feature of the disorder. As in previous cases, the transcobalamin II deficiency was accompanied by findings in the serum of complexing of the patient's R binder and the relative prominence of a cobalamin-binding peak eluting at a molecular weight of approximately 70,000 on Sephadex G-200 gel chromatography. In addition, the total serum R binder (free and complexed) level was low. This case demonstrates that transcobalamin II deficiency should be considered in any infant with a low serum cobalamin level in the first few months of life.

Agammaglobulinemia↗
PubMed1993

Endocytosis of transcobalamin in male rabbit germ cells: electron microscope radioautography study.

The binding of 125I-iodinated transcobalamin to a suspension of isolated rabbit germ cells was studied by Scatchard plot. The number of binding sites was evaluated to about 1000 per cell, and its association constant (Kass) in order of 14.6 l/nmole. The distribution to structures related to endocytosis was determined by ultrastructural histomorphometric studies. Both coated and uncoated structures were present regardless of maturation stage. The number of coated vesicles was at its highest in the initial maturation steps, whereas the number of uncoated vesicles was highest in the final maturation steps. The endocytosis of 125I-iodinated transcobalamin by the suspension of germ cells was studied by electron microscope radioautography. The tracer was mostly detected over the plasma membrane, coated vesicles and multivesicular bodies of germ cells. The grains were observed mainly over spermatocytes and round spermatids; 31.6% and 32% of these cells, respectively, were labeled. In contrast the tracer was detected in only 8.11% of elongated spermatids. In conclusion, iodinated transcobalamin is internalized in rabbit germ cells by receptor-mediated endocytosis. This phenomenon was predominant in the early stages of germ cell maturation.

Animals↗
PubMed1994

Serum vitamin B12 and transcobalamin levels in early HIV disease.

A cohort of asymptomatic human immunodeficiency virus (HIV) seropositive patients was followed over a 2 1/2-year period, to establish changes in serum vitamin B12 (B12) concentrations. Serum B12, CD4 count, and clinical progression to acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) were measured. The unsaturated B12 binding capacities of the transcobalamins were also determined at the start of the study and compared to those from a homosexual HIV seronegative control group. The geometric mean of serum B12 in 218 asymptomatic HIV seropositive patients was significantly lower than of a homosexual HIV seronegative control group (P = 0.02) and the unsaturated B12 binding capacities of transcobalamins I and II were significantly higher in the asymptomatic patients compared with the same control group (P < 0.03, P < 0.0001, respectively). Fifty-nine of the asymptomatic HIV seropositive patients were followed over a 2 1/2-year period during which most had falling serum B12 levels (64%). Twelve patients progressed clinically to ARC or AIDS, of which nine had repeat serum B12 estimation prior to progression. All nine patients had or developed falling serum B12 levels without any evidence of an HIV-related bowel disorder. All patients progressing had falling CD4 counts. Subnormal serum B12 levels are common in HIV disease and occur at an early stage. B12 levels fall in most patients with time and may help predict those patients whose disease will progress the most rapidly.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Cytogenetic findings of a child with transcobalamin II deficiency.

Transcobalamin II deficiency is a rare, probably autosomal recessive, inborn error of protein metabolism [Hakami et al., 1971]. Several authors have described the morphological characteristics of bone marrow aspirates from patients with this disorder; no reports have detailed the cytogenetic findings [Hitzig et al., 1974; Hakami et al., 1971; Niebrugge et al., 1982]. We report the cytogenetic findings of the bone marrow aspirates from an infant with transcobalamin II deficiency and identify fragile site expression in the hematopoietic cells in this patient.

Chromosome Aberrations↗
PubMed2006

Study of four genes belonging to the folate pathway: transcobalamin 2 is involved in the onset of non-syndromic cleft lip with or without cleft palate.

Cleft lip with or without cleft palate (CL/P) is the most common inborn craniofacial anomaly. Affected individuals require extensive medical and psychosocial support. Although CL/P has a complex and poorly understood etiology, increasing evidence of folate pathway involvement has been collected. So far, only the MTHFR gene has been extensively investigated as a risk factor for CL/P, while little has been done to test genetic variations in the folate biosynthetic pathways that may influence the infant's susceptibility to these birth defects. To date, this paper presents the first attempt to verify the involvement of four genes belonging to the folate pathway in nonsyndromic cleft onset. We used a case-parent triad design to test for linkage disequilibrium in the case of seven SNPs mapping on four different genes: transcobalamin 1 and 2 (TCN1 and TCN2), methionine synthase (MTR), and MTR reductase (MTRR). Our finding suggests that TCN2 is involved in causing CL/P. Indeed, significant overtransmission of the C allele was observed at the polymorphism c.776C>G (p.Pro259Arg) to the affected offspring (P=0.01). Results obtained with additional TCN2 polymorphisms suggest that c.776C>G may be functionally related to CL/P. However, because conflicting data exist with regard to the effect of the polymorphism in transcobalamin 2 function or in perturbing plasma levels of key molecules in the folate pathway, further investigation is warranted to confirm our data.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1979

Evidence for 15 genetically determined electrophoretic variants of transcobalamin II in rabbit serum.

By starch gel electrophoresis and autoradiography two classes of vitamin B12 binding proteins were detected in rabbit serum. By analogy to the nomenclature used in man, the two classes of proteins were named "transcobalamin I" (TCI) and "transcobalamin II" (TCII). Fifteen TCII phenotypes were observed, and family data indicated that they are controlled by five allelic codominant genes. The possibility that the five genes arise from the action of at least two polymorphic and closely linked structural loci is discussed.

Animals↗
PubMed1983

Effect of dexamethasone on serum transcobalamin II concentration in women undergoing pelvic surgery.

Dexamethasone (120 mg/day for 2 days) was administered intramuscularly to young females undergoing pelvic surgery for infertility. The therapy was shown to cause a transient increase in the serum level of the granulocyte-produced transcobalamins (TCI and TCIII) and more significantly in the monocyte-produced transcobalamin (TCII), from 1220 +/- 70 to 1980 +/- 158 pg/ml (P less than 0.001). The change closely followed a transient elevation of EA rosette forming cells in the peripheral blood (from 20 to 50% of the total mononuclear cell population), which are mainly monocytes. The observed effects were shown to be independent of the surgical trauma. The results indicate that the increase in serum TCII can be attributed to an effect of dexamethasone on monocytes.

Blood Cell Count↗
PubMed2003

Transcobalamin II receptor interacts with megalin in the renal apical brush border membrane.

Purified human transcobalamin II receptor (TC II-R) binds to megalin, a 600 kDa endocytic receptor with an association constant, K(a), of 66 n M and bound(max) of 1.1 mole of TC II-R/mole of megalin both in the presence and absence of its ligand, transcobalamin II (TC II). Immunoprecipitation followed by immunoblotting of Triton X-100 extracts of the apical brush border membrane (BBM) from rabbit renal cortex revealed association of these two proteins. (35)[S]-TC II complexed with cobalamin (Cbl; Vitamin B(12)) bound to Sepharose-megalin affinity matrix and the binding was enhanced 5-fold when TC II-R was prebound to megalin. Megalin antiserum inhibited both the TC II-R-dependent and -independent binding of (35)[S]-TC II-Cbl to megalin, while TC II-R antiserum inhibited only the TC II-R-dependent binding. In rabbits with circulating antiserum to megalin, renal apical BBM megalin was present as an immune complex, but its levels were not altered. However, the protein levels of both TC II-R and the cation-independent mannose 6-phosphate receptor (CIMPR) were drastically reduced and the urinary excretion of TC II, albumin, and other low-molecular weight proteins was significantly increased. These results suggest that megalin contains a distinct single high-affinity binding site for TC II-R and their association in the native renal BBM is important for tubular reabsorption of many proteins, including TC II.

Animals↗
PubMed1987

Receptors for transferrin and transcobalamin II display segregated distribution on microvilli of leukemia L1210 cells.

Simultaneous addition of uniform latex particles derivatized with transferrin (0.532 micron) and transcobalamin II (0.345 micron) to leukemia L1210 cells resulted in segregated binding to individual microvilli as demonstrated by scanning electron microscopy. This segregated distribution suggests that individual microvilli are endowed either transferrin or transcobalamin II receptors but not both. Intracellular sorting and segregation of newly synthesized or recycling receptors probably occur prior to expression on the plasmalemma microvilli.

Animals↗
PubMed1982

Transcobalamin II in protein-energy malnutrition among residents of the Kivu area.

Transcobalamin II, the crucial transport protein for vitamin B12, was measured in protein-energy malnutrition patients and healthy controls. No significant difference between these two groups was observed. Treated patients showed higher concentrations than those on admission. The striking observation was, however, that all African subjects studied in Lwiro, Zaïre, had very high transcobalamin II levels compared to Europeans living either in Brussels or in Lwiro, and compared to Africans living in Brussels. This observation seems therefore not simply related to genetic or to environmental factors. No evident explanation is yet available.

Adolescent↗
PubMed1985

Synthesis of transcobalamin II by cultured human hepatocytes.

Cultured HepG2 cells, derived from a human hepatoma synthesized and released unsaturated, immunoreactive transcobalamin II. Synthesis was confirmed by the blocking with inhibitors of protein synthesis and by incorporation of tritiated leucine into transcobalamin II.

Apoproteins↗
PubMed1987

The interaction of human transcobalamin isopeptides in cerebrospinal fluid and plasma with cobalamin and the cellular acceptor.

By isoelectric focusing, transcobalamin from human cerebrospinal fluid was separated into the phenotypes X, M, MX, SX and MS. The corresponding plasma transcobalamins were of identical phenotypes. The unsaturated cobalamin-binding capacity in the cerebrospinal fluid was 0.12-0.54 nmol.1(-1), median 0.23 nmol.1(-1); no difference in binding capacity was found between the individual phenotypes. The isopeptides M, X and S bound cyano[57Co]cobalamin from pH 6 to 10. The apparent affinity constant was the same for all the isopeptides (0.4.10(12) l.mol-1, pH 7.4). The isopeptide-cobalamin complexes bound to acceptors on human placenta membranes with an apparent affinity constant of 11.10(9) l.mol-1, pH 7.4.

Adult↗