The Transport of Endogenous Vitamin B12 in Normal Human Serum

1976 ◽  
Vol 51 (1) ◽  
pp. 47-52
Author(s):  
J. M. England ◽  
Margaret C. Down ◽  
Irene J. Wise ◽  
J. C. Linnell

1. Serum from normal subjects has been chromatographed on Sephadex G-200 columns and the fractions containing transcobalamins 0, I and II have been identified. 2. The fractions corresponding to transcobalamin I contained, on average, 90% of the endogenous vitamin B12. Only 3% was attached to transcobalamin 0, and 7% was bound to transcobalamin II.

1977 ◽  
Vol 53 (5) ◽  
pp. 453-457 ◽  
Author(s):  
C. A. Hall

1. After fractionation of the vitamin B12-binding proteins of ten normal sera the components containing transcobalamin II and R-type binders of vitamin B12 respectively were studied for endogenous vitamin B12 content by two distinct systems of vitamin B12 assay. 2. The measurements of total serum vitamin B12 by either bioassay with Euglena gracilis or a radioisotope dilution assay agreed closely. 3. The native vitamin B12 carried by transcobalamin II was higher as measured by bioassay than by isotope dilution assay. 4. The presence of the transcobalamin II fraction of human serum altered the key reaction between the binding reagent of the isotope dilution assay, so that this assay failed to measure vitamin B12 quantitatively. 5. Probably, the mean fraction of plasma vitamin B12 carried by transcobalamin II is in the range 20–30%.


1981 ◽  
Vol 97 (2) ◽  
pp. 231-242 ◽  
Author(s):  
F. A. O. Mendelsohn ◽  
Christine D. Kachel

Abstract. Normal human serum markedly stimulated aldosterone production from rat adrenal glomerulosa cells incubated in Krebs Ringer bicarbonate medium (KRBGA). The effect was dose-related. In [K+] 3.6 mm KRBGA medium, serum stimulated aldosterone output to higher levels than those produced by maximal doses of serotonin (5 HT), angiotensin II (AII) or high [K+] (8.4 mm). Cells maximally stimulated by high [K+], 5 HT or AII in KRBGA medium were further stimulated by serum. The angiotensin analogue, [Sar1, Ala8]-AII abolished the effect of AII but not that of high [K+] or serum. Basal and ACTH-stimulated corticosterone outputs of rat fasciculata cells were not significantly affected by sera known to stimulate glomerulosa cells. Aldosterone stimulating activity of serum was dialysable and fully recovered in a serum ultrafiltrate. The serotonin blockers methysergide and metergoline abolished the aldosterone stimulating activity of serum but also depressed basal aldosterone output and methysergide reduced K+-stimulated output. Chymotrypsin digestion abolished the aldosterone stimulating activity of AII but not that of serotonin or serum. 5 HT concentration of sera was measured and found to be near the threshold for aldosterone stimulation. Sodium loading and depletion of 4 normal subjects did not consistently modify the aldosterone stimulating activity of their sera. In a supplemented medium (RPMI 1640), basal and K+-stimulated aldosterone outputs were higher than in KRBGA medium. Under these conditions serum stimulated aldosterone output in normal [K+] medium but only marginally in high [K+] medium. In RPMI medium, serum did not further stimulate cells maximally stimulated with serotonin. Serum appears to stimulate aldosterone production from glomerulsoa cells by two different mechanisms: One is probably due to a serotonin-like substance. A separate effect of serum, seen only in KRBGA medium, is to enhance aldosterone output of glomerulosa cells maximally stimulated by K+, 5 HT or AII.


2009 ◽  
Vol 11 (1) ◽  
pp. 8-12 ◽  
Author(s):  
David W. Sonneborn ◽  
Ann B. Baskerville ◽  
William Regelson

Nature ◽  
1968 ◽  
Vol 217 (5125) ◽  
pp. 272-274 ◽  
Author(s):  
EVANGELOS GIZIS ◽  
LEO M. MEYER

1997 ◽  
Vol 1 (4) ◽  
pp. 196-202
Author(s):  
Gerald G. Krueger ◽  
Cynthia M. Jorgensen

Background: A framework hypothesis for the pathogenesis of psoriasis states that “there is an aberration throughout the skin of patients with psoriasis that is modified to disease expression by circulating factors.” Objective: A question to emerge from this hypothesis concerns whether fibroblasts could be more central to the aberration than other cells of the skin? This article focuses on the modulation of growth of fibroblasts from uninvolved and involved sites of patients with psoriasis as a function of the type of serum in which they are grown. Methods: Fibroblasts were generated from normal subjects and from involved and uninvolved sites of six untreated psoriatic subjects and their growth in vitro was assessed as a function of the type of serum (fetal bovine serum, normal human serum, and serum from psoriatic subjects) in which they are grown. Results: The data show (a) that fibroblasts from psoriatic subjects, especially from uninvolved sites, have an inherent capacity to proliferate at an enhanced rate relative to normal fibroblasts; (b) that this enhanced proliferation can be augmented by normal human serum and to a greater degree by serum from psoriatic subjects; (c) that ≈ 40% of the enhanced proliferation is secondary to the psoriasis serum phenotype; (d) that ≈ 30% of enhanced proliferation is secondary to the psoriasis fibroblast phenotype; and (e) that the magnitude of these features are independent of the severity of psoriasis, as assessed at the time of donation of biopsies for generation of test fibroblasts or of blood for serum. Conclusion: These data support the hypothesis that there is an aberration throughout the skin of patients with psoriasis (enhanced proliferation of fibroblasts in vitro, especially from uninvolved sites) that is modified by circulating factors (serum).


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