scholarly journals Role of transferrin in determining internal iron distribution

Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 957-966
Author(s):  
P Pootrakul ◽  
A Christensen ◽  
B Josephson ◽  
CA Finch
Keyword(s):  
Isotope Ratio ◽  
Hepatic Uptake ◽  
The Other ◽  
Iron Salts ◽  
Iron Deficient ◽  
Loading And Unloading ◽  
The Mean

The behavior in vivo of transferrin in loading and unloading iron from its two sites was examined in rats. Radioiron entering the plasma from the gastrointestinal tract in iron-deficient, normal and iron-loaded rats did not differ in its subsequent tissue distribution between erythroid marrow and liver of normal recipients from a second isotope added to the same plasma in vitro. Loading studies in vitro were then carried out employing a reticulocyte incubation model designed to place one isotope predominantly on one site of transferrin, more available to the erythron, and the second isotope on the other site, more available to the liver. In 15 groups of animals in which 3 different iron salts were employed to load transferrin with iron, the mean isotope ratio in the erythron was 1.03 (+/-0.06 SD) and the mean liver ratio was 0.75 (+/-0.21 SD). It was found that the incubation of plasma with reticulocytes resulted in contamination of the plasma by radioactive hemoglobin. After allowance was made for hepatic uptake of radiohemoglobin in the 13 groups in which proper correction could be made, the isotope ratio in the liver became 0.97 (+/-0.17 SD). It is concluded that iron atoms from the two sites of transferrin have similar tissue distributions in vivo in the experimental situations examined.

scholarly journals Role of transferrin in determining internal iron distribution

Blood ◽  
1977 ◽  
Vol 49 (6) ◽  
pp. 957-966 ◽  
Author(s):  
P Pootrakul ◽  
A Christensen ◽  
B Josephson ◽  
CA Finch
Keyword(s):  
Isotope Ratio ◽  
Hepatic Uptake ◽  
The Other ◽  
Iron Salts ◽  
Iron Deficient ◽  
Loading And Unloading ◽  
The Mean

Abstract The behavior in vivo of transferrin in loading and unloading iron from its two sites was examined in rats. Radioiron entering the plasma from the gastrointestinal tract in iron-deficient, normal and iron-loaded rats did not differ in its subsequent tissue distribution between erythroid marrow and liver of normal recipients from a second isotope added to the same plasma in vitro. Loading studies in vitro were then carried out employing a reticulocyte incubation model designed to place one isotope predominantly on one site of transferrin, more available to the erythron, and the second isotope on the other site, more available to the liver. In 15 groups of animals in which 3 different iron salts were employed to load transferrin with iron, the mean isotope ratio in the erythron was 1.03 (+/-0.06 SD) and the mean liver ratio was 0.75 (+/-0.21 SD). It was found that the incubation of plasma with reticulocytes resulted in contamination of the plasma by radioactive hemoglobin. After allowance was made for hepatic uptake of radiohemoglobin in the 13 groups in which proper correction could be made, the isotope ratio in the liver became 0.97 (+/-0.17 SD). It is concluded that iron atoms from the two sites of transferrin have similar tissue distributions in vivo in the experimental situations examined.

Binding of 63Ni(II) to Ultrafiltrable Constituents of Rabbit Serum In Vivo and In Vitro

1975 ◽  
Vol 21 (4) ◽  
pp. 521-527 ◽  
Author(s):  
Noritake Asato ◽  
Maria van Soestbergen ◽  
F William Sunderman
Keyword(s):  
Rabbit Serum ◽  
Total Serum ◽  
In Vivo Experiments ◽  
The Mean ◽  
Layer Chromatography ◽  
In Vivo Administration ◽  
Mean Concentration

Abstract Binding of 63Ni(Il) to ultrafiltrable constituents of rabbit serum was studied (a) after in vitro incubation (2 h, 37 °C) of rabbit serum with 63NiCl2 (10-100 µmol/liter), and (b) at intervals (0.25-2 h) after in vivo administration of 63NiCl2 (40-160 µmol/kg body wt, i.v.). Serum ultrafiltrates were fractionated by thin-layer chromatography, and the separated compounds made visible by autoradiography and by ninhydrin staining. Several (≃5) ultrafiltrable 63Ni-complexes were demonstrable as distinct radiodense 63Ni-bands with chromatographic mobilities corresponding to those of ninhydrin-positive bands. Unbound 63Ni(II) was not detected in serum ultrafiltrates in either the in vitro or in vivo experiments. In sera (n = 10) incubated in vitro with 63Ni(II) (10 µmol/ liter), the mean percentage of ultrafiltrable 63Ni was 36% (range = 33-38) of total serum 63Ni. In contrast, in sera (n = 10) obtained 2 h after i.v. injection of 63Ni(II) (40 µmol/kg), the mean concentration of total serum 63Ni was 10.8 µmol/liter (range = 6-14), and the mean percentage of ultrafiltrable 63Ni was 15% (range = 9-21) of total serum 63Ni. The disparity between the percentages of ultrafiltrable 63Ni obtained in vitro and in vivo was obviated when the in vivo experiments were performed in rabbits bilaterally nephrectomized, with ligated common bile ducts. This investigation confirms the existence of several nickel receptors in serum ultrafiltrates and substantiates the role of ultrafiltrable complexes in the excretion of nickel.

Anionic and cationic exchange mechanisms in the skin of anurans, with special reference to Leptodactylidae in vivo

1971 ◽  
Vol 262 (842) ◽  
pp. 163-174 ◽  
Keyword(s):  
Transport Mechanism ◽  
Selective Inhibition ◽  
The Other ◽  
Sodium Absorption ◽  
Experimental Conditions ◽  
Net Flux ◽  
Cationic Exchange

In several species of anurans, the in vivo skin has been shown to absorb Na + and Cl - independently from dilute external solutions. That the mechanism for sodium absorption is different from that of chloride absroption is born out by the following: (1) Either of these ions is absorbed without an accompanying ion when this latter is impermeant. (2) From NaCl solutions there can be an unequal absorption of sodium and chloride. (3) A selective inhibition of the absorption of one of the ions can be produced experimentally, while the net flux of the other remains unchanged. In all these situations, the absorbed ion has to be exchanged against an endogenous ion of the same charge. In Calyptocephalella gayi , H + and HCO - 3 are exchanged against sodium and chloride respectively. A comparison of the relationships between H + excretion and Na + absorption in vivo skins and shortcircuited in vitro skins shows that in the latter no H + excretion occurs, only the Na + transport being maintained under these experimental conditions. From this, one must conclude that the active Na + transport is the motive factor of the transport mechanism. H + excretion by the in vivo skin plays the role of physiologically short-circuiting the Na + transport.

scholarly journals Investigation of the Role of CD8+ T Cells in Bovine Tuberculosis In Vivo

2003 ◽  
Vol 71 (8) ◽  
pp. 4297-4303 ◽  
Author(s):  
B. Villarreal-Ramos ◽  
M. McAulay ◽  
V. Chance ◽  
M. Martin ◽  
J. Morgan ◽  
...  
Keyword(s):  
Lymph Node ◽  
Bovine Tuberculosis ◽  
The Other ◽  
Cd8 Cells ◽  
Cd8 Cell ◽  
Ifn Γ ◽  
Mycobacterial Antigens

ABSTRACT Mycobacterium bovis is the causative agent of bovine tuberculosis (TB), and it has the potential to induce disease in humans. CD8+ T cells (CD8 cells) have been shown to respond to mycobacterial antigens in humans, cattle, and mice. In mice, CD8 cells have been shown to play a role in protection against mycobacterial infection. To determine the role of CD8 cells in bovine TB in vivo, two groups of calves were infected with the virulent M. bovis strain AF2122/97. After infection, one group was injected with a CD8 cell-depleting monoclonal antibody (MAb), and the other group was injected with an isotype control MAb. Immune responses to mycobacterial antigens were measured weekly in vitro. After 8 weeks, the animals were killed, and postmortem examinations were carried out. In vitro proliferation responses were similar in both calf groups, but in vitro gamma interferon (IFN-γ) production in 24-h whole-blood cultures was significantly higher in control cattle than in CD8 cell-depleted calves. Postmortem examination showed that calves in both groups had developed comparable TB lesions in the lower respiratory tract and associated lymph nodes. Head lymph node lesion scores, on the other hand, were higher in control calves than in CD8 cell-depleted calves. Furthermore, there was significant correlation between the level of IFN-γ and the head lymph node lesion score. These experiments indicate that CD8 cells play a role in the immune response to M. bovis in cattle by contributing to the IFN-γ response. However, CD8 cells may also play a deleterious role by contributing to the immunopathology of bovine TB.

scholarly journals Hepatoprotective and antineoplastic potencial of red propolis produced by the bees Apis mellifera in the semiarid of Rio Grande do Norte, Brazil

2019 ◽  
Vol 39 (9) ◽  
pp. 744-756
Author(s):  
Jardel B. Silva ◽  
Kaliane A.R. Paiva ◽  
Kizzy M.F.M. Costa ◽  
Geysa A. Viana ◽  
Hélio N. Araújo Júnior ◽  
...  
Keyword(s):  
Ethanolic Extract ◽  
The Other ◽  
Hepatoprotective Effect ◽  
Normal Cells ◽  
Propolis Extract ◽  
Regenerative Nodules ◽  
Serum Biochemical ◽  
The Mean

ABSTRACT: The objective of this study was to evaluate the hepatoprotective effect of the honey bee Apis mellifera ethanolic extract of the red propolis, obtained in four municipalities of the Rio Grande do Norte semi-arid region, through an in vitro evaluation of the antineoplastic potential in human hepatic carcinoma (HepG2) and normal cell lines (L929), and from the comet assay in hepatic cell lines (ZF-L hepatocytes) to evaluate the genoprotective potential of the extract. The hepatoprotective effect was also evaluated in vivo by the induction of chronic experimental hepatic lesions in rodents (Rattus norvegicus Berkenhout, 1769), Wistar line, by intraperitoneal administration of thioacetamide (TAA) at the dose of 0.2g/kg. The animals were distributed in the following experimental groups: G1 (control), G2 (treated with 500mg/kg ethanolic extract of propolis), G3 (treated with 500mg/kg of ethanolic extract and TAA) and G4 (treated with TAA). All rats were submitted to serum biochemical, macroscopic, histological and stereological biochemical exams of the liver. It was verified the genoprotective effect of red propolis since the mean damages promoted to DNA in cells tested with the extract were significantly lower than the mean of the positive control damage (hydrogen peroxide). The red propolis extract did not present cytotoxic activity to the tumor cells of human liver cancer, as well as to normal ones. The absence of cytotoxicity in normal cells may indicate safety in the use of the propolis extract. The results of the serum biochemical evaluation showed that the serum levels of the aminotransferase enzymes (AST) did not differ significantly between G1, G2 and G3 when compared to each other. G4 showed significant increase in levels compared to the other groups, indicating that the administration of the extract did not cause liver toxicity, as well as exerted hepatoprotective effect against the hepatic damage induced by TAA. The G3 and G4 animals developed cirrhosis, but in G3 the livers were characterized by the presence of small regenerative nodules and level with the surface of the organ, whereas in G4 the livers showed large regenerative nodules. The livers of the G1 and G2 animals presented normal histological appearance, whereas the livers of the G3 animals showed regenerative nodules surrounded by thin septa of connective tissue, and in G4 the regenerative nodules were surrounded by thick septa fibrous connective tissue. The analysis of the hepatic tissues by means of stereology showed that there was no statistical difference between the percentage of hepatocytes, sinusoids, and collagens in G1 and G2. In G3 the percentage of hepatocytes, sinusoids, and collagen did not differ significantly from the other groups. It was concluded that the ethanolic extract of the red propolis exerted a hepatoprotective effect, because it promoted in vitro reduction of the damage to the DNA of liver cells, antineoplastic activity in human hepatocellular carcinoma cell line (HepG2) and did not exert cytotoxic effect in normal cells or was able to reduce liver enzyme activity and the severity of cirrhosis induced by TAA in vivo.

Antihepcidin antibody treatment modulates iron metabolism and is effective in a mouse model of inflammation-induced anemia

Blood ◽  
2010 ◽  
Vol 115 (17) ◽  
pp. 3616-3624 ◽  
Author(s):  
Barbra J. Sasu ◽  
Keegan S. Cooke ◽  
Tara L. Arvedson ◽  
Cherylene Plewa ◽  
Aaron R. Ellison ◽  
...  
Keyword(s):  
Iron Metabolism ◽  
Response To Treatment ◽  
Antibody Testing ◽  
Antibody Treatment ◽  
Amino Acid Peptide ◽  
Iron Deficient ◽  
Anemia Treatment

Abstract Iron maldistribution has been implicated in multiple diseases, including the anemia of inflammation (AI), atherosclerosis, diabetes, and neurodegenerative disorders. Iron metabolism is controlled by hepcidin, a 25-amino acid peptide. Hepcidin is induced by inflammation, causes iron to be sequestered, and thus, potentially contributes to AI. Human hepcidin (hHepc) overexpression in mice caused an iron-deficient phenotype, including stunted growth, hair loss, and iron-deficient erythropoiesis. It also caused resistance to supraphysiologic levels of erythropoiesis-stimulating agent, supporting the hypothesis that hepcidin may influence response to treatment in AI. To explore the role of hepcidin in inflammatory anemia, a mouse AI model was developed with heat-killed Brucella abortus treatment. Suppression of hepcidin mRNA was a successful anemia treatment in this model. High-affinity antibodies specific for hHepc were generated, and hHepc knock-in mice were produced to enable antibody testing. Antibody treatment neutralized hHepc in vitro and in vivo and facilitated anemia treatment in hHepc knock-in mice with AI. These data indicate that antihepcidin antibodies may be an effective treatment for patients with inflammatory anemia. The ability to manipulate iron metabolism in vivo may also allow investigation of the role of iron in a number of other pathologic conditions.

scholarly journals Decreased Fast Ripples in the Hippocampus of Rats with Spontaneous Recurrent Seizures Treated with Carbenoxolone and Quinine

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Consuelo Ventura-Mejía ◽  
Laura Medina-Ceja
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
High Frequency Oscillations ◽  
The Mean ◽  
Eeg Recordings ◽  
The Right ◽  
Spontaneous Recurrent Seizures

Background. In models of temporal lobe epilepsy and in patients with this pathology, high frequency oscillations called fast ripples (FRs, 250–600 Hz) can be observed. FRs are considered potential biomarkers for epilepsy and, in the light of manyin vitroandin silicostudies, we thought that electrical synapses mediated by gap junctions might possibly modulate FRsin vivo.Methods. Animals with spontaneous recurrent seizures induced by pilocarpine administration were implanted with movable microelectrodes in the right anterior and posterior hippocampus to evaluate the effects of gap junction blockers administered in the entorhinal cortex. The effects of carbenoxolone (50 nmoles) and quinine (35 pmoles) on the mean number of spontaneous FR events (occurrence of FRs), as well as on the mean number of oscillation cycles per FR event and their frequency, were assessed using a specific algorithm to analyze FRs in intracranial EEG recordings.Results. We found that these gap junction blockers decreased the mean number of FRs and the mean number of oscillation cycles per FR event in the hippocampus, both during and at different times after carbenoxolone and quinine administration.Conclusion. These data suggest that FRs may be modulated by gap junctions, although additional experimentsin vivowill be necessary to determine the precise role of gap junctions in this pathological activity associated with epileptogenesis.

Platelet Involvement After Myocardial Infarction

1979 ◽  
Author(s):  
J.R. O’Brien ◽  
R.I. Handin ◽  
M.D. Etherington ◽  
R.D. Shuttleworth ◽  
W. Calwell
Keyword(s):  
Myocardial Infarction ◽  
Inverse Correlation ◽  
The Other ◽  
Interim Report ◽  
Clotting Time ◽  
Enzymatic Process ◽  
Acid Glycoprotein ◽  
The Mean

After myocardial Infarction (MI) the Heparin Thrombin Clotting Time (HTCT) of platelet (plt) poor plasma is short, indicating an increase in Heparin Neutralizing Activity (HNA). Plt. Factor 4 (PF4) released in vitro also neutralizes heparin. Does the plasma HTCT in MI reflect PF4 released in vivo? Fifteen patients with MI were compared with 23 controls. The mean HTCT was 43.9 sees, in controls and 14.8 sees, in patients. Plasma PF4 measured by RIA was abnormal in 3 patients but strictly normal in the other 12 (n = 12, mean 3.96 ng/ml; controls n = 22, mean 3.54). There was no correlation between the plasma PF4 and the HTCT. The plts, were frozen and thawed and the patients’ plts, released less HNA (0.17 units/109 plts.) relative to the controls (0.70 units/109plts.) and there was a tight inverse correlation between the plasma HTCT and the intra-plt. HNA. Plts, were isolated and stimulated maximally with thrombin; then malondialdehyde (MDA) production reflecting PG synthesis was monitored fluorometrically. Patients liberated less MDA. (415 ng/109plts.) than the controls (911 ng/plts.). All differences are significant, except the PF4. Plasma fibrinogen and α1 acid glycoprotein were also measured. Thus after an MI and presumably as a result of it, plts, are damaged or “exhausted” as reflected both by a decrease in an enzymatic process - PG synthesis and by a decrease in the content of HNA (? PF4). This interim report also clearly demonstrates that the plasma HTCT does not reflect the same attribute as plasma PF4 detected by RIA.

Peritoneal Sclerosis: Role of Plasticizers in Stimulating Interleukin-1 Production

1993 ◽  
Vol 13 (2_suppl) ◽  
pp. 517-519 ◽  
Author(s):  
Agostino Fracasso ◽  
Lorenzo Calo ◽  
Silvano Landini ◽  
Paolo Morachiello ◽  
Flavio Righetto ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Final Concentration ◽  
The Other ◽  
Fibroblast Proliferation ◽  
Two Cultures

The role of plasticizers (PLS) in inducing water flow inhibition and peritoneal sclerosis has been demonstrated in both In vivo and In vitro studies. Interleukin-1 (IL-1) has been shown to be a regulator of fibroblast proliferation as well as collagenase production. The aim of this study was to evaluate the role of PLS in stimulating mononuclear ce1l1L-1 secretion. Two cultures containing 103 cells/mL were obtained from 14 healthy subjects. One was used as the control, and the other was mixed with diethylhexylphthalate (DEHP) to reach a final concentration of 2.8x10” M. After 4 hours the samples were centrifuged, and the supernatants were tested by radioimmunoassay for IL-1α and IL-1β. The results showed a significant increase In both IL-1α and IL-1 β production In DEHP-stimulated cells in comparIson to the controls: 42.6±15.4 versus 29.3±10 ng/L (p<0.015) for IL-1α. and 153.6±55 versus 113.6±32 ng/L (p<0.03) for IL-1β In conclusion, PLS added to mononuclear cells were able to Induce IL-1 secretion. This mechanism could be responsible, at least in part, for the development of peritoneal sclerosis. Thus the employment of plasticlzer-free bags should be elective in peritoneal dialysis.

scholarly journals Tumor-induced granulopoiesis unrelated to colony-stimulating factor

Blood ◽  
1983 ◽  
Vol 62 (3) ◽  
pp. 693-696
Author(s):  
H Burlington ◽  
EP Cronkite ◽  
B Heldman ◽  
N Pappas ◽  
RK Shadduck
Keyword(s):  
The Other ◽  
Mammary Adenocarcinoma ◽  
Colony Stimulating Factor ◽  
Original Tumor ◽  
Distinct Morphology ◽  
Stimulating Factor

A transplantable granulocytosis-inducing mammary adenocarcinoma of mice was used to provide evidence about the role of tumor-generated factors in granulopoiesis. The original tumor produced high levels of colony- stimulating factor (CSF) in culture as well as inhibitor to CSF. The tumor was passaged repeatedly, both in host mice and in culture, and eventually displayed a varying capacity to induce granulocytosis. Tumors that were associated with either the induction of extreme granulocytosis or near-normal granulocyte levels were selected and passaged intermittently in vivo and in culture. Two tumor lines were thus isolated: one, line C-4a, inducing granulocytosis, and the other, line 34–4H, failing to induce granulocytosis. Both lines grow at the same rate in host mice, but in culture, each displays a distinct morphology. Measurement of CSF and inhibitor produced by each line in culture showed that line 34–4H retained the capacity to produce CSF and inhibitor in spite of losing the ability to influence granulopoiesis in vivo. This suggests that the various factors shown to influence granulopoiesis in vitro may have little or no role as physiologic regulators in vivo.

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