scholarly journals Iron metabolism in the Belgrade rat

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 623-628 ◽  
Author(s):  
J Edwards ◽  
H Huebers ◽  
C Kunzler ◽  
C Finch
Keyword(s):  
Iron Metabolism ◽  
Iron Uptake ◽  
Iron Concentration ◽  
Release Mechanism ◽  
Iron Release ◽  
Intracellular Iron ◽  
Plasma Iron ◽  
Body Tissues ◽  
Erythroid Hyperplasia ◽  
Iron Deficient

Iron metabolism in the Belgrade rat was examined in the intact animal and in the reticulocyte suspensions. The plasma iron turnover was increased. However, when allowance was made for the effect of the elevated plasma iron concentration, erythroid marrow capacity for iron uptake was at basal levels. Numbers of erythroid cells in marrow and spleen measured by the radioiron dilution technique were increased. Thus iron uptake was not proportionate to the erythroid hyperplasia in the b/b rat, despite a more than adequate plasma iron supply. This relative deficiency in iron uptake was reflected in a severe microcytosis and elevated red cell protoporphyrin. Reticulocyte incubation studies demonstrated an unimpaired uptake of the transferrin- iron-receptor complex but a marked reduction in iron accumulation. The diferric transferrin molecule, when it did give up iron within the cell, released both of its iron atoms so that only apotransferrin was returned to the media. In contrast to the nearly complete release of iron within the normal reticulocyte, the major portion of iron taken up by the Belgrade reticulocyte was returned to the plasma. The release mechanism that can be impaired in iron-deficient reticulocytes by EDTA or cadmium was shown to be affected by lower concentrations of these substances in the Belgrade reticulocyte. It is concluded that the Belgrade rat has an abnormality of iron release within the absorptive vacuole that is responsible for a state of intracellular iron deficiency, involving the erythron and other body tissues.

scholarly journals Iron metabolism in the Belgrade rat

Blood ◽  
1986 ◽  
Vol 67 (3) ◽  
pp. 623-628 ◽  
Author(s):  
J Edwards ◽  
H Huebers ◽  
C Kunzler ◽  
C Finch
Keyword(s):  
Iron Metabolism ◽  
Iron Uptake ◽  
Iron Concentration ◽  
Release Mechanism ◽  
Iron Release ◽  
Intracellular Iron ◽  
Plasma Iron ◽  
Body Tissues ◽  
Erythroid Hyperplasia ◽  
Iron Deficient

Abstract Iron metabolism in the Belgrade rat was examined in the intact animal and in the reticulocyte suspensions. The plasma iron turnover was increased. However, when allowance was made for the effect of the elevated plasma iron concentration, erythroid marrow capacity for iron uptake was at basal levels. Numbers of erythroid cells in marrow and spleen measured by the radioiron dilution technique were increased. Thus iron uptake was not proportionate to the erythroid hyperplasia in the b/b rat, despite a more than adequate plasma iron supply. This relative deficiency in iron uptake was reflected in a severe microcytosis and elevated red cell protoporphyrin. Reticulocyte incubation studies demonstrated an unimpaired uptake of the transferrin- iron-receptor complex but a marked reduction in iron accumulation. The diferric transferrin molecule, when it did give up iron within the cell, released both of its iron atoms so that only apotransferrin was returned to the media. In contrast to the nearly complete release of iron within the normal reticulocyte, the major portion of iron taken up by the Belgrade reticulocyte was returned to the plasma. The release mechanism that can be impaired in iron-deficient reticulocytes by EDTA or cadmium was shown to be affected by lower concentrations of these substances in the Belgrade reticulocyte. It is concluded that the Belgrade rat has an abnormality of iron release within the absorptive vacuole that is responsible for a state of intracellular iron deficiency, involving the erythron and other body tissues.

scholarly journals Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Vitamin E ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Plasma Iron ◽  
Erythroid Hyperplasia

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.

scholarly journals Regulation of iron absorption and storage iron turnover

Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 30-37
Author(s):  
A Rosenmund ◽  
S Gerber ◽  
H Huebers ◽  
C Finch
Keyword(s):  
Iron Absorption ◽  
Iron Concentration ◽  
Iron Release ◽  
Plasma Iron ◽  
Iron Supply ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Humoral Mechanism ◽  
And Storage ◽  
Male Rate

The regulation of iron supply to plasma was studied in male rate. Repeated exchange transfusions were first carried out with plasma from iron-deficient or iron-loaded animals. There was no recognizable effect on the amount of iron entering the plasma as evidenced by plasma iron concentration or iron absorption by recipient animals. In other studies, iron compounds having different tissue distribution were injected. Subsequent iron release was greater from reticuloendothelial cells than from other iron-loaded tissues. When requirements for transferrin iron were increased by exchange transfusion with high reticulocyte blood, within minutes there was a doubling of the rate of tissue iron donation. It was concluded from these studies that (1) iron turnover in the plasma is primarily determined by the number of tissue receptors for iron, particularly those of the erythron, (2) that the amount of iron supplied by each donor tissue is dependent on the output of other donor tissues, and (3) that a humoral mechanism regulating iron exchange is unlikely in view of the speed of response and magnitude of changes in plasma iron turnover. It is proposed that there is some direct mechanism that determines the movement of iron from donor tissues to unsaturated transferrin binding sites.

scholarly journals Regulation of iron absorption and storage iron turnover

Blood ◽  
1980 ◽  
Vol 56 (1) ◽  
pp. 30-37 ◽  
Author(s):  
A Rosenmund ◽  
S Gerber ◽  
H Huebers ◽  
C Finch
Keyword(s):  
Iron Absorption ◽  
Iron Concentration ◽  
Iron Release ◽  
Plasma Iron ◽  
Iron Supply ◽  
Tissue Iron ◽  
Iron Deficient ◽  
Humoral Mechanism ◽  
And Storage ◽  
Male Rate

Abstract The regulation of iron supply to plasma was studied in male rate. Repeated exchange transfusions were first carried out with plasma from iron-deficient or iron-loaded animals. There was no recognizable effect on the amount of iron entering the plasma as evidenced by plasma iron concentration or iron absorption by recipient animals. In other studies, iron compounds having different tissue distribution were injected. Subsequent iron release was greater from reticuloendothelial cells than from other iron-loaded tissues. When requirements for transferrin iron were increased by exchange transfusion with high reticulocyte blood, within minutes there was a doubling of the rate of tissue iron donation. It was concluded from these studies that (1) iron turnover in the plasma is primarily determined by the number of tissue receptors for iron, particularly those of the erythron, (2) that the amount of iron supplied by each donor tissue is dependent on the output of other donor tissues, and (3) that a humoral mechanism regulating iron exchange is unlikely in view of the speed of response and magnitude of changes in plasma iron turnover. It is proposed that there is some direct mechanism that determines the movement of iron from donor tissues to unsaturated transferrin binding sites.

scholarly journals Abnormalities of iron metabolism and erythropoiesis in vitamin E- deficient rabbits

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Vitamin E ◽  
Iron Metabolism ◽  
Iron Absorption ◽  
Iron Concentration ◽  
Vitamin E Deficiency ◽  
Deficient Diet ◽  
Plasma Iron ◽  
Erythroid Hyperplasia

Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.

Marginally excessive iron loading transiently blocks mucosal iron uptake in iron-deficient rats

2014 ◽  
Vol 307 (1) ◽  
pp. G89-G97 ◽  
Author(s):  
Shoko Shinoda ◽  
Shiho Yoshizawa ◽  
Eriko Nozaki ◽  
Kouki Tadai ◽  
Anna Arita
Keyword(s):  
Iron Uptake ◽  
Iron Concentration ◽  
Iron Loading ◽  
Short Acting ◽  
Excess Iron ◽  
Rapid Induction ◽  
Cellular Iron ◽  
Iron Load ◽  
Iron Deficient ◽  
Cellular Iron Uptake

Regular “mucosal block” is characterized by decreased uptake of a normal iron load 3–72 h after the administration of excess iron (generally 10 mg) to iron-deficient animals. We found that short-acting mucosal block could be induced by much lower iron concentration and much shorter induction time than previously reported, without affecting levels of gene expression. A rapid endocytic mechanism was reported to decrease intestinal iron absorption after a high iron load, but the activating iron load and the time to decreased absorption were undetermined. We assessed the effects of 30–2,000 μg iron load on iron uptake in the duodenal loop of iron-deficient and iron-sufficient rats under anesthesia. One hour later, mucosal cellular iron uptake in iron-deficient rats administered 30 μg iron was 76.1%, decreasing 25% to 50.7% in rats administered 2,000 μg iron. In contrast, iron uptake by iron-sufficient rats was 63% (range 60.3–65.5%) regardless of iron load. Duodenal mucosal iron concentration was significantly lower in iron-deficient than in iron-sufficient rats. Iron levels in portal blood were consistently higher in iron-deficient rats regardless of iron load, in contrast to the decreased iron uptake on the luminal side. Iron loading blocked mucosal uptake of marginally excess iron (1,000 μg), with a greater effect at 15 min than at 30 min. The rapid induction of short-acting mucosal block only in iron-deficient rats suggests DMT1 internalization.

Relationship among plasma iron, plasma iron turnover, and reticuloendothelial iron release

Blood ◽  
1983 ◽  
Vol 61 (4) ◽  
pp. 799-802 ◽  
Author(s):  
T Uchida ◽  
T Akitsuki ◽  
H Kimura ◽  
T Tanaka ◽  
S Matsuda ◽  
...  
Keyword(s):  
Ferrous Sulfate ◽  
Iron Concentration ◽  
Normal Subjects ◽  
Reticuloendothelial System ◽  
Iron Level ◽  
Iron Release ◽  
Lower Plasma ◽  
Plasma Iron ◽  
Normal Males ◽  
Composite Data

A circadian rhythm was demonstrated in 10 males and 10 females with respective mean decreases in plasma iron concentration at 18 hr of 62% and 47% of morning values. Ferrokinetic studies performed on 5 normal males and 5 normal females showed a more rapid disappearance rate and lower plasma iron turnover in the evening. Parallel studies were done on 6 normal males in the morning and 4 normal males in the evening of the release of reticuloendothelial iron at 8 and 18 hr after intravenous injection of 59Fe chondroitin ferrous sulfate. The 6-hr release in the morning was 54.1% and in the evening 25.9%. Composite data from morning and evening showed a correlation between plasma iron level and plasma iron turnover (r = 0.76, p less than 0.001). A similar correlation existed between the plasma iron level and the percent of radioiron released from the reticuloendothelial system (r = 0.67, 0.02 less than p less than 0.05). These data are consistent with a fluctuating iron release from the reticuloendothelial cell in normal subjects, which would account for the diurnal variation in plasma iron.

scholarly journals Role of copper in mitochondrial iron metabolism

Blood ◽  
1976 ◽  
Vol 48 (1) ◽  
pp. 77-85 ◽  
Author(s):  
DM Williams ◽  
D Loukopoulos ◽  
GR Lee ◽  
GE Cartwright
Keyword(s):  
Cytochrome Oxidase ◽  
Iron Metabolism ◽  
Oxidase Activity ◽  
Ferrous Iron ◽  
Iron Uptake ◽  
Ferric Iron ◽  
Intracellular Iron ◽  
Cytochrome Oxidase Activity ◽  
Heme Synthesis

Abstract Heme synthesis by copper-deficient cells was investigated to elucidate the nature of the defect in intracellular iron metabolism. Iron uptake from transferrin by copper-deficient reticulocytes was 52% of normal, and the rate of heme synthesis was 33% of normal. Hepatic mitochondria isolated from copper-deficient animals were deficient in cytochrome oxidase activity and failed to synthesize heme from ferric iron (Fe III) and protoporphyrin at the normal rate. The rate of heme synthesis correlated with the cytochrome oxidase activity. Heme synthesis from Fe(III) and protoporphyrin by normal mitochondria was enhanced by succinate and inhibited by malonate, antimycin A, azide, and cyanide. It is proposed that an intact electron transport system is required for the reduction of Fe(III), thereby providing a pool of ferrous iron (Fe II) for protoheme and heme a synthesis.

Diminished iron acquisition by cells and tissues of Belgrade laboratory rats

1992 ◽  
Vol 262 (2) ◽  
pp. R220-R224 ◽  
Author(s):  
E. A. Farcich ◽  
E. H. Morgan
Keyword(s):  
Iron Uptake ◽  
Iron Acquisition ◽  
Genetic Defect ◽  
In Vivo Studies ◽  
Intracellular Iron ◽  
Iron Transfer ◽  
Laboratory Rats ◽  
Iron Deficient

Iron uptake from transferrin by a variety of cells and tissues of homozygous Belgrade laboratory rats was compared with heterozygotes, and normal and iron-deficient Wistar rats. In all cases the results for homozygous Belgrade rats were lower than for the other animals. The maximal rate of iron uptake by fibroblasts cultured in vitro and iron passage to homozygous fetuses in utero was less than 60% of control values. In vivo studies of 15-day-old Belgrade rats revealed a defect in the homozygotes with reduced iron transfer to heart, liver, brain, and femurs. In addition, adult Belgrade laboratory rats had impaired intestinal iron absorption compared with the genetically normal animals. It is concluded that the defect in iron metabolism in the Belgrade laboratory rat is a ubiquitous one that affects transport of iron across membranes of many types of cells, resulting in low intracellular iron levels. This suggests that the genetic defect leads to a widely expressed abnormality in the structure and/or function of a membrane carrier for iron.

The Case for an Estrogen-iron Axis in Health and Disease

2019 ◽  
Vol 128 (04) ◽  
pp. 270-277 ◽  
Author(s):  
Mawieh Hamad ◽  
Khuloud Bajbouj ◽  
Jalal Taneera
Keyword(s):  
Iron Overload ◽  
Postmenopausal Women ◽  
Iron Metabolism ◽  
Premenopausal Women ◽  
Cardiovascular Complications ◽  
Iron Release ◽  
Intracellular Iron ◽  
Uterine Growth ◽  
Clinical Consequences ◽  
Health And Disease

AbstractClinical and experimental evidence suggest that estrogen manipulates intracellular iron metabolism and that elevated levels of estrogen associate with increased systemic iron availability. This has been attributed to the ability of estrogen to suppress hepcidin synthesis, maintain ferroportin integrity and enhance iron release from iron-absorbing duodenal enterocytes and iron-storing macrophages and hepatocytes. These observations speak of a potential “estrogen-iron” axis that manipulates iron metabolism in response to hematologic (erythropoiesis) and non-hematologic (uterine growth, pregnancy, lactation) needs for iron. Such an axis could contribute to minimizing iron deficiency in premenopausal women and iron overload in postmenopausal women. It could also exacerbate iron overload and related clinical consequences including cancer, osteoporosis, cardiovascular complications and neurodegenerative symptoms, especially in postmenopausal women on hormonal replacement therapy. Understanding the role of estrogen in iron metabolism may shed some light on the pleotropic, but often paradoxical, roles of estrogen in human health and disease.

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