Effects of hypoxia on iron absorption and mobilization in the rat

1964 ◽  
Vol 207 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Georg W. Strohmeyer ◽  
Stephen A. Miller ◽  
Robert W. Scarlata ◽  
Edward W. Moore ◽  
Mortimer S. Greenberg ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Iron Absorption ◽  
Test Dose ◽  
Oral Iron ◽  
Base Line ◽  
Tissue Storage ◽  
Iron Load ◽  
Tissue Iron ◽  
Iron Deficient

Rats exposed to an atmosphere of 10% oxygen increase their absorption of a test dose of iron after 6 8 hr. Release of tissue storage iron begins within 2 hr of the start of hypoxia and continues for at least 8 hr. An oral iron load does not prevent the release of tissue iron in response to hypoxia. Iron-loaded rats also release iron from storage depots and increase their minimal absorption in response to hypoxia. Iron-deficient rats apparently have a diminished tissue release and also increase absorption above their elevated base-line levels. Xanthine loading had no effect on the release of tissue iron or changes in absorption with hypoxia, and there was no evidence that changes in xanthine oxidase activity in the liver or bowel were directly associated with tissue release or absorption of iron.

Zinc, cadmium, and iron interactions during intestinal absorption in iron-deficient mice

1978 ◽  
Vol 56 (3) ◽  
pp. 384-389 ◽  
Author(s):  
D. L. Hamilton ◽  
J. E. C. Bellamy ◽  
J. D. Valberg ◽  
L. S. Valberg
Keyword(s):  
Zinc Chloride ◽  
Binding Sites ◽  
Iron Absorption ◽  
High Capacity ◽  
Test Dose ◽  
The Body ◽  
Zinc Uptake ◽  
Iron Deficient ◽  
Zinc Cadmium ◽  
Iron And Zinc

Zinc absorption from a test dose of (65Zn) zinc chloride was increased in mice with a high capacity to absorb iron induced by a low-iron diet. When radiolabelled zinc chloride in concentrations varying from 0.025 to 0.30 mM was perfused through open-ended duodenal loops of mice fed this diet, the proportion of zinc taken up from the lumen and transferred to the body was greater from lower than from higher doses. The addition of iron to the perfusate inhibited zinc uptake and transfer, and zinc had a similar effect on iron absorption. Cadmium, a potent inhibitor of iron uptake in mice fed a low-iron diet, impaired zinc uptake under these dietary conditions. These results suggest that in dietary-induced iron deficiency there are analogous mucosal binding sites for the uptake of iron and zinc. There also appear to be mutually exclusive binding sites for the absorption of these metals: radiolabeled iron absorption from an intragastric test dose was enhanced in mice with a high capacity to absorb iron produced by bleeding, whereas the absorption of zinc was not increased.

scholarly journals Iron Absorption in Iron-Deficient Women, Who Received 65 mg Fe with an Indonesian Breakfast, Is Much Better from NaFe(III)EDTA than from Fe(II)SO4, with an Acceptable Increase of Plasma NTBI. A Randomized Clinical Trial

2018 ◽  
Vol 11 (3) ◽  
pp. 85 ◽  
Author(s):  
Eka Ginanjar ◽  
Lilik Indrawati ◽  
Iswari Setianingsih ◽  
Djumhana Atmakusumah ◽  
Alida Harahap ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Absorption ◽  
Normal Values ◽  
Test Dose ◽  
Food Fortification ◽  
Double Blind ◽  
Blood Tests ◽  
Oral Test ◽  
Iron Deficient ◽  
Fe Complexes

Plasma non-transferrin-bound iron (NTBI) is potentially harmful due to the generation of free radicals that cause tissue damage in vascular and other diseases. Studies in iron-replete and iron-deficient subjects, receiving a single oral test dose of Fe(II)SO4 or NaFe(III)EDTA with water, revealed that FeSO4 was well absorbed when compared with NaFeEDTA, while only the Fe(II) compound showed a remarkable increase of NTBI. As NaFeEDTA is successfully used for food fortification, a double-blind randomized cross-over trial was conducted in 11 healthy women with uncomplicated iron deficiency. All subjects received a placebo, 6.5 mg FeSO4, 65 mg FeSO4, 6.5 mg NaFeEDTA, and 65 mg NaFeEDTA with a traditional Indonesian breakfast in one-week intervals. Blood tests were carried out every 60 min for five hours. NTBI detection was performed using the fluorescein-labeled apotransferrin method. Plasma iron values were highly increased after 65 mg NaFeEDTA, twice as high as after FeSO4. A similar pattern was seen for NTBI. After 6.5 mg of NaFeEDTA and FeSO4, NTBI was hardly detectable. NaFeEDTA was highly effective for the treatment of iron deficiency if given with a meal, inhibiting the formation of nonabsorbable Fe-complexes, while NTBI did not exceed the range of normal values for iron-replete subjects.

Copper deficiency increases iron absorption in the rat

2003 ◽  
Vol 285 (5) ◽  
pp. G789-G795 ◽  
Author(s):  
Carla Thomas ◽  
Phillip S. Oates
Keyword(s):  
Kupffer Cells ◽  
Oxidase Activity ◽  
Copper Deficiency ◽  
Iron Absorption ◽  
Nonheme Iron ◽  
Iron Accumulation ◽  
Strong Correlations ◽  
Liver Iron ◽  
Iron Deficient ◽  
Ferroxidase Activity

Release of iron from enterocytes and hepatocytes is thought to require the copper-dependent ferroxidase activity of hephaestin (Hp) and ceruloplasmin (Cp), respectively. In swine, copper deficiency (CD) impairs iron absorption, but whether this occurs in rats is unclear. By feeding a diet deficient in copper, CD was produced, as evidenced by the loss of copper-dependent plasma ferroxidase I activity, and in enterocytes, CD reduced copper levels and copper-dependent oxidase activity. Hematocrit was reduced, and liver iron was doubled. CD reduced duodenal mucosal iron and ferritin, whereas CD increased iron absorption. Duodenal mucosal DMT1-IRE and ferroportin1 expression remained constant with CD. When absorption in CD rats was compared with that seen normally and in iron-deficient anemic animals, strong correlations were found among mucosal iron, ferritin, and iron absorption, suggesting that the level of iron absorption was appropriate given that the erythroid and stores stimulators of iron absorption are opposed in CD. Because CD reduced the activity of Cp, as evidenced by copper-dependent plasma ferroxidase I activity and hepatocyte iron accumulation, but iron absorption increased, it is unlikely that the ferroxidase activity of Hp is important and suggests another function for this protein in the export of iron from the enterocyte during iron absorption. Also, the copper-dependent ferroxidase activity of Cp does not appear important for iron efflux from macrophages, because Kupffer cells of the liver and nonheme iron levels of the spleen were normal during copper deficiency, suggesting another role for Cp in these cells.

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.

Proton Pump Inhibitor Use and the Ability to Replete Iron Stores

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1039-1039
Author(s):  
Alina M Huang ◽  
Christine M Ho ◽  
John L. Reagan ◽  
Eric Winer
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Proton Pump ◽  
Iron Absorption ◽  
Oral Iron ◽  
Deficiency Anemia ◽  
Care Clinic ◽  
Iron Stores ◽  
Iron Deficient ◽  
Iron Replacement

Abstract Abstract 1039 Background: Oral iron absorption occurs in the duodenum and requires increased gastric acidity to allow iron to remain in the more soluble, ferrous form. Many patients with iron deficiency anemia who require oral iron repletion are on proton pump inhibitors (PPIs) for management of various conditions that require acid suppression for treatment. In vitro studies suggest that inhibition of gastric acid secretion decreases the bioavailability of iron. In patients with established iron deficiency anemia who are on PPIs, there is a paucity of data regarding the efficacy of iron replacement with concomitant PPI use. Sharma et al. published a case report on 2 patients who were iron deficient and on PPI therapy (Sharma et. al. Southern Medical Journal 2004). Their findings showed that discontinuation of the PPI resulted in improvement of iron deficiency anemia on the same dose of oral iron replacement. Additionally, Hutchinson et al. demonstrated that in individuals with hereditary hemachromatosis, those on PPIs had a significant reduction in phlebotomy requirements needed to keep serum ferritin ∼50μg (Hutchinson et. al. Gut 2007). We conducted a retrospective study to assess whether a difference exists in terms of iron repletion between patients on a PPI versus those not on a PPI. Methods: Patients were selected from the medical primary care clinic from charts dating January 2000 until January 2009. Included patients were adults older than 18 years of age, a diagnosis of iron deficiency based on ferritin < 30 with at least one follow up ferritin value, and recipients of oral iron replacement. Excluded patients were those with chronic active bleeding and anemia of chronic disease. Indices examined include iron (Fe), total iron binding capacity (TIBC), ferritin, transferrin saturation, hemoglobin (Hb), hematocrit (Hct), and mean corpuscular volume (MCV). The primary endpoint of interest is repletion of iron stores defined by ferritin > 30. Those who were able to replete their iron stores are termed “responders” and those who were not are termed “nonresponders”. Results: Forty-five patients have been identified who have met the above criteria. Of these patients, 14 were on a PPI and 31 were not on a PPI. Of the patients not on a PPI, 38.7% responded to oral iron. Of the patients on a PPI, 50.0% responded to oral iron. The average initial and final values of indices of interest were compared between the groups (Table 1). Discussion: Our data suggests that patients both on and off PPIs show the ability to replete their iron stores. Furthermore, it appears that a slightly greater percentage of patients on a PPI compared with those not on a PPI are able to replete their iron stores, though the numbers remain small. Most importantly, these findings challenge the commonly held belief that PPI use impairs oral iron absorption. A prospective study is warranted to further confirm these observational data. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Relationship between Down-Regulation of Copper-Related Genes and Decreased Ferroportin Protein Level in the Duodenum of Iron-Deficient Piglets

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 104
Author(s):  
Aneta Jończy ◽  
Rafał Mazgaj ◽  
Rafał Radosław Starzyński ◽  
Piotr Poznański ◽  
Mateusz Szudzik ◽  
...  
Keyword(s):  
Iron Absorption ◽  
Underlying Mechanism ◽  
Metabolic Effects ◽  
Deficiency Anemia ◽  
Copper Transporter ◽  
Cellular Iron ◽  
Iron Deficient ◽  
Copper Distribution ◽  
Iron Deposits ◽  
Neonatal Iron Deficiency

In mammals, 2 × 1012 red blood cells (RBCs) are produced every day in the bone marrow to ensure a constant supply of iron to maintain effective erythropoiesis. Impaired iron absorption in the duodenum and inefficient iron reutilization from senescent RBCs by macrophages contribute to the development of anemia. Ferroportin (Fpn), the only known cellular iron exporter, as well as hephaestin (Heph) and ceruloplasmin, two copper-dependent ferroxidases involved in the above-mentioned processes, are key elements of the interaction between copper and iron metabolisms. Crosslinks between these metals have been known for many years, but metabolic effects of one on the other have not been elucidated to date. Neonatal iron deficiency anemia in piglets provides an interesting model for studying this interplay. In duodenal enterocytes of young anemic piglets, we identified iron deposits and demonstrated increased expression of ferritin with a concomitant decline in both Fpn and Heph expression. We postulated that the underlying mechanism involves changes in copper distribution within enterocytes as a result of decreased expression of the copper transporter—Atp7b. Obtained results strongly suggest that regulation of iron absorption within enterocytes is based on the interaction between proteins of copper and iron metabolisms and outcompetes systemic regulation.

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