scholarly journals In Vitro and In Vivo Evaluations of Mesoporous Iron Particles for Iron Bioavailability

2019 ◽  
Vol 20 (21) ◽  
pp. 5291
Author(s):  
Lin ◽  
Wu ◽  
Liao ◽  
Jakfar ◽  
Tang ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Cell Model ◽  
Deficiency Anemia ◽  
Iron Particles ◽  
Standard Drug ◽  
Iron Deficient ◽  
Commercial Iron

Chronic renal failure involving hemodialysis results in blood loss during filtration. Iron deficiency and iron deficiency anemia can result. A compensatory increase in iron dosage has many side effects including discomfort. Elemental iron is a highly-pure iron source, which reduces the frequency of dosages; the solubility decreases with increased particle size or pore size. In this study, synthesized mesoporous iron particles (MIPs) were used to relieve iron deficiency anemia. Their bioavailability was measured in vitro by a Caco-2 cell model and in vivo in iron-deficient rats. In vitro bioavailability of MIPs was examined by measuring ferritin content in the Caco-2 cell model. Iron uptake of MIPs was significantly higher than commercial iron particles, which were less porous. In vivo bioavailability of MIPs was examined by measuring body weight gain and red blood cell-related parameters, compared with the bioavailability of standard drug ferrous sulfate in iron-deficient anemic rats. Finally, average hemoglobin content and hemoglobin regeneration efficiency were significantly higher in anemic rats supplemented with commercial iron particles, compared to anemic controls. In the 28-day oral toxicity test, MIPs were not significantly toxic to rat physiology or tissue histopathology. Thus, MIPs may allow effective recovery of hemoglobin in iron deficiency anemia.

scholarly journals Iron-Deficiency Anemia Results in Transcriptional and Metabolic Remodeling in the Heart Toward a Glycolytic Phenotype

2021 ◽  
Vol 7 ◽  
Author(s):  
Yu Jin Chung ◽  
Pawel Swietach ◽  
M. Kate Curtis ◽  
Vicky Ball ◽  
Peter A. Robbins ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Cardiac Contraction ◽  
Deficiency Anemia ◽  
Resonance Spectroscopy ◽  
Pyruvate Metabolism ◽  
Iron Deficient ◽  
Metabolic Remodeling

Iron deficiency is the most prevalent micronutrient disorder globally. When severe, iron deficiency leads to anemia, which can be deleterious to cardiac function. Given the central role of iron and oxygen in cardiac biology, multiple pathways are expected to be altered in iron-deficiency anemia, and identifying these requires an unbiased approach. To investigate these changes, gene expression and metabolism were studied in mice weaned onto an iron-deficient diet for 6 weeks. Whole-exome transcriptomics (RNAseq) identified over 1,500 differentially expressed genes (DEGs), of which 22% were upregulated and 78% were downregulated in the iron-deficient group, relative to control animals on an iron-adjusted diet. The major biological pathways affected were oxidative phosphorylation and pyruvate metabolism, as well as cardiac contraction and responses related to environmental stress. Cardiac metabolism was studied functionally using in vitro and in vivo methodologies. Spectrometric measurement of the activity of the four electron transport chain complexes in total cardiac lysates showed that the activities of Complexes I and IV were reduced in the hearts of iron-deficient animals. Pyruvate metabolism was assessed in vivo using hyperpolarized 13C magnetic resonance spectroscopy (MRS) of hyperpolarized pyruvate. Hearts from iron-deficient and anemic animals showed significantly decreased flux through pyruvate dehydrogenase and increased lactic acid production, consistent with tissue hypoxia and induction of genes coding for glycolytic enzymes and H+-monocarboxylate transport-4. Our results show that iron-deficiency anemia results in a metabolic remodeling toward a glycolytic, lactic acid-producing phenotype, a hallmark of hypoxia.

scholarly journals PREPARATION AND EVALUATION OF IRON OXIDE NANOPARTICLES FOR TREATMENT OF IRON DEFICIENCY ANEMIA

2018 ◽  
Vol 10 (1) ◽  
pp. 142 ◽  
Author(s):  
Fahima Hashem ◽  
Mohamed Nasr ◽  
Yomna Ahmed
Keyword(s):  
Folic Acid ◽  
Iron Oxide ◽  
Iron Deficiency ◽  
Iron Oxide Nanoparticles ◽  
Deficiency Anemia ◽  
Oxide Nanoparticles ◽  
Prepared Nanoparticles ◽  
Commercial Iron

Objective: The objective of this research was to formulate and evaluate iron oxide nanoparticles for treatment of iron deficiency anemia (IDA).Methods: Iron oxide nanoparticles were prepared by co-precipitation method and stabilized by coating with folic acid or chitosan. The prepared nanoparticles were characterized in vitro for morphology, particle size, zeta potential, crystallinity and ultraviolet-visible (UV-Vis) absorption. In vivo studies were performed to evaluate the efficacy of the prepared nanoparticles in treating iron-deficient anemic rats compared to the commercial iron product.Results: In vitro results revealed that particle sizes were 65.95±5 nm, 220.2±12 nm and 295.3±19 nm for uncoated iron oxide nanoparticles, folic acid-coated iron oxide nanoparticles and chitosan coated iron oxide nanoparticles, respectively. UV-Vis absorption spectrum and x-ray diffraction (XRD) patterns confirmed that the prepared nanoparticles were iron oxide nanoparticles. In vivo results indicated that folic acid-coated iron oxide nanoparticles showed effective restorative action, returning haemoglobin (Hb) concentration to normal levels, where not only complete recovery of Hb within short time from the anemic state to the high normal level, but also improved Hb concentrations compared to the commercial iron product.Conclusion: The results obtained in this research work clearly indicated a promising potential of folic acid-coated iron oxide nanoparticles for the effective treatment of IDA.

scholarly journals Glycolysis and Lactate Dehydrogenase A in Iron-Mediated Suppression of Osteoblast Function

2020 ◽  
Vol 3 ◽  
Author(s):  
Pete Hunter ◽  
Daniel Edwards ◽  
Christopher Miller ◽  
Erica Clinkenbeard
Keyword(s):  
Bone Marrow ◽  
Lactate Dehydrogenase ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Deficiency Anemia ◽  
Bone Homeostasis ◽  
Western Blots ◽  
Osteoblast Function

Background/Objective:   An estimated 37 million Americans have Chronic Kidney Disease (CKD), a condition in characterized by gradual decline in kidney function1. Patients with CKD are often afflicted with skeletal fractures, increasing morbidity and mortality. CKD has also shown a strong correlation with iron-deficiency anemia. The underlying mechanisms of how iron-deficiency anemia of CKD affects bone loss are not well understood. Based on RNA-sequencing results, we hypothesize that lactate dehydrogenase A (LDHA) may play a role in iron-deficiency mediated suppression of osteoblast differentiation and function.    Methods:   Mouse Progenitor Cells (MPC2) were incubated in osteogenic media along with deferoxamine (DFO) to induce differentiation in chronic iron deficiency; samples were collected after 7 and 14 days. Quantitative real-time PCR and western blot were used to validate LDHA mRNA and protein levels in DFO treated MPCs versus control cells. RNA levels of osteoblast genes and LDHA were also assessed in a pre-clinical mouse model of CKD.    Results:   In vitro, MPCs cultured in DFO media showed a significant increase of LDHA mRNA at 7 days (p=0.015) and returned to near control levels by day 14. Western blots showed a slight increase of total LDHA protein in DFO treated MPCs at 7 days and a large increase of protein at the 14-day mark (p=0.051). In vivo, CKD bone marrow showed a reduction in osteoblast gene expression (osteocalcin and type 1 collagen; p<0.05). LDHA mRNA expression was increased in CKD mice bone marrow when compared to wild-type mice (p=0.051), suggesting an inverse relationship.    Conclusion and Potential Impact:   Inappropriate activation of glycolysis and LDHA appears to play a role in iron-deficiency mediated suppression of osteoblast function in relation to CKD, both in vitro and in vivo. Further exploration of this relationship could be critical to the development of improved treatment options to maintain bone homeostasis during CKD. 

Maturation, iron deficiency, and ligands in enteric radioiron transport in vitro

1963 ◽  
Vol 204 (1) ◽  
pp. 171-175 ◽  
Author(s):  
W. S. Ruliffson ◽  
J. M. Hopping
Keyword(s):  
Ascorbic Acid ◽  
Iron Deficiency ◽  
Iron Absorption ◽  
Deficiency Anemia ◽  
Anaerobic Incubation ◽  
Reverse Effect ◽  
Factors Affecting ◽  
Everted Gut Sac

The effects in rats, of age, iron-deficiency anemia, and ascorbic acid, citrate, fluoride, and ethylenediaminetetraacetate (EDTA) on enteric radioiron transport were studied in vitro by an everted gut-sac technique. Sacs from young animals transported more than those from older ones. Proximal jejunal sacs from anemic animals transported more than similar sacs from nonanemic rats, but the reverse effect appeared in sacs formed from proximal duodenum. When added to media containing ascorbic acid or citrate, fluoride depressed transport as did anaerobic incubation in the presence of ascorbic acid. Anaerobic incubation in the presence of EDTA appeared to permit elevated transport. Ascorbic acid, citrate, and EDTA all enhanced the level of Fe59 appearing in serosal media. These results appear to agree with previously established in vivo phenomena and tend to validate the in vitro method as one of promise for further studies of factors affecting iron absorption and of the mechanism of iron absorption.

scholarly journals Iron supplementation in goitrous, iron-deficient children improves their response to oral iodized oil

2000 ◽  
pp. 217-223 ◽  
Author(s):  
M Zimmermann ◽  
P Adou ◽  
T Torresani ◽  
C Zeder ◽  
R Hurrell
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Iron Supplementation ◽  
Thyroid Volume ◽  
Oral Iron ◽  
Deficiency Anemia ◽  
Urinary Iodine Concentration ◽  
Iodized Oil ◽  
Iron Deficient ◽  
Group 2

OBJECTIVE: In developing countries, many children are at high risk for both goiter and iron-deficiency anemia. Because iron deficiency may impair thyroid metabolism, the aim of this study was to determine if iron supplementation improves the response to oral iodine in goitrous, iron-deficient anemic children. DESIGN: A trial of oral iodized oil followed by oral iron supplementation in an area of endemic goiter in the western Ivory Coast. METHODS: Goitrous, iodine-deficient children (aged 6-12 years; n=109) were divided into two groups: Group 1 consisted of goitrous children who were not anemic; Group 2 consisted of goitrous children who were iron-deficient anemic. Both groups were given 200mg oral iodine as iodized oil. Thyroid gland volume using ultrasound, urinary iodine concentration (UI), serum thyroxine (T(4)) and whole blood TSH were measured at baseline, and at 1, 5, 10, 15 and 30 weeks post intervention. Beginning at 30 weeks, the anemic group was given 60mg oral iron as ferrous sulfate four times/week for 12 weeks. At 50 and 65 weeks after oral iodine (8 and 23 weeks after completing iron supplementation), UI, TSH, T(4) and thyroid volume were remeasured. RESULTS: The prevalence of goiter at 30 weeks after oral iodine in Groups 1 and 2 was 12% and 64% respectively. Mean percent change in thyroid volume compared with baseline at 30 weeks in Groups 1 and 2 was -45.1% and -21.8% respectively (P<0.001 between groups). After iron supplementation in Group 2, there was a further decrease in mean thyroid volume from baseline in the anemic children (-34.8% and -38.4% at 50 and 65 weeks) and goiter prevalence fell to 31% and 20% at 50 and 65 weeks. CONCLUSION: Iron supplementation may improve the efficacy of oral iodized oil in goitrous children with iron-deficiency anemia.

scholarly journals Effects of Iron Deficiency Anemia and Its Rapid Correction on the Serum Metabolomic Profile of Rhesus Infants

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1070-1070
Author(s):  
Brian Sandri ◽  
Gabriele Lubach ◽  
Eric Lock ◽  
Michael Georgieff ◽  
Pamela Kling ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Acid Production ◽  
Iron Status ◽  
Deficiency Anemia ◽  
Iron Dextran ◽  
Metabolomic Profile ◽  
Intramuscular Injections ◽  
Iron Deficient ◽  
Rapid Correction

Abstract Objectives To determine whether rapid correction of iron deficiency using intramuscular iron dextran normalizes serum metabolomic changes in a nonhuman primate model of iron deficiency anemia (IDA). Methods Blood was collected from naturally iron-sufficient (IS; n = 10) and IDA (n = 12) male and female infant rhesus monkeys (Macaca mulatta) at 6 months of age. IDA infants were treated with intramuscular injections of iron dextran, 10 mg/weekly for 4–8 weeks. Iron status was reevaluated following treatment using hematological measurements and sera were metabolically profiled using HPLC/MS with isobaric standards for identification and quantification. Results Early-life iron deficiency anemia negatively affects many cellular metabolic processes, including energy production, electron transport, and oxidative degradation of toxins. Slow iron repletion with dietary supplementation restores iron deficient monkeys from a hematological perspective, but the serum metabolomic profile remains differed from monkeys that had been iron sufficient their entire life. Whether rapid iron restoration through intramuscular injections of iron dextran normalizes serum metabolomic profile is not known. A total of 654 metabolites were measured with differences in 53 metabolites identified between IS and IDA monkeys at 6 months (P 0.05). Pathway analyses provided evidence of altered liver function, hypometabolic state, differential essential fatty acid production, irregular inosine and guanosine metabolism, and atypical bile acid production in IDA infants. After treatment, iron-related hematological parameters had recovered, but the formerly IDA infants remained metabolically distinct from the IS infants, with 225 metabolites differentially expressed between the groups. Conclusions As with slow iron repletion, rapid iron repletion does not normalize the altered serum metabolomic profile in rhesus infants with IDA, suggesting the need for iron supplementation in the pre-anemic stage. Funding Sources National Institutes of Health.

In vitro cytokine production in patients with iron deficiency anemia

2004 ◽  
Vol 113 (3) ◽  
pp. 340-344 ◽  
Author(s):  
Michael Bergman ◽  
Hanna Bessler ◽  
Hertzel Salman ◽  
Dimitri Siomin ◽  
Rachel Straussberg ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Cytokine Production ◽  
Deficiency Anemia

scholarly journals Eye-Blinking Rates Are Slower in Infants with Iron-Deficiency Anemia than in Nonanemic Iron-Deficient or Iron-Sufficient Infants

2010 ◽  
Vol 140 (5) ◽  
pp. 1057-1061 ◽  
Author(s):  
Betsy Lozoff ◽  
Rinat Armony-Sivan ◽  
Niko Kaciroti ◽  
Yuezhou Jing ◽  
Mari Golub ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Deficiency Anemia ◽  
Iron Deficient

scholarly journals Effect of Maternal Iron Deficiency Anemia on the Iron Store of Newborns in Ethiopia

Anemia ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Betelihem Terefe ◽  
Asaye Birhanu ◽  
Paulos Nigussie ◽  
Aster Tsegaye
Keyword(s):  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Serum Ferritin ◽  
Complete Blood Count ◽  
Iron Status ◽  
Hemoglobin Concentration ◽  
Deficiency Anemia ◽  
Iron Store ◽  
Cross Sectional ◽  
Iron Deficient

Iron deficiency anemia among pregnant women is a widespread problem in developing countries including Ethiopia, though its influence on neonatal iron status was inconsistently reported in literature. This cross-sectional study was conducted to compare hematologic profiles and iron status of newborns from mothers with different anemia status and determine correlation between maternal and neonatal hematologic profiles and iron status in Ethiopian context. We included 89 mothers and their respective newborns and performed complete blood count and assessed serum ferritin and C-reactive protein levels from blood samples collected from study participants. Maternal median hemoglobin and serum ferritin levels were 12.2 g/dL and 47.0 ng/mL, respectively. The median hemoglobin and serum ferritin levels for the newborns were 16.2 g/dL and 187.6 ng/mL, respectively. The mothers were classified into two groups based on hemoglobin and serum ferritin levels as iron deficient anemic (IDA) and nonanemic (NA) and newborns of IDA mothers had significantly lower levels of serum ferritin (P=0.017) and hemoglobin concentration (P=0.024). Besides, newborns’ ferritin and hemoglobin levels showed significant correlation with maternal hemoglobin (P=0.018;P=0.039) and ferritin (P=0.000;P=0.008) levels. We concluded that maternal IDA may have an effect on the iron stores of newborns.

Iron Deficiency Anemia: Recovery from in vitro Oxidative Stress

1993 ◽  
Vol 90 (2) ◽  
pp. 94-98 ◽  
Author(s):  
M. Bartal ◽  
D. Mazor ◽  
A. Dvilansky ◽  
N. Meyerstein
Keyword(s):  
Oxidative Stress ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Deficiency Anemia
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