Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
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PMID:Ferritin- and apoferritin-induced immune complex glomerulonephritis in mice. 49 22

Tissue ferritin metabolism was compared in control and ascorbic acid (AA) deficient guinea-pigs. Concentrations of ferritin protein in the liver (0.98 +/- 0.61 mg/g wet weight) and spleen (0.48 +/- 0.23 mg/g) of control animals did not change after tissue depletion of AA. Iron dextran (75 mg/kg weight, i.m.) caused a 4-5-fold increase in tissue ferritin concentrations in controls whereas no increase in tissue ferritin occurred in scorbutic animals. The rise in tissue total iron concentration was similar in the two groups. Liver ferritin synthesis was similar in control and scorbutic animals. After stimulation with iron (8 mg/kg iron dextran i.v.), ferritin synthesis rose in both groups of animals. However, the pattern of response differed. At 24 h after iron dextran, ferritin synthesis in controls was still significantly elevated (P less than 0.001) and liver ferritin protein continued to rise, whereas in scorbutic animals, ferritin synthesis had declined to pre-iron injection levels, and no rise in ferritin protein values occurred. It is concluded that the ferritin synthetic apparatus in AA deficient tissues remained intact and capable of responding to added iron. The absence of a sustained elevation in tissue ferritin protein after an iron load appeared to be due to inadequate stimulation of ferritin synthesis by intracellular iron. It is suggested that AA has a physiological role in the reduction of intracellular iron and that it is the reduced form of iron which stimulates ferritin synthesis. Abnormalities of iron metabolism occur in AA depleted tissues when the quantity of Fe3+ entering cells exceeds the residual reducing capacity of those cells.
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PMID:Tissue ferritin in scorbutic guinea-pigs. 661 28

Enzymatic tracer techniques to study normal and pathologic strial capillary transport pose various problems. The use of electron opaque tracers can circumvent many of these problems. Iron dextran (mol. diam 20--70 A) and ferritin (mol. diam 110 A) were injected intravenously and the mice sacrificed at intervals of 1/2, 1, 2, 5, and 24 h. The iron dextran results were unusual in that from 1/2 to 5 h after administration the tracer was present within the cytoplasmic matrix of endothelia, but by 24 h it had been cleared out. No transendothelial exchange was noted. The ferritin results were in conflict and previous results using horse-radish peroxidase. Transport of ferritin was minimal regardless of time sacrificed. No more than a few molecules were scattered about the capillary basal limina. Those molecules transported across capillaries were apparently delivered by means of the micropinocytotic system. The results suggest a blood-strial barrier similar to the blood-thymic and blood-myenteric barriers. Experimental as well as control animals exhibited strial light cells which contained ferritin-like particles within their cytoplasmic matrices. These light cells are probably reticuloendothelial type cells. Ferritin may be useful to gauge strial capillary transport alterations associated with auditory pathologies.
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PMID:An evaluation of normal strial capillary transport using the electron-opaque tracers ferritin and iron dextran. 740 70

The cost-effectiveness impact of iron dextran administration on the use of epoetin alfa and blood in hemodialysis patients was studied. Subjects were ambulatory hemodialysis patients who had been receiving hemodialysis for at least six months before the start of an iron dextran protocol and who had been given epoetin alfa for at least four of those six months. Clinical data were collected for six months before and six months after the protocol was implemented. Successful treatment was defined as a hematocrit of 33-36%, a transferrin saturation of >10%, a ferritin concentration of >100 ng/mL, and no blood use except for acute blood loss. A total of 33 patients completed the study. Fifty units of blood were used in the first six months and nine units in the second six months. There was significant improvement in mean hematocrit, ferritin, and transferrin saturation values after the protocol began. Average epoetin alfa doses did not change significantly. There was significant improvement in success rates for ferritin and blood use and in the overall success rate. Ten patients met all success criteria in the preprotocol period, versus 27 in the postprotocol period. Monthly cost-effectiveness analysis for the preprotocol and postprotocol periods indicated costs of $1350 and $526, per successful treatment, respectively. The incremental cost-effectiveness of iron dextran was $42 per successful treatment. Iron dextran improved iron indices and reduced the need for blood transfusions but did not reduce the average dose of epoetin alfa. The additional cost of therapy per month seemed justified by the clinical benefits.
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PMID:Cost-effectiveness impact of iron dextran on hemodialysis patients' use of epoetin alfa and blood. 987 88

Iron supplementation has become an integral part of the management of patients receiving epoetin therapy, and clinicians have found it necessary to learn how and when to use it to the best advantage. Three routes of administration for iron are available: oral, intramuscular, and intravenous. Oral iron has the advantage of being simple and cheap, but it is limited by side-effects, poor compliance, poor absorption, and low efficacy. Intravenous iron is the best means of guaranteeing delivery of readily available iron to the bone marrow, but it requires greater clinical supervision. The i.v. iron preparations vary widely in their degradation kinetics, bioavailability, side-effect profiles, and maximum dose for single administration. Iron dextran is hampered by a small but significant risk of anaphylaxis, whereas all i.v. iron preparations can induce "free iron" reactions if the circulating plasma transferrin is overloaded. Intravenous iron may be given in advance of epoetin therapy, as concomitant treatment to prevent the development of iron deficiency, as treatment of absolute or functional iron deficiency, or as adjuvant therapy to enhance the response to epoetin in iron-replete patients. Markers of iron status that may indicate a need for i.v. iron include a serum ferritin of less than 100 microg/liter, a transferrin saturation of less than 20%, and a percentage of hypochromic red cells more than 10%. Various regimens are available for giving i.v. iron: low-dose administration of 20 to 60 mg every dialysis session in hemodialysis patients, medium-dose administration of 100 to 400 mg, and high-dose administration of 500 to 1000 mg. Iron sodium gluconate can only be given as a low-dose regimen because of toxicity, whereas the only preparation suitable for high-dose administration is iron dextran. Although concerns have been raised regarding iron overload and long-term toxicity with i.v. iron therapy in terms of increased risk of infections, cardiovascular disease, and malignancy, there is little evidence to substantiate this in patients receiving epoetin. Care should be taken, however, to prevent the serum ferritin rising above 800 to 1000 microg/liter and the transferrin saturation above 50%. Provided this is done, the benefits of i.v. iron almost certainly outweigh the risks in terms of optimizing the response to epoetin therapy.
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PMID:Strategies for iron supplementation: oral versus intravenous. 1008 88

To evaluate the effect of body iron stores on the vulnerability of the brain to ischemia, a focal permanent brain ischemia was induced by photothrombotic occlusion of cortical vessels in rats with or without chronic treatment with iron dextran (25 mg iron/kg, every other day for 20 days, intraperitoneally). Iron dextran induced systemic iron overload as evidenced by high ferritin (Ft) ( x 5) and total iron levels ( x 3) in serum as well as increased Ft expression in the liver and heart. Conversely, neither serum free iron levels nor Ft expression in the brain were changed by iron dextran. Finally, infarct volume was not modified by iron dextran. In addition, induction of ischemia in rats treated with FeCl(3) (560 microg iron/kg, intravenously) as a means of increasing serum free iron levels during the ischemic period did not enlarge infarct volume. We then explored the effect of brain ischemia itself on serum Ft by measuring serum Ft before and after induction of brain ischemic insults with different neurologic outcomes in rats (brain embolization with microspheres, photothrombotic occlusion of cortical vessels, four-vessel occlusion). Serum Ft levels were found higher at day 1 after ischemia than before ischemia only in rats subjected to the most severe insult (brain embolization). In conclusion, our study showed that increased body iron stores do not increase the vulnerability of the brain to ischemia and that brain ischemia, if severe, results in the elevation of serum Ft levels.
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PMID:Serum ferritin in stroke: a marker of increased body iron stores or stroke severity? 1590 98

Tannic acid (TA), a water soluble natural polyphenol with 8 gallic acids groups, is abundantly present in various medicinal plants. Previously TA has been investigated for its antimicrobial and antifungal properties. Being a large polyphenol, TA chelates more than 1 metal. Hence TA has been explored for potent antioxidant activities against reactive oxygen species (ROS), reactive nitrogen species (RNS) and as iron chelator in vitro thereby mitigating iron-overload induced hepatotoxicity in vivo. Iron dextran was injected intraperitoneally in Swiss albino mice to induce iron-overload triggered hepatotoxicity, followed by oral administration of TA for remediation. After treatment, liver, spleen, and blood samples were processed from sacrificed animals. The liver iron, serum ferritin, serum markers, ROS, liver antioxidant status, and liver damage parameters were assessed, followed by histopathology and protein expression studies. Our results show that TA is a prominent ROS and RNS scavenger as well as iron chelator in vitro. It also reversed the ROS levels in vivo and restricted the liver damage parameters as compared to the standard drug, desirox. Moreover, this natural polyphenol exclusively ameliorates the histopathological and fibrotic changes in liver sections reducing the iron-overload, along with chelation of liver iron and normalization of serum ferritin. The protective role of TA against iron-overload induced apoptosis in liver was further supported by changed levels of caspase 3, PARP as well as Bax/BCl-2 ratio. Thus, TA can be envisaged as a better orally administrable iron chelator to reduce iron-overload induced hepatotoxicity through ROS regulation.
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PMID:A natural antioxidant, tannic acid mitigates iron-overload induced hepatotoxicity in Swiss albino mice through ROS regulation. 2944 34

Intravenous infusions of iron have evolved from a poorly effective and dangerous intervention to a safe cornerstone in the treatment of iron deficiency. Modern iron formulations are composite nanoparticles composed of carbohydrate ferric oxy-hydroxides. Iron dextran, iron derisomaltose (formely known as iron isomaltoside 1000), ferric carboxymaltose, ferrumoxytol, iron sucrose and sodium ferric gluconate can be infused at different doses and allow correction of total iron deficit with single or repeated doses in 1-2 weeks depending on the specific formulation. All iron preparations are associated with a risk of severe infusion reactions. In recent prospective clinical trials, the risk of moderate to severe infusion reactions was comparable among all modern preparations affecting <1% of patients. Hence, intravenous iron therapy is reserved for iron deficiency anemia patients with intolerance or unresponsiveness of oral iron. As per European drug label, intravenous iron may also be preferred when rapid correction of the iron deficit is required. In patients with inflammation, iron-deficiency should also be suspected as anemia cause when transferrin saturation is low because serum ferritin can be spuriously normal. The main treatment target for i.v. iron is an improvement of the quality of life, for which hemoglobin is a surrogate marker. An emerging complication affecting 50-74% of patients treated with ferric carboxymaltose in prospective clinical trials is hypophosphatemia - or more accurately the 6H syndrome (hyperphosphaturic hypophosphatemia triggered by high fibroblast growth factor 23 that causes hypovitaminosis D, hypocalcemia and secondary hyperparathyroidism). These biochemical changes can cause severe and potentially irreversible clinical complications, such a bone pain, osteomalacia and fractures. Individual selection of the appropriate iron therapy and evaluation of treatment response are mandatory to safely deliver improved outcome through intravenous iron therapies.
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PMID:Intravenous iron supplementation therapy. 3244 12