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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extended X-ray absorption fine structure (EXAFS) associated with the iron K-edge has been measured and interpreted for ferritin and haemosiderin extracted from horse spleen, and haemosiderin extracted from the livers of humans with treated primary haemochromatosis, and from the spleens of humans with treated secondary haemochromatosis. For ferritin, the data are consistent with, on average, each iron atom being in an environment comprised of approx. six oxygen atoms at 1.93 +/- 0.02 A, approx. 1.5 iron atoms at 2.95 +/- 0.02 A and approx. 1.1 iron atoms at 3.39 +/- 0.02 A, with a further shell of oxygens at approx. 3.6 A. Iron in horse spleen haemosiderin is in an essentially identical local environment to that in horse spleen ferritin. In contrast, the EXAFS data for primary haemochromatosis haemosiderin indicate that the iron-oxide core is amorphous; only a single shell of approx. six oxygen atoms at approx. 1.94 +/- 0.02 A being apparent. Secondary haemochromatosis haemosiderin shows an ordered structure with approx. 1.4 iron atoms at both 2.97 +/- 0.02 and 3.34 +/- 0.02 A. This arrangement of iron atoms is similar to that in horse spleen haemosiderin, but the first oxygen shell is split with approx. 2.9 atoms at 1.90 +/- 0.02 A and approx. 2.7 at 2.03 +/- 0.02 A, indicative of substantial structural differences between secondary haemochromatosis haemosiderin and horse spleen haemosiderin.
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PMID:Iron K-edge absorption spectroscopic investigations of the cores of ferritin and haemosiderins. 176 66

Anaesthetic drugs can induce reversible as well as irreversible changes in cell membranes and intracellular proteins as well as lipid peroxidation in the liver. Low molecular weight iron species (LMWI) can by their catalytic activity contribute to the generation of free radicals (hydroxyl radicals). Free radicals are a recognisable cause of intracellular damage. Impaired mitochondrial function is also a sign of intracellular damage, which is usually irreversible. Thus, an agent may be cytotoxic when it causes a significant increase in intracellular LMWI. Whether the LMWI arise from ferritin or is released from iron containing proteins, the same reaction occurs. As long as LMWI can undergo redox cycling, hydroxyl radicals can be formed. We investigated the effect of various mixtures of diethylether, halothane, nitrous oxide and oxygen on the intracellular LMWI content and mitochondrial function of the rat myocardium. Hearts isolated from rats anaesthetised with diethylether showed an increase in the cytosolic LMWI compared to the control group. No increase in mitochondrial LMWI was demonstrated. Subsequent perfusion of the isolated hearts showed a further increase in the LMWI. On perfusion the mitochondrial LMWI increased in comparison with controls. Mitochondrial function was significantly impaired as measured by the QO2 (state 3), ADP/O ratio and oxidative phosphorylation rate (OPR). Exposure of rats to 50% nitrous oxide for 15 minutes increased the myocardial LMWI, but had no effect on mitochondrial function. Exposure to room air for 30 minutes before isolating the hearts, still showed a significant increase in LMWI with no detectable change in mitochondrial function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of various mixtures of diethylether, halothane, nitrous oxide and oxygen on low molecular weight iron content and mitochondrial function of the rat myocardium. 177 41

Evidence from the literature and from our laboratory demonstrates a pronounced and rapid flow of fluids and associated solutes through the extravascular spaces in bone. Minutes after injection, large molecules such as ferritin and horseradish peroxidase (HRP) have been localized throughout the osteocytic lacunae and canaliculi of cortical bone in the chick, rat and dog. Patterns of marker movement preclude diffusion as the mechanism for solute movement and suggest a centrifugal bulk flow of fluids. We have developed a computer model of bone fluid flow that has led to the conclusion that the pattern and rate of fluid movement is governed by the pressure differential across the bone, the vascular architecture, and the porosity of the mineralized matrix. The validity of simulations in which a substance is injected and monitored over time has been tested by comparisons with actual injections of markers in the rat. Evidence is presented for a relationship between blood flow and bone dynamics in growth, repair and pathology of bone. We employed the tail suspension model of weightlessness in the rat to test the effect of posture on the perfusion of cortical bone using injections of HRP. Data indicated that perfusion of the femur was reduced by this treatment. We propose a "rheostat" mechanism, which suggests that bone perfusion may set limits for bone growth and remodeling. Therefore, bone mass reflects the ability of the vasculature to supply oxygen and nutrients to the cells on and within the mineralized matrix.
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PMID:Fluid movement in bone: theoretical and empirical. 149 Oct 26

Ferritin is the principal protein of iron storage (in the Fe(III) state). The UV-A irradiation of 0.25 microM ferritin solutions (from horse spleen) loaded with 530 microM Fe(III) induces Fe2+ release in the medium. The initial quantum yield is wavelength dependent (phi(365 nm) approximately 2 x 10(-3) but pH and oxygen independent. The Fe2+ release reaches a plateau which strongly depends on pH and oxygen. The amino acid composition of the apoprotein is not altered by the UV irradiation. Addition of formate ions enhances the Fe2+ production, suggesting that the ferritin photoreduction involves an electron transfer from an OH- ligand. The possible importance of this phenomenon in skin photobiology is discussed.
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PMID:Ferrous ion release from ferritin by ultraviolet-A radiations. 179 53

We have used the carrageenan-induced pouch-granuloma in rats to investigate how changes in low-molecular-mass iron chelate levels in the exudate, induced by iron loading (iron-dextran) or chelation (desferrioxamine) influence cellular and systemic inflammatory parameters. In the iron-treated group we observed a rapid decrease in the number of leukocytes and exudate volume; there was also an increase in ferritin iron and low-molecular-mass iron chelates, and on the eighth day a systemic response. In the desferrioxamine-treated group we detected a decrease in low-molecular-mass iron chelates, ferritin iron, and an increase in the number of leukocytes. We describe the protective effects of desferrioxamine against the deleterious effects of ferrous iron and relate this to its chelating and scavenging activity. The results suggest that the levels of low-molecular-mass iron chelates modulate the inflammatory response, possibly through their contribution to the oxygen free radical generation, which is responsible for the cell membrane damage and subsequently its death. The modulatory action of iron-dextran and desferrioxamine support our hypothesis.
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PMID:Modulation of exudate inflammation parameters in rat carrageenan-induced granuloma by modification of exudate iron levels. 186 39

Anaerobic threshold (AT) has been advocated as an objective method of evaluating exercise capacity in patients with chronic congestive heart failure. The factors that determine AT, however, remain still unclear. To assess the influence of oxygen transport capacity on AT, patients with iron deficiency anemia were studied before and after treatment with iron. Twenty-nine female subjects were studied. They were divided into the following 3 groups: 1) iron deficiency anemia (group IDA: Hgb less than 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes and 6 non-athletes, 2) latent iron deficiency (group Lat-ID: Hgb greater than or equal to 11 g/dl and ferritin less than 10 ng/ml) consisting of 4 athletes, and normal (group Nor: Hgb greater than or equal to 11 g/dl and ferritin greater than or equal to 10 ng/ml) consisting of 15 athletes and 6 non-athletes. By bicycle ergometer using ramp protocol, peak oxygen uptake (peak VO2) and AT were measured in each group. Following the 1st exercise testing, groups IDA and Lat-ID were treated by oral iron for 1-1.5 months. The 2nd exercise testing was then performed. Furthermore, to investigate whether muscle cell energy metabolism itself is altered by iron deficiency, P magnetic resonance spectroscopy (MRS) was performed in 2 relatively severe anemic patients during forearm exercise while assessing the changes in phosphocreatine and inorganic phosphate. Peak VO2 and AT in non-athletes were significantly lower in IDA group than Nor group (peak VO2 (ml/min/kg): 23.7 +/- 5.1 vs 33.3 +/- 3.8, p less than 0.01, AT (ml/min/kg): 15.9 +/- 3.3 vs 21.3 +/- 1.3, p less than 0.01). After iron administration, Hgb was increased significantly in IDA group (from 9.0 +/- 1.8 to 12.1 +/- 0.8 g/dl, p less than 0.01) accompanied by an improvement in peak VO2 and AT (peak VO2 (ml/min/kg): from 34.2 +/- 12.4 to 40.0 + 13.0, p less than 0.001, AT (ml/min/kg): from 20.9 +/- 6.3 to 25.0 +/- 8.0, p less than 0.001). Lat-ID and Nor groups showed no changes. MRS indices of cell energy metabolism of the 2 severely anemic patients did not differ from those of normal controls, and no changes were observed after iron treatment. It is concluded from these results in iron deficiency anemia that oxygen transport is a determinant of anaerobic threshold.
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PMID:[Effect of blood hemoglobin concentration on anaerobic threshold]. 191 24

Neuroblastoma cells accumulate ascorbic acid and iron. It was hypothesized that these features could be exploited for sensitizing neuroblastoma cells for therapy in combination with reactive oxygen intermediates. In the present study the effects of 6-hydroxydopamine (6-OHDA) and H2O2 on metabolic parameters critical for cell survival were investigated in cells with low and high ferritin content in the presence and absence of ascorbate. Human neuroblastoma SK-N-SH cells were pretreated with 100 microM FeSO4 and 10 microM desferrioxamine, respectively, for 24 h yielding cells with different ferritin contents. The effects of 6-OHDA and H2O2 (25 microM-250 microM) in the absence and presence of 1 mM ascorbic acid on DNA strand break formation, activation of poly(ADP-ribose) polymerase, and finally decrease in NAD+ and ATP concentration were investigated. All these parameters were influenced by 6-OHDA and H2O2 in a concentration-dependent manner in a similar way. The effects were most pronounced in ferritin-rich cells and in the presence of ascorbic acid. Using isolated CCC PM2 DNA, 6-OHDA and ascorbic acid caused strand breaks that were prevented in the presence of mannitol or desferrithiocine. H2O2-mediated strand breaks were observed only in the presence of ascorbic acid. Based on these data and data published by others a model explaining the deleterious effects of ascorbic acid on neuroblastoma cells is presented. It is suggested that continuous application of a high dosage of ascorbic acid might be a useful approach in neuroblastoma therapy.
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PMID:Ascorbic acid enhances the effects of 6-hydroxydopamine and H2O2 on iron-dependent DNA strand breaks and related processes in the neuroblastoma cell line SK-N-SH. 193 70

Bovine heart microsomes have been found to contain a non-heme iron protein which serves as an electron acceptor for NADPH-cytochrome P-450 reductase and therefore stimulates NADPH oxidation. This protein, tentatively referred to as Microsomal Iron Protein (MIP), has been extracted with Triton N-101 and purified by ion exchange chromatography on CM- and DEAE-celluloses and gel filtration on Sepharose 6B. MIP is an Mr = 66,000 monomer with 17 atoms of Fe(III)/molecule. Incubation with dithionite removes iron from MIP and abolishes the stimulation of NADPH oxidation, but subsequent incubation with nitrilotriacetic-Fe(III) reincorporates iron and restores the stimulation of NADPH oxidation. Oxygen is the ultimate electron acceptor. In the presence of oxygen, the enzymatic reduction of MIP Fe(III) is followed by the reoxidation of Fe(II) at the expense of oxygen, generating superoxide anion and regenerating MIP Fe(III) for the continuous oxidation of NADPH. In the absence of oxygen, electron transfer from the reductase to MIP Fe(III) causes the release of Fe(II), which limits the ability of MIP to serve as an electron acceptor and stimulate NADPH oxidation. The--NH2-terminal of MIP has been sequenced, and no homology has been found with the sequence of other iron storage or transport proteins such as ferritin or transferrin.
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PMID:Bovine heart microsomes contain an Mr = 66,000 non-heme iron protein which stimulates NADPH oxidation. 193 64

ADR-529 [(+)-1,2-bis(3,5-dioxopiperazin-1-yl)propane], a nonpolar, cyclic analogue of EDTA, protects against anthracycline cardiotoxicity in vivo. The protective mechanism presumably involves chelation of iron by a hydrolysis product of ADR-529, thus preventing the formation of reactive iron/oxygen species which can damage membrane lipids. We investigated the effects of ADR-529 and its hydrolysis products (the tetraacid and the diacid diamide) on NADPH- and ADP-Fe(3+)-dependent lipid peroxidation of rat liver microsomes and liposomes in the presence of cytochrome P-450 reductase. Hydrolyzed ADR-529 products caused inhibition of lipid peroxidation when in excess of the iron concentration. However, no inhibition of lipid peroxidation was detected by similar concentrations of nonhydrolyzed ADR-529. Microsomes did not affect the inhibition of lipid peroxidation, suggesting that rat liver microsomes do not hydrolyze ADR-529. Similarly, the diacid diamide hydrolysis product of ADR-529 inhibited ferritin- and adriamycin-iron-dependent liposomal lipid peroxidation in a concentration-dependent manner. No correlation between partially reduced oxygen species (O2.- and .OH; as measured by electron spin resonance) and lipid peroxidation (as assayed by malondialdehyde formation) was observed, suggesting that liposomal lipid peroxidation was strictly an iron-dependent phenomenon. These results suggest that inhibition of lipid peroxidation by iron chelation may be related to the protective effects of ADR-529 on in vivo anthracycline toxicity.
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PMID:Effects of (+)-1,2-bis(3,5-dioxopiperazin-1-yl)propane (ADR-529) on iron-catalyzed lipid peroxidation. 196 87

Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal death, due to their ability to promote formation of oxygen radicals.
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PMID:Brain iron and ferritin in Parkinson's and Alzheimer's diseases. 207 10


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