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)

Effects of physical training on fasting erythrocyte and plasma zinc distributions were studied on seven previously sedentary male students. The training consisted of running over 5 km, 6 times/week for 10 weeks. Maximum aerobic capacity (VO2max) and 12 min walk-run performance increased significantly (p less than 0.01) after training. The erythrocyte concentrations of total zinc and of zinc derived from carbonic anhydrase I (CA-I) rose significantly (p less than 0.05) after training, whereas no such effects were noted in CA-II-derived zinc, Cu2Zn2 superoxide dismutase-derived zinc, and other zinc. On the other hand, no effect of training was found in total or alpha 2-macroglobulin-bound zinc in plasma, although albumin-bound zinc concentration declined significantly (p less than 0.05). Following the training period, however, the response to a VO2max test of the van Beaumont quotient (J Appl Physiol 1973;34:102-6) for total plasma zinc had decreased significantly (p less than 0.05), suggesting a relative reduction of the circulating exchangeable zinc. In addition, there were significant (p less than 0.05) decreases in plasma iron and ferritin concentrations after training, indicating latent iron deficiency anemia. These results may suggest that the changes in CA-I-derived zinc and/or albumin-bound zinc portend zinc deficiency during running training and that sports anemia precedes hypozincemia in athletes.
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PMID:Training effects on blood zinc levels in humans. 212 94

In four patients with trisomy 21 (three constitutional, one acquired) with a morphological undifferentiated leukemia, diagnosis of erythroid leukemia was established by both immunophenotyping and ultrastructural studies. Indeed, a majority of blasts from three patients expressed several erythroid markers such as carbonic anhydrase 1, spectrin beta chain, and glycophorin A. In addition, band 3 and hemoglobin were immunologically detected in a fraction of the blast cells from two cases. At ultrastructural level, a majority or all blast cells exhibited erythroid differentiation features such as theta granules and ferritin molecules. However, platelet glycoproteins GP Ib, GP IIb, and GP IIIa were also immunologically detected in a fraction (from 14-82%) of the blasts. Since the ultrastructural study indicated that some promegakaryoblasts were also present in three patients, double labeling between erythroid markers (glycophorin A or carbonic anhydrase I) and platelet glycoprotein (Ib or IIIa) was performed and showed a clear overlap between the two kinds of markers. A similar approach was performed at ultrastructural level and indicated that blast cells with ultrastructural erythroid features of differentiation may have three distinct phenotypes, i.e., presence of glycophorin A without platelet glycoproteins or, conversely, the presence of platelet glycoproteins without glycophorin A and coexpression of glycophorin A and platelet glycoproteins. Expression of glycophorin A correlated directly with the differentiation level of the erythroid blasts, whereas platelet glycoproteins were essentially expressed in the more primitive leukemic erythroid cells. The GP Ib synthesized by these blasts was subsequently studied. The GP Ib alpha mRNA analyzed by Northern blot from these erythroid cells was identical in size with that from megakaryocytic cells as was the molecular weight of the GP Ib molecule from both after immunoprecipitation by a monoclonal antibody. Therefore, "in vivo" erythroid leukemic cells may express the main platelet glycoproteins including GP Ib.
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PMID:Expression of platelet glycoproteins by erythroid blasts in four cases of trisomy 21. 252 26

With use of iron histochemistry and immunohistochemistry, regional changes in the appearance of iron, ferritin, transferrin, glial fibrillary acidic protein-positive astrocytes, and activated microglia were examined from 1 to 24 weeks after transient forebrain ischemia (four-vessel occlusion model) in rat brain. Expression of the C3bi receptor and the major histocompatibility complex class II antigen was used to identify microglia. Neuronal death was confirmed by hematoxylin-eosin staining only in pyramidal cells of the hippocampal CA1 region, which is known as the area most vulnerable to ischemia. Perls' reaction with 3,3'-diaminobenzidine intensification revealed iron deposits in the CA1 region after week 4, which gradually increased and formed clusters by week 24. Iron also deposited in layers III-V of the parietal cortex after week 8 and gradually built up as granular deposits in the cytoplasm of pyramidal cells in frontocortical layer V. An increasing astroglial reaction and the appearance of ferritin-immunopositive microglia paralleled the iron accumulation in the hippocampal CA1 region, indicating that iron deposition was probably produced in the process of gliosis. Neither neuronal death nor atrophy was found in the cerebral cortex. Nevertheless, an astroglial and ferritin-immunopositive microglial reaction became evident at week 8 in the parietal cortex. On the other hand, the granular iron deposition in the pyramidal neurons of frontocortical layer V was not accompanied by any glial reaction in the chronic stage of ischemia. Three different types of iron deposition in the chronic phase after transient forebrain ischemia were shown in this study. In view of the neuronal damage caused by iron-catalyzed free radical formation, the late-onset iron deposition may be relevant to the pathogenesis of the chronic brain dysfunction seen at a late stage after cerebral ischemia.
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PMID:Regional differences in late-onset iron deposition, ferritin, transferrin, astrocyte proliferation, and microglial activation after transient forebrain ischemia in rat brain. 786 Jun 55

A fifty five-year-old male presenting as FAB M6 had blasts that were positive both for erythroblastic and megakaryocytic surface makers, i.e., carbonic anhydrase I, CD36 and CD41. HLA-DR and cD71 were also positive. In a very small portion, CD33 and glycophorin A were also positive. By Giemsa staining, these blasts were relatively large and had basophilic cytoplasm. By electroscopic study, PPO was negative and showed ferritin particles, theta granules and iron containing mitochondria in cytoplasm. Chromosome analysis revealed major karyotypic abnormality (MAKA). After initial treatment with blood transfusion, prednisolone and exymetholone, CD41b increased in positive ratio. Trial of remission induction with BHAC-DMP failed and patient died in 5 months.
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PMID:[Acute erythroblastic leukemia presenting as FAB M6 with surface marker positive for megakaryocytic and erythroid: report of a case]. 813 10

Analyzing the distribution pattern of transferrin (Tf) and ferritin, we investigated the changes in iron metabolism related proteins in the process of neuronal death induced by 5 min ischemia. In the control animals, Tf immunoreactivity was localized in the oligodendrocytes. Ferritin was distributed in both neurons and gliacytes, particularly microglia. In parallel with the delayed neuronal death, Tf-positive atrophied neurons and numerous ferritin-positive gliacytes appeared in the CA1 subfield of the hippocampus 4 days after ischemia, when glia fibrillary acidic protein (GFAP)-positive astrocytes also appeared throughout the hippocampal structure. A considerable number of ferritin-positive phagocytes (reactive microglia) appeared in the stratum pyramidale from the seventh day. Our data show clearly that the mobilization of Tf and ferritin-positive phagocytes are linked with the degeneration of neurons induced by cerebral ischemia. These events may suggest an activation of iron handling system under the postischemic condition.
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PMID:Activation of iron handling system within the gerbil hippocampus after cerebral ischemia. 883 41

Quantitative T2 magnetic resonance (MR) imaging was used to examine gerbil brains 1, 3, 10, and 30 days after 5 min forebrain ischemia. T2 was increased in the dorsal-lateral striatum 1 and 3 days post-ischemia, and in the hippocampus 3 days post-ischemia. T2 was normal 10 days post-ischemia, and decreased in the hippocampus and dorsal-lateral striatum 30 days post-ischemia. Neuronal counts in the dorsal-lateral striatum and CA1 hippocampal region were uniformly decreased 30 days post-ischemia. The increase in T2 shortly after ischemia is attributed to brain edema localized to regions where neuronal injury developed. The late decrease in T2 may be due to decreased water in gliotic tissue, or to ferritin-positive microglia, following forebrain ischemia. Tissue atrophy at later times gave enlarged ventricles on MR images.
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PMID:Temporal profile of magnetic resonance imaging changes following forebrain ischemia in the gerbil. 986 38

Iron may catalyse the production of reactive oxygen species during post-ischemic reoxygenation and subsequently lead to brain damage. Ferritin, an iron sequestering and storage protein, can also be a source of iron after ischemic insult. However, its role in ischemia-reperfusion has not been carefully investigated. In the present study, we examined the temporal and spatial induction profiles of both H- and L-ferritin messenger RNA and protein in a well-defined focal cerebral ischemia model. Results of northern blot analysis showed a delayed and prolonged induction of both H- and L-ferritin messenger RNA in the ischemic cortex of rats subjected to 60min ischemic insult. A significant induction of both H- and L-ferritin messenger RNA was observed at 12h and remained elevated for up to 336h after the onset of reperfusion. At the peak level, quantitative analysis of the blot indicated a 2.5-fold and a six-fold increase in H- and L-ferritin messenger RNA, respectively, compared with the sham-operated controls. No apparent change in the levels of either messenger RNA was observed in the contralateral side. Results of in situ hybridization studies revealed constitutive expression of both H- and L-ferritin messenger RNA throughout the brain in sham-operated animals, in particular the hippocampus and the piriform cortex. Nevertheless, the signal intensity of H-ferritin messenger RNA was much higher than that of L-ferritin messenger RNA. Seventy-two hours after 60min ischemia, marked expression of H-ferritin messenger RNA was observed in the area surrounding the middle cerebral artery irrigated cortex, the medial part of the caudoputamen and in the subfield of the CA1 hippocampal region of the ipsilateral hemisphere. Similarly, a large induction of L-ferritin messenger RNA was also noted in several areas, including the middle cerebral artery irrigated cortex, the lateral part of the caudoputamen and the stratum pyramidale of the CA1 hippocampal region, which were totally different from areas where H-ferritin messenger RNA was found. At 336h after ischemia, increased expression of H-ferritin messenger RNA was observed in the peri-necrosis and ipsilateral thalamus regions, while L-ferritin messenger RNA was noted exclusively at the edge within the necrosis. Results of immunohistochemical study further revealed that ferritin immunoreactivity was present in the same areas where increased ferritin messenger RNA was found. Sixty-minute ischemia also led to iron deposition in discrete areas. Iron deposition was highly associated with the induction of ferritin, particularly in the macrophage- and microglia-positive areas where cell death or tissue necrosis was noted.In summary, our initial findings indicate that ischemic insult leads to induction of both H- and L-ferritin messenger RNA. In the present study, although the temporal induction profiles were similar, the major expression areas for these two genes were totally different. Ferritin immunoreactivity was observed in the same areas where increased ferritin messenger RNA was found. Ischemia also resulted in iron deposition, which highly associated with the ferritin immunoreactivity. The exact regulatory mechanism and pathological significance for the differential expression of H- and L-ferritin genes following ischemia/reperfusion remain to be clarified.
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PMID:Differential regulation of H- and L-ferritin messenger RNA subunits, ferritin protein and iron following focal cerebral ischemia-reperfusion. 1109 10

Iron deficiency (ID), the most prevalent nutritional disorder in the world, impairs cognition in early development. The involvement of hippocampus in cognition has prompted investigation into distribution of the iron storage protein ferritin (FER) in rat hippocampus. (a) In normal rats, FER positive cells appeared first in lateral CA3 and hilus of dentate gyrus and then spread over the entire mossy fiber (MF) system. No such spread was observed in CA1 field. (b) Nutritional iron deficiency retarded development of FER in the MF system. No change in FER was observed in CA1 field. (c) Zinc distribution can be altered by iron deficiency. Thus, the effect of zinc added to iron supplementation was tested in iron-deficient rats. Significant FER recovery was observed only in hippocampal MF of rats receiving both zinc and iron. It is apparent that for accelerating recovery of hippocampal function in iron deficiency, both zinc and iron are required.
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PMID:The effects of iron deficiency and iron and zinc supplementation on rat hippocampus ferritin. 1237 58

We have previously demonstrated that psychological stress (PS) can cause iron to accumulate in the cerebral cortex, hippocampus, and striatum of rats. However, why iron accumulates and in what oxidation state iron it accumulates in the brain of PS-exposed rats has not been well elucidated. In the present study, we investigated the influence of PS on the low molecular weight iron pool (LMWIP) in the rat brain. The results showed that: (1) PS significantly expanded LMWIP in the cerebral cortex, hippocampus, and striatum in rats; (2) PS caused derangement of pyramidal cells and reduced the layers of pyramidal CA1 and CA2 neurons; (3) PS exposure greatly lowered the expression of ferritin (Fn) and hephaestin (HP) in the rat cortex and hippocampus; and (4) PS decreased superoxide dismutase, glutathione peroxidase, and glutathione level and increased malondialdehyde level in the cerebral cortex, hippocampus, and striatum in rats. These results indicated that PS could expand LMWIP significantly, which may be attributed to PS-induced decrease in Fn, HP expression, and the subsequent reduction in iron storage and utilization, and expansion of LMWIP could in turn lead to aggravation of oxidative damage.
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PMID:Psychological stress expands low molecular weight iron pool in cerebral cortex, hippocampus, and striatum of rats. 2199 66

Oxidative stress is one of the possible mechanisms of neurodegeneration. One of the elements of this mechanism are altered iron homeostasis and changes concerning of iron metabolism regulatory proteins. The primary iron storage protein in cells is ferritin, composed of heavy (H) and light (L) chains. In brain tissue neurons contain mainly ferritin H-chains, whereas glial cells are rich in L-chains. To the best of our knowledge, this is the first study that compares structure of ferritin and histopathological hallmarks in hippocampal tissue affected by the pathological process of Alzheimer's disease (AD). Our data indicate a statistically significant correlation between the concentration of L chains of ferritin, the H/L ratio and the amount of senile plaques in the subiculum, CA1 and CA4 sectors of the hippocampus (p<0.001, p=0.025, p=0.029). A significant correlation was also found between the concentration of L-ferritin and neuronal loss (p=0.0026). These findings indicate an important role of ferritin light chains in neurodegeneration, that is linked to chronic inflammation processes and the associated activation of the microglia rich of L chains.
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PMID:Relationships between typical histopathological hallmarks and the ferritin in the hippocampus from patients with Alzheimer's disease. 2699 18


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