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1.
Brain iron and ferritin in Parkinson's and Alzheimer's diseases   总被引:14,自引:0,他引:14  
Summary 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 dath, due to their ability to promote formation of oxygen radicals.Ferritin antisera were kindly provided by Dr. J. G. Joshi, Department of Biochemistry, University of Tennessee, Knoxville, TN, U.S.A.  相似文献
2.
Summary A strong immunoreactivity for ferritin was observed in the neuritic (senile) plaques in Alzheimer's disease hippocampus. The ferritin accumulation was almost exclusively associated with the microglia, which appeared to have proliferated greatly. These cells were also positive for HLA-DR, a putative marker for reactive microglia. In contrast, in the diffuse plaques, which were without neuritic pathology, the ferritin-stained microglia appeared to be normal. Microglia were seen frequently in contact with neurons undergoing neurofibrillary changes but only the tangles in the extracellular space were ferritin positive. No ferritin was detected, by Western blots, in paired helical filaments isolated from Alzheimer's disease brain, suggesting that ferritin was most likely weakly associated with and was not a constituent of these fibrils. No correlation between increased ferritin/microglia activity and blood-brain barrier leakage was detected. Ferritin, an iron-storage protein, might have a role in the formation of amyloid through the action of free radicals generated during the release of iron from the ferritin molecule. Alternatively, the ferritin/microglia system might be secondarily involved in the removal and processing of the amyloid.Supported in part by the New York State Office of Mental Retardation and Developmental Disabilities and National Institutes of Health grants NS18105, AG05892 and AG04220. H. L. was funded by a grant from the Ministry for Science and Research, Austria, J. G. J. and J. F. were funded by the Council for Tobacco Research. Parts of this paper have been reported at the 9th International Conference on Proteins of Iron Transport and Storage, Brisbane, Australia, June 1989 and at the 2nd International Conference on Aluminium and Health, Orlando, Fla, USA, December 1989  相似文献
3.
By the use of a radioimmunoassay, ferritin was detected in the cerebrospinal fluid (CSF) of apparently healthy individuals at a mean concentration of 5.1 arb U/l, i.e. a level about 5 % of the mean normal serum-ferritin concentration. Fourteen patients with acute cerebrovascular stroke or transient ischemic attacks (one case) were followed by serial determinations of CSF-ferritin during 2 weeks or more from onset of symptoms. After cerebral stroke all patients exhibited an increase of CSF-ferritin with peak levels between 4 and 6 days from admission. Those three patients in whom computed tomography showed cerebral bleeding had the highest peak CSF-ferritin concentrations (mean value 249 ± 65 (SEM) arb U/l). The mean peak CSF-ferritin was 28 ± 11 arb U/l in the patients who had cerebral infarction without signs of bleeding. In seven patients CSF-ferritin returned to the control range after 2 weeks. The extent of the rise of ferritin in CSF could not be explained by damaged blood-CSF barrier. We suggest that the increment of ferritin in CSF of patients with cerebrovascular lesions may reflect an inflammatory response within the brain possibly mediated by macrophages.  相似文献
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5.
目的 探讨脑脊液中肿瘤坏死因子α(TNF-α)、β2微球蛋白(β2M)和铁蛋白(F)对于中枢神经系统白血病(CNSL)诊断的意义.方法 采用酶联免疫吸附和放射免疫方法检测CNSL组,无CNSL组和对照组脑脊液中TNF-α、β2M和F的变化.结果 CNSL组脑脊液中TNF-α、β2M和F均高于无CNSL组和对照组,有显著性差异(P<0.05)).TNF-α、β2M和F联合检测CNSL的约登指数均高于单一指标检测CNSL.结论 脑脊液中TNF-α、β2M和F在CNSL的诊断中有重要意义,提示其联合检测可以早期诊断CNSL.  相似文献
6.
Summary Anionic groups on cerebral arteriolar endothelium were localized using cationized ferritin (CF), and alterations in the distribution of these groups were documented in arterioles with increased permeability to horseradish peroxidase (HRP) in angiotensin-induced acute hypertension.Normotensive animals showed a uniform distribution of anionic groups on the endothelial luminal plasma membrane when fixed or live vessels were reacted with CF. Anionic groups were localized at the mouth of pinocytotic vesicles in both preparations; however, only live cells demonstrated CF particles within vesicles, and the possibility that these represent pinocytosed CF particles cannot be ruled out. Cationized ferritin particles were not observed on the plasma membranes within interendothelial spaces in either of the preparations.Sixty percent of hypertensive animals with pressures over 200 mmHg showed increased arteriolar permeability to HRP. At 2.5 min, permeable arteriolar segments with active vesicular transport of HRP showed marked reduction or loss of CF binding. Capillaries and venules in the adjacent cortex and nonpermeable arterioles demonstrated linear endothelial CF binding similar to controls. Most permeable vessels of animals killed 6–20 min after onset of acute hypertension when the blood-brain barrier is usually closed showed CF binding on endothelium indicating that there is rapid restoration of the net negative charge.These studies demonstrate that increased arteriolar permeability in acute hypertension is associated with a transient alteration of surface charge. The mechanism by which charge is altered remains to be determined.Supported by Ontario Heart Foundation 2-6  相似文献
7.
Cytochemical demonstration of negative surface charges in central myelin   总被引:2,自引:0,他引:2  
Homogenates of central myelin were treated with ferritin derivatives having different isoelectric points. It was found that considerable amounts of cationic ferritin (pI 8.5-9.5) had access to the extracellular space, but that anionic ferritin (pI 4.0) and native ferritin (pI 4.5) did not. The electrostatic nature of the binding of cationic ferritin was demonstrated by treating the homogenates with poly-L-lysine and 1 M NaCl:both reagents led to a complete displacement of the bound cationic ferritin. Neither extensive trypsination nor neuraminidase treatment showed a significant effect on the intralamellar distribution of the bound cationic ferritin molecules. This suggests that the net negative charge on the extracellular myelin face stems primarily from acidic lipid groups in the membrane.  相似文献
8.
血清铁蛋白对急性脑梗死患者的临床评估   总被引:2,自引:0,他引:2  
目的评估脑梗死急性期血清铁蛋白与患者病损的程度及恢复情况的关系.方法用化学发光法检测48例脑梗死患者急性期血清铁蛋白, 行中国神经功能缺损程度(CSS)评分(入院及住院3周时), 患者恢复情况以CSS减分值表示.结果入院时CSS≥15分组血清铁蛋白水平明显高于CSS<15分组(P<0.01), 两者呈正相关(r=13.47,P<0.01).入院3周时CSS减分值少组血清铁蛋白水平高, 且在CSS≥15分组中差异有显著性(P<0.05).结论脑梗死患者急性期血清铁蛋白的含量与脑梗死病损的严重程度及恢复密切相关.  相似文献
9.
Hypertrophic cardiomyopathy is a common complication of Friedreich's ataxia (FRDA). Histological sections reveal abnormal cardiomyocytes, muscle fiber necrosis, reactive inflammation, and increased endomysial connective tissue. Scattered muscle fibers display perinuclear collections of minute iron-positive granules that lie in rows between myofibrils. Frataxin deficiency in FRDA causes mitochondrial iron dysmetabolism. We studied total iron and the iron-related proteins ferritin, mitochondrial ferritin, divalent metal transporter 1 (DMT1), and ferroportin in FRDA hearts by biochemical and histological techniques. Total iron in the left ventricular wall of FRDA patients (30.7+/-19.3 mg/100 g dry weight) was not significantly higher than normal (31.3+/-24.1 mg/100 g dry weight). Similarly, cytosolic holoferritin levels in FRDA hearts (230+/-172 microg/g wet weight) were not significantly elevated above normal (148+/-86 microg/g wet weight). The iron-positive granules exhibited immunoreactivity for cytosolic ferritin, mitochondrial ferritin, and ferroportin. Electron microscopy showed enhanced electron density of mitochondrial deposits after treatment with bismuth subnitrate supporting ferritin accumulation. The inflammatory cells in the endomysium were reactive for CD68, cytosolic ferritin, and the DMT1 isoform(s) translated from messenger ribonucleic acids containing iron-responsive elements (DMT1+). Progressive cardiomyopathy in FRDA is the likely result of iron-catalyzed mitochondrial damage followed by muscle fiber necrosis and a chronic reactive myocarditis.  相似文献
10.
It is shown here that transferrin (Tf), the iron transport protein and carbonic anhydrase C (CA C) are specifically located within oligodendrocytes in murine brain cell cultures. Ferritin (F), the major iron storage protein, was demonstrated in oligodendrocytes, as well as in astrocytes and microglial cells and was more prominent in the former. CA C and Tf were seen first after 6-7 days in culture. CA C and F positivity increased rapidly and at day 20, 80-85% of galactocerebroside + oligodendrocytes were positive for both proteins. Only a small number of oligodendrocytes was Tf+ up to day 14, after which their numbers increased rapidly until day 20, when 67% of the oligodendrocytes were Tf+. Because of the presence of Tf and F in oligodendrocytes it is suggested that these cells may play an important role in the metabolism of iron within the central nervous system.  相似文献
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