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  1 / 1010 MEDLINE  
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[PMID]:28536273
[Au] Autor:Aydemir TB; Kim MH; Kim J; Colon-Perez LM; Banan G; Mareci TH; Febo M; Cousins RJ
[Ad] Endereço:Food Science and Human Nutrition Department, Center for Nutritional Sciences, College of Agricultural and Life Sciences.
[Ti] Título:Metal Transporter ( ) Deletion in Mice Increases Manganese Deposition and Produces Neurotoxic Signatures and Diminished Motor Activity.
[So] Source:J Neurosci;37(25):5996-6006, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in human have been linked to symptoms of the early onset of Parkinsonism and Dystonia. This phenotype is likely related to excess manganese accumulation in the CNS. The metal transporter ZIP14 (SLC39A14) is viewed primarily as a zinc transporter that is inducible via proinflammatory stimuli. evidence shows that ZIP14 can also transport manganese. To examine a role for ZIP14 in manganese homeostasis, we used knock-out (KO) male and female mice to conduct comparative metabolic, imaging, and functional studies. Manganese accumulation was fourfold to fivefold higher in brains of KO mice compared with young adult wild-type mice. There was less accumulation of subcutaneously administered Mn in the liver, gallbladder, and gastrointestinal tract of the KO mice, suggesting that manganese elimination is impaired with ablation. Impaired elimination creates the opportunity for atypical manganese accumulation in tissues, including the brain. The intensity of MR images from brains of the KO mice is indicative of major manganese accumulation. In agreement with excessive manganese accumulation was the impaired motor function observed in the KO mice. These results also demonstrate that ZIP14 is not essential for manganese uptake by the brain. Nevertheless, the upregulation of signatures of brain injury observed in the KO mice demonstrates that normal ZIP14 function is an essential factor required to prevent manganese-linked neurodegeneration. Manganese is an essential micronutrient. When acquired in excess, manganese accumulates in tissues of the CNS and is associated with neurodegenerative disease, particularly Parkinson-like syndrome and dystonia. Some members of the ZIP metal transporter family transport manganese. Using mutant mice deficient in the ZIP14 metal transporter, we have discovered that ZIP14 is essential for manganese elimination via the gastrointestinal tract, and a lack of ZIP14 results in manganese accumulation in critical tissues such as the brain, as measured by MRI, and produces signatures of brain injury and impaired motor function. Humans with altered ZIP14 function would lack this gatekeeper function of ZIP14 and therefore would be prone to manganese-related neurological diseases.
[Mh] Termos MeSH primário: Proteínas de Transporte de Cátions/genética
Proteínas de Transporte de Cátions/metabolismo
Intoxicação por Manganês/genética
Intoxicação por Manganês/metabolismo
Manganês/metabolismo
Atividade Motora/genética
[Mh] Termos MeSH secundário: Animais
Química Encefálica/genética
Feminino
Motilidade Gastrointestinal/genética
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Distribuição Tecidual
Zinco/metabolismo
Zinco/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cation Transport Proteins); 0 (SLC39A14 protein, mouse); 42Z2K6ZL8P (Manganese); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0285-17.2017


  2 / 1010 MEDLINE  
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[PMID]:28417441
[Au] Autor:Pfalzer AC; Bowman AB
[Ad] Endereço:Departments of Pediatrics, Vanderbilt University Medical Center (VUMC), Nashville, TN, USA.
[Ti] Título:Relationships Between Essential Manganese Biology and Manganese Toxicity in Neurological Disease.
[So] Source:Curr Environ Health Rep;4(2):223-228, 2017 Jun.
[Is] ISSN:2196-5412
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Manganese (Mn) is critical for neurodevelopment but also has been implicated in the pathophysiology of several neurological diseases. We discuss how Mn requirements intersect with Mn biology and toxicity, and how these requirements may be altered in neurological disease. Furthermore, we discuss the emerging evidence that the level of Mn associated with optimal overall efficiency for Mn biology does not necessarily coincide with optimal cognitive outcomes. RECENT FINDINGS: Studies have linked Mn exposures with urea cycle metabolism and autophagy, with evidence that exposures typically neurotoxic may be able to correct deficiencies in these processes at least short term. The line between Mn-dependent biology and toxicity is thus blurred. Further, new work suggests that Mn exposures correlating to optimal cognitive scores in children are associated with cognitive decline in adults. This review explores relationships between Mn-dependent neurobiology and Mn-dependent neurotoxicity. We propose the hypothesis that Mn levels/exposures that are toxic to some biological processes are beneficial for other biological processes and influenced by developmental stage and disease state.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Central
Intoxicação por Manganês/fisiopatologia
Manganês/efeitos adversos
Síndromes Neurotóxicas
[Mh] Termos MeSH secundário: Envelhecimento
Doenças do Sistema Nervoso Central/etiologia
Seres Humanos
Manganês/metabolismo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
42Z2K6ZL8P (Manganese)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1007/s40572-017-0136-1


  3 / 1010 MEDLINE  
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[PMID]:28394286
[Au] Autor:Li SJ; Ou CY; He SN; Huang XW; Luo HL; Meng HY; Lu GD; Jiang YM; Vieira Peres T; Luo YN; Deng XF
[Ad] Endereço:Department of Toxicology, School of Public Health, Guangxi Medical University, Nanning 530021, China. lishaojun0613@163.com.
[Ti] Título:Sodium p-Aminosalicylic Acid Reverses Sub-Chronic Manganese-Induced Impairments of Spatial Learning and Memory Abilities in Rats, but Fails to Restore γ-Aminobutyric Acid Levels.
[So] Source:Int J Environ Res Public Health;14(4), 2017 Apr 10.
[Is] ISSN:1660-4601
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Excessive manganese (Mn) exposure is not only a health risk for occupational workers, but also for the general population. Sodium para-aminosalicylic acid (PAS-Na) has been successfully used in the treatment of manganism, but the involved molecular mechanisms have yet to be determined. The present study aimed to investigate the effects of PAS-Na on sub-chronic Mn exposure-induced impairments of spatial learning and memory, and determine the possible involvements of γ-aminobutyric acid (GABA) metabolism in vivo. Sprague-Dawley male rats received daily intraperitoneal injections MnCl2 (as 6.55 mg/kg Mn body weight, five days per week for 12 weeks), followed by daily subcutaneous injections of 100, 200, or 300 mg/kg PAS-Na for an additional six weeks. Mn exposure significantly impaired spatial learning and memory ability, as noted in the Morris water maze test, and the following PAS-Na treatment successfully restored these adverse effects to levels indistinguishable from controls. Unexpectedly, PAS-Na failed to recover the Mn-induced decrease in the overall GABA levels, although PAS-Na treatment reversed Mn-induced alterations in the enzyme activities directly responsible for the synthesis and degradation of GABA (glutamate decarboxylase and GABA-transaminase, respectively). Moreover, Mn exposure caused an increase of GABA transporter 1 (GAT-1) and decrease of GABA A receptor (GABA ) in transcriptional levels, which could be reverted by the highest dose of 300 mg/kg PAS-Na treatment. In conclusion, the GABA metabolism was interrupted by sub-chronic Mn exposure. However, the PAS-Na treatment mediated protection from sub-chronic Mn exposure-induced neurotoxicity, which may not be dependent on the GABA metabolism.
[Mh] Termos MeSH primário: Ácido Aminossalicílico/farmacologia
Intoxicação por Manganês/patologia
Manganês/toxicidade
Memória/efeitos dos fármacos
Aprendizagem Espacial/efeitos dos fármacos
Ácido gama-Aminobutírico/sangue
[Mh] Termos MeSH secundário: Animais
Esquema de Medicação
Masculino
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
42Z2K6ZL8P (Manganese); 56-12-2 (gamma-Aminobutyric Acid); 5B2658E0N2 (Aminosalicylic Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE


  4 / 1010 MEDLINE  
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[PMID]:27843694
[Au] Autor:Juurmaa J; Menke RA; Vila P; Müürsepp A; Tomberg T; Ilves P; Nigul M; Johansen-Berg H; Donaghy M; Stagg CJ; Stepens A; Taba P
[Ad] Endereço:Department of Neurology and Neurosurgery University of Tartu Tartu Estonia.
[Ti] Título:Grey matter abnormalities in methcathinone abusers with a Parkinsonian syndrome.
[So] Source:Brain Behav;6(11):e00539, 2016 Nov.
[Is] ISSN:2162-3279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A permanent Parkinsonian syndrome occurs in intravenous abusers of the designer psychostimulant methcathinone (ephedrone). It is attributed to deposition of contaminant manganese, as reflected by characteristic globus pallidus hyperintensity on T1-weighted MRI. METHODS: We have investigated brain structure and function in methcathinone abusers ( = 12) compared to matched control subjects ( = 12) using T1-weighted structural and resting-state functional MRI. RESULTS: Segmentation analysis revealed significant ( < .05) subcortical grey matter atrophy in methcathinone abusers within putamen and thalamus bilaterally, and the left caudate nucleus. The volume of the caudate nuclei correlated inversely with duration of methcathinone abuse. Voxel-based morphometry showed patients to have significant grey matter loss ( < .05) bilaterally in the putamina and caudate nucleus. Surface-based analysis demonstrated nine clusters of cerebral cortical thinning in methcathinone abusers, with relative sparing of prefrontal, parieto-occipital, and temporal regions. Resting-state functional MRI analysis showed increased functional connectivity within the motor network of patients ( < .05), particularly within the right primary motor cortex. CONCLUSION: Taken together, these results suggest that the manganese exposure associated with prolonged methcathinone abuse results in widespread structural and functional changes affecting both subcortical and cortical grey matter and their connections. Underlying the distinctive movement disorder caused by methcathinone abuse, there is a more widespread pattern of brain involvement than is evident from the hyperintensity restricted to the basal ganglia as shown by T1-weighted structural MRI.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Substância Cinzenta/efeitos dos fármacos
Transtornos Parkinsonianos/induzido quimicamente
Propiofenonas/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Atrofia/induzido quimicamente
Encéfalo/patologia
Encéfalo/fisiopatologia
Estudos de Casos e Controles
Feminino
Substância Cinzenta/patologia
Substância Cinzenta/fisiopatologia
Seres Humanos
Imagem por Ressonância Magnética/métodos
Masculino
Intoxicação por Manganês/sangue
Intoxicação por Manganês/etiologia
Transtornos Parkinsonianos/patologia
Transtornos Parkinsonianos/fisiopatologia
Transtornos Relacionados ao Uso de Substâncias/patologia
Transtornos Relacionados ao Uso de Substâncias/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Propiophenones); 386QA522QG (monomethylpropion)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE


  5 / 1010 MEDLINE  
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[PMID]:27814772
[Au] Autor:Peres TV; Schettinger MR; Chen P; Carvalho F; Avila DS; Bowman AB; Aschner M
[Ad] Endereço:Department of Molecular Pharmacology, Albert Einstein College of Medicine, Forchheimer, 209, 1300 Morris Park Ave, Bronx, 10461, NY, USA. tanara.peres-vieira@einstein.yu.edu.
[Ti] Título:"Manganese-induced neurotoxicity: a review of its behavioral consequences and neuroprotective strategies".
[So] Source:BMC Pharmacol Toxicol;17(1):57, 2016 Nov 04.
[Is] ISSN:2050-6511
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Manganese (Mn) is an essential heavy metal. However, Mn's nutritional aspects are paralleled by its role as a neurotoxicant upon excessive exposure. In this review, we covered recent advances in identifying mechanisms of Mn uptake and its molecular actions in the brain as well as promising neuroprotective strategies. The authors focused on reporting findings regarding Mn transport mechanisms, Mn effects on cholinergic system, behavioral alterations induced by Mn exposure and studies of neuroprotective strategies against Mn intoxication. We report that exposure to Mn may arise from environmental sources, occupational settings, food, total parenteral nutrition (TPN), methcathinone drug abuse or even genetic factors, such as mutation in the transporter SLC30A10. Accumulation of Mn occurs mainly in the basal ganglia and leads to a syndrome called manganism, whose symptoms of cognitive dysfunction and motor impairment resemble Parkinson's disease (PD). Various neurotransmitter systems may be impaired due to Mn, especially dopaminergic, but also cholinergic and GABAergic. Several proteins have been identified to transport Mn, including divalent metal tranporter-1 (DMT-1), SLC30A10, transferrin and ferroportin and allow its accumulation in the central nervous system. Parallel to identification of Mn neurotoxic properties, neuroprotective strategies have been reported, and these include endogenous antioxidants (for instance, vitamin E), plant extracts (complex mixtures containing polyphenols and non-characterized components), iron chelating agents, precursors of glutathione (GSH), and synthetic compounds that can experimentally afford protection against Mn-induced neurotoxicity.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Transtornos Cognitivos/prevenção & controle
Manganês/toxicidade
Transtornos das Habilidades Motoras/prevenção & controle
Fármacos Neuroprotetores/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Transtornos Cognitivos/induzido quimicamente
Transtornos Cognitivos/metabolismo
Alimentos/efeitos adversos
Seres Humanos
Manganês/metabolismo
Intoxicação por Manganês/metabolismo
Intoxicação por Manganês/prevenção & controle
Transtornos das Habilidades Motoras/induzido quimicamente
Transtornos das Habilidades Motoras/metabolismo
Fármacos Neuroprotetores/metabolismo
Doença de Parkinson/metabolismo
Doença de Parkinson/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neuroprotective Agents); 42Z2K6ZL8P (Manganese)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


  6 / 1010 MEDLINE  
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[PMID]:27665767
[Au] Autor:Li SJ; Luo YN; Li Y; Chen JW; Mo YH; Yuan ZX; Ou SY; Ou CY; Jiang YM; Deng XF
[Ad] Endereço:Department of Toxicology, School of Public Health, Guangxi Medical University, China.
[Ti] Título:Sodium para-aminosalicylate protected cultured basal ganglia astrocytes from manganese-induced DNA damages and alteration of amino acid neurotransmitter levels.
[So] Source:J Toxicol Sci;41(5):573-81, 2016.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Sodium para-aminosalicylate (PAS-Na) was first applied successfully in clinical treatment of two manganism patients with good prognosis. However, the mechanism of how PAS-Na protects against Mn-induced neurotoxicity is still elusive. The current study was conducted to explore the effects of PAS-Na on Mn-induced basal ganglia astrocyte injury, and the involvement of amino acid neurotransmitter in vitro. Basal ganglia astrocytes were exposed to 500 µM manganese chloride (MnCl2) for 24 hr, following by 50, 150, or 450 µM PAS-Na treatment for another 24 hr. MnCl2 significantly decreased viability of astrocytes and induced DNA damages via increasing the percentage of tail DNA and Olive tail moment of DNA. Moreover, Mn interrupted amino acid neurotransmitters by decreasing Gln levels and increasing Glu, Gly levels. In contrast, PAS-Na treatment reversed the aforementioned Mn-induced toxic effects on basal ganglia astrocytes. Taken together, our results demonstrated that excessive Mn exposure may induce toxic effects on basal ganglia astrocytes, while PAS-Na could protect basal ganglia astrocytes from Mn-induced neurotoxicity.
[Mh] Termos MeSH primário: Ácido Aminossalicílico/farmacologia
Astrócitos/efeitos dos fármacos
Gânglios da Base/efeitos dos fármacos
Cloretos/toxicidade
Dano ao DNA/efeitos dos fármacos
Ácido Glutâmico/metabolismo
Glutamina/metabolismo
Glicina/metabolismo
Intoxicação por Manganês/prevenção & controle
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Astrócitos/metabolismo
Astrócitos/patologia
Gânglios da Base/metabolismo
Gânglios da Base/patologia
Células Cultivadas
Citoproteção
Relação Dose-Resposta a Droga
Compostos de Manganês
Intoxicação por Manganês/genética
Intoxicação por Manganês/metabolismo
Intoxicação por Manganês/patologia
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Manganese Compounds); 0 (Protective Agents); 0RH81L854J (Glutamine); 3KX376GY7L (Glutamic Acid); 5B2658E0N2 (Aminosalicylic Acid); QQE170PANO (manganese chloride); TE7660XO1C (Glycine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE
[do] DOI:10.2131/jts.41.573


  7 / 1010 MEDLINE  
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[PMID]:27310289
[Au] Autor:Selikhova M; Tripoliti E; Fedoryshyn L; Matvienko Y; Stanetska H; Boychuk M; Komnatska I; Lees AJ; Sanotsky Y
[Ad] Endereço:Institute of Neurology, Reta Lila Weston Institute of Neurological Studies, UCL, United Kingdom. Electronic address: m.selikhova@talk21.com.
[Ti] Título:Analysis of a distinct speech disorder seen in chronic manganese toxicity following Ephedrone abuse.
[So] Source:Clin Neurol Neurosurg;147:71-7, 2016 Aug.
[Is] ISSN:1872-6968
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: In the last fifteen years a new cause of chronic manganese toxicity has been recognized. It follows recreational intravenous injections of Ephedrone, synthesized from a cold remedies contained pseudoephedrine. Potassium permanganate is used as an oxidant. It presents with severe parkinsonism-dystonia and a characteristic dysarthria. OBJECTIVES: We performed a focus perceptual study of dysarthria in Ephedrone induced parkinsonism and compared the findings with the speech disorders seen in Parkinson's disease (PD) and Progressive Supranuclear Palsy (PSP). METHODS: A digital voice recording, perceptual speech analysis (Darley, 1975) [18], serial neurological assessment and Brain Magnetic Resonance (MR) imaging were performed at the Lviv regional Clinical Hospital. The results were analysed at the Institute of Neurology in London. RESULTS: Dysarthria developed after 8.5±3.2months of daily intravenous Ephedrone abuse and was an initial symptom in a third of cases. It was characterised by a robotic-flat prosody, whispering or continuous phonation, an inability to regulate pitch and volume, frozen lip articulation, a variable degree of dystonic tightness, difficulties in speech initiation and palladia, There was no nasality and swallowing was normal. In some patients speech deteriorated even after the discontinuation of Ephedrone. MR imaging, performed soon after drug cessation showed T1 signal hyperintesity in striatum and pallidum, especially in the Globus Pallidum interna. CONCLUSION: Ephedrone induced chronic manganese toxicity can lead to a mixed hypokinetic-dystonic dysarthria with a distinct dystonic pattern. Perceptual speech analysis can be a helpful ancillary investigation in the differential diagnosis of parkinsonism, and may permit the recognition of chronic manganese toxicity.
[Mh] Termos MeSH primário: Disartria/etiologia
Globo Pálido/diagnóstico por imagem
Intoxicação por Manganês/complicações
Neostriado/diagnóstico por imagem
Doença de Parkinson Secundária/complicações
Propiofenonas/toxicidade
[Mh] Termos MeSH secundário: Adulto
Disartria/induzido quimicamente
Seres Humanos
Masculino
Intoxicação por Manganês/etiologia
Doença de Parkinson Secundária/induzido quimicamente
Doença de Parkinson Secundária/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Propiophenones); 386QA522QG (monomethylpropion)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE


  8 / 1010 MEDLINE  
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[PMID]:27193731
[Au] Autor:Saputra D; Chang J; Lee BJ; Yoon JH; Kim J; Lee K
[Ad] Endereço:Inhalation Toxicology Center, Korea Institute of Toxicology, Korea.
[Ti] Título:Short-term manganese inhalation decreases brain dopamine transporter levels without disrupting motor skills in rats.
[So] Source:J Toxicol Sci;41(3):391-402, 2016.
[Is] ISSN:1880-3989
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Manganese (Mn) is used in industrial metal alloys and can be released into the atmosphere during methylcyclopentadienyl manganese tricarbonyl combustion. Increased Mn deposition in the brain after long-term exposure to the metal by inhalation is associated with altered dopamine metabolism and neurobehavioral problems, including impaired motor skills. However, neurotoxic effects of short-term exposure to inhaled Mn are not completely characterized. The purpose of this study is to define the neurobehavioral and neurochemical effects of short-term inhalation exposure to Mn at a high concentration using rats. Male Sprague-Dawley rats were exposed to MnCl2 aerosol in a nose-only inhalation chamber for 3 weeks (1.2 µm, 39 mg/m(3)). Motor coordination was tested on the day after the last exposure using a rotarod device at a fixed speed of 10 rpm for 2 min. Also, dopamine transporter and dopamine receptor protein expression levels in the striatum region of the brain were determined by Western blot analysis. At a rotarod speed of 10 rpm, there were no significant differences in the time on the bar before the first fall or the number of falls during the two-minute test observed in the exposed rats, as compared with controls. The Mn-exposed group had significantly higher Mn levels in the lung, blood, olfactory bulb, prefrontal cortex, striatum, and cerebellum compared with the control group. A Mn concentration gradient was observed from the olfactory bulb to the striatum, supporting the idea that Mn is transported via the olfactory pathway. Our results demonstrated that inhalation exposure to 39 mg/m(3) Mn for 3 weeks induced mild lung injury and modulation of dopamine transporter expression in the brain, without altering motor activity.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Cloretos/toxicidade
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Exposição por Inalação
Intoxicação por Manganês/etiologia
Atividade Motora/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Cloretos/metabolismo
Lesão Pulmonar/induzido quimicamente
Lesão Pulmonar/patologia
Masculino
Compostos de Manganês/metabolismo
Intoxicação por Manganês/metabolismo
Intoxicação por Manganês/fisiopatologia
Intoxicação por Manganês/psicologia
Ratos Sprague-Dawley
Receptores Dopaminérgicos/metabolismo
Medição de Risco
Teste de Desempenho do Rota-Rod
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Dopamine Plasma Membrane Transport Proteins); 0 (Manganese Compounds); 0 (Receptors, Dopamine); QQE170PANO (manganese chloride)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160520
[St] Status:MEDLINE
[do] DOI:10.2131/jts.41.391


  9 / 1010 MEDLINE  
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[PMID]:27163837
[Au] Autor:Hines EQ; Soomro I; Howland MA; Hoffman RS; Smith SW
[Ad] Endereço:a Division of Medical Toxicology, Ronald O. Perelman Department of Emergency Medicine , NYU School of Medicine , New York , NY , USA ;
[Ti] Título:Massive intravenous manganese overdose due to compounding error: minimal role for hemodialysis.
[So] Source:Clin Toxicol (Phila);54(6):523-5, 2016 Jul.
[Is] ISSN:1556-9519
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Manganese-associated parkinsonism is well described in occupational settings, in chronic methcathinone users, and in patients receiving long-term total parenteral nutrition. We present a unique case of acute intravenous manganese poisoning with a systematic evaluation of hemodialysis efficacy. CASE DETAILS: A 52-year-old woman was inadvertently administered a single intravenous dose of 800 mg compounded manganese chloride at an outpatient chelation center. In an attempt to minimize central nervous system (CNS) manganese deposition, she underwent urgent hemodialysis followed by five days of therapy with calcium disodium EDTA (1 g/m(2) over eight hours daily). Her initial whole blood manganese concentration, obtained six hours after exposure and prior to treatment, was 120 mcg/L (2.19 micromol/L); normal <5 mcg/L (< 0.09 micromol/L). Following the first four-hour hemodialysis session her blood manganese concentration decreased to 20 mcg/L (0.36 micromol/L). Despite the fall in her blood manganese concentration, analysis of dialysate revealed a total elimination of only 604 mcg (11 micromol) manganese (∼1.4% of manganese burden). Although she remained asymptomatic, an MRI on hospital day two revealed T1 hyperintensities within the bilateral globus pallidi, consistent with manganese exposure. DISCUSSION: Manganese poisoning is associated with irreversible neurologic toxicity. Hemodialysis did not appear to significantly enhance elimination in this case of acute intravenous manganese toxicity, beyond supportive care and calcium disodium EDTA chelation.
[Mh] Termos MeSH primário: Overdose de Drogas/terapia
Intoxicação por Manganês/terapia
Manganês/administração & dosagem
Manganês/sangue
Diálise Renal
[Mh] Termos MeSH secundário: Administração Intravenosa
Quelantes/uso terapêutico
Relação Dose-Resposta a Droga
Overdose de Drogas/sangue
Ácido Edético/uso terapêutico
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Intoxicação por Manganês/sangue
Meia-Idade
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/terapia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chelating Agents); 42Z2K6ZL8P (Manganese); 9G34HU7RV0 (Edetic Acid)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160511
[St] Status:MEDLINE
[do] DOI:10.1080/15563650.2016.1178390


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Fotocópia
[PMID]:27012047
[Au] Autor:Dastych M; Dastych M; Senkyrík M
[Ti] Título:Manganese in Whole Blood and Hair in Patients with Long-Term Home Parenteral Nutrition.
[So] Source:Clin Lab;62(1-2):173-7, 2016.
[Is] ISSN:1433-6510
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Manganese is an essential trace element and indispensable component of nutrition mixtures in long-term home parenteral nutrition (HPN) of patients. On the other hand, neurotoxic effects of excess manganese in the organism have been known for a long time. The objective of the present study was to determine manganese concentration in whole blood and hair of patients with long-term home parenteral nutrition. METHODS: We examined 16 patients (7 men and 9 women) aged from 28 to 68 years on long-term HPN lasting from 4 to 96 months. The short bowel syndrome was an indication for HPN. The daily dose of manganese ranged between 80 and 470 microg/day (1.2 to 8.5 pg/kg/day). RESULTS: In the investigated patients we detected approximately a doubled value of manganese concentration in whole blood in comparison to the control group (16.2 microg/L; 12.9-20.4 microg/L and 7.4 microg/L; 6.4-8.4 microg/L). In five patients with symptoms of cholestatic hepatopathy, Mn concentration in whole blood exceeded the value of 20.0 microg/L. Magnetic resonance of the brain in four of these patients detected a hyperintense T1-signal in the globus pallidus without any clinical symptoms similar to the Parkinson's syndrome. The content of manganese in the patients' hair was also significantly increased (p < 0.04). CONCLUSIONS: The results of our study corroborate the necessity of careful monitoring of the manganese concentration in the organism during HPN, especially in patients with liver disorders. Individualized HPN with greater accessibility of variable mixtures of trace elements would certainly be greatly beneficial, at least with regard to problems associated with manganese substitution.
[Mh] Termos MeSH primário: Cabelo/metabolismo
Manganês/sangue
Nutrição Parenteral no Domicílio
Síndrome do Intestino Curto/terapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Encéfalo/patologia
Estudos de Casos e Controles
Feminino
Seres Humanos
Hepatopatias/sangue
Hepatopatias/complicações
Imagem por Ressonância Magnética
Masculino
Intoxicação por Manganês/sangue
Intoxicação por Manganês/etiologia
Intoxicação por Manganês/patologia
Meia-Idade
Nutrição Parenteral no Domicílio/efeitos adversos
Valor Preditivo dos Testes
Fatores de Risco
Síndrome do Intestino Curto/sangue
Síndrome do Intestino Curto/complicações
Síndrome do Intestino Curto/diagnóstico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 42Z2K6ZL8P (Manganese)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:160325
[Lr] Data última revisão:
160325
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160326
[St] Status:MEDLINE



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