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[PMID]:29431328
[Au] Autor:Vokina VA; Sosedova LM; Filippova TM
[Ti] Título:[The study of neurotoxicity of toluene in conditions of experimental modeling of prenatal hypoxic damage of the brain].
[So] Source:Gig Sanit;95(9):895-9, 2016.
[Is] ISSN:0016-9900
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:There was executed the study of the impact of toluene on indices of behavior, cognitive capabilities and bioelectric activity of the brain in white rats with normal course of the period of antenatal development and against background ofprenatal hemic hypoxia Prenatal hypoxia was modeled in pregnant female rats by subcutaneous injection of sodium nitrite in a dose of 50 mg/kg at from the 10 to the 19 day of gestation. At the age of 3 months the males from the obtained offspring were exposed to inhalation exposure of toluene (150 ppm, 4 weeks). After exposure to toluene in animals there was evaluated the pattern of individual behavior, indices of cognitive capabilities and also bioelectric activity of the brain. There were revealed such common consistencies of transformations in the behavior of exposed to toluene animals with normal and impaired embryogenesis as disturbed motor activity, reduction of exploratory behavior and cognitive functions, impaired bioelectric potentials of the brain. Features of changes in behavior and EEG indices in toluene-exposed rats with prenatal hypoxia are characterized by inhibition of motor activity, increased anxiety and latency of main peaks of auditory and visual evoked potentials. Prenatal hypoxic damage of the central nervous system was shown to be an aggravating factor in toluene intoxication in rats.
[Mh] Termos MeSH primário: Comportamento Animal
Encéfalo
Cognição
Hipóxia-Isquemia Encefálica
Complicações na Gravidez/fisiopatologia
Tolueno/farmacologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Comportamento Animal/fisiologia
Encéfalo/efeitos dos fármacos
Encéfalo/fisiopatologia
Mapeamento Encefálico/métodos
Cognição/efeitos dos fármacos
Cognição/fisiologia
Modelos Animais de Doenças
Feminino
Hipóxia-Isquemia Encefálica/complicações
Hipóxia-Isquemia Encefálica/fisiopatologia
Neurotoxinas/farmacologia
Gravidez
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); 3FPU23BG52 (Toluene)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180213
[St] Status:MEDLINE


  2 / 11674 MEDLINE  
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[PMID]:28942274
[Au] Autor:Andersson M; Karlsson O; Brandt I
[Ad] Endereço:Department of Environmental Toxicology, Uppsala University, SE-752 36 Uppsala, Sweden.
[Ti] Título:The environmental neurotoxin ß-N-methylamino-l-alanine (l-BMAA) is deposited into birds' eggs.
[So] Source:Ecotoxicol Environ Saf;147:720-724, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The neurotoxic amino acid ß-N-methylamino-L-alanine (BMAA) has been implicated in the etiology of neurodegenerative disorders. BMAA is also a known developmental neurotoxin and research indicates that the sources of human and wildlife exposure may be more diverse than previously anticipated. The aim of the present study was therefore to examine whether BMAA can be transferred into birds' eggs. Egg laying quail were dosed with C-labeled BMAA. The distribution of radioactivity in the birds and their laid eggs was then examined at different time points by autoradiography and phosphoimaging analysis. To evaluate the metabolic stability of the BMAA molecule, the distribution of C-methyl- and C-carboxyl-labeled BMAA were compared. The results revealed a pronounced incorporation of radioactivity in the eggs, predominantly in the yolk but also in the albumen. Imaging analysis showed that the concentrations of radioactivity in the liver decreased about seven times between the 24h and the 72h time points, while the concentrations in egg yolk remained largely unchanged. At 72h the egg yolk contained about five times the concentration of radioactivity in the liver. Both BMAA preparations gave rise to similar distribution pattern in the bird tissues and in the eggs, indicating metabolic stability of the labeled groups. The demonstrated deposition into eggs warrants studies of BMAAs effects on bird development. Moreover, birds' eggs may be a source of human BMAA exposure, provided that the laying birds are exposed to BMAA via their diet.
[Mh] Termos MeSH primário: Diamino Aminoácidos/toxicidade
Aves/metabolismo
Monitoramento Ambiental/métodos
Poluentes Ambientais/toxicidade
Neurotoxinas/toxicidade
Óvulo/metabolismo
[Mh] Termos MeSH secundário: Diamino Aminoácidos/metabolismo
Animais
Autorradiografia
Poluentes Ambientais/metabolismo
Seres Humanos
Neurotoxinas/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids, Diamino); 0 (Environmental Pollutants); 0 (Neurotoxins); 108SA6URTV (beta-N-methylamino-L-alanine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


  3 / 11674 MEDLINE  
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[PMID]:28468639
[Au] Autor:Sasajima H; Yagi S; Osada H; Zako M
[Ad] Endereço:Department of Ophthalmology, Aichi Medical University, Nagakute, Aichi, Japan.
[Ti] Título:Botulinum toxin-induced acute anterior uveitis in a patient with Behçet's disease under infliximab treatment: a case report.
[So] Source:J Med Case Rep;11(1):124, 2017 May 04.
[Is] ISSN:1752-1947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Injections of lipopolysaccharide in animal models generate acute anterior uveitis (also known as endotoxin-induced uveitis), but the effects of lipopolysaccharide injection are unknown in humans. We describe an unusual case in which acute anterior uveitis was dramatically activated subsequent to botulinum toxin injection in a patient with Behçet's disease but the acute anterior uveitis was satisfactorily attenuated by infliximab. CASE PRESENTATION: A 53-year-old Japanese man had normal ocular findings at his regularly scheduled appointment. He had been diagnosed as having incomplete-type Behçet's disease 11 years before. Three years after the diagnosis he was given systemic infusions of 5 mg/kg infliximab every 8 weeks and he had not experienced a uveitis attack for 8 years with no treatment other than infliximab. Two days after the eye examination, he received intracutaneous botulinum toxin injections to treat axillary hyperhidrosis on both sides. Three hours after the injections, he noted rapidly increasing floaters in his right eye. Four days after the injections, his right eye showed severe acute anterior uveitis with deteriorated aqueous flare and anterior vitreous opacity. He received his scheduled infliximab injection, and the right acute anterior uveitis immediately attenuated. CONCLUSIONS: Botulinum toxin may have clinical effects similar to those of lipopolysaccharide in endotoxin-induced uveitis models. To the best of our knowledge, this is the first report to suggest that botulinum toxin may trigger acute anterior uveitis, although the precise mechanism is still unclear.
[Mh] Termos MeSH primário: Síndrome de Behçet/tratamento farmacológico
Toxinas Botulínicas/efeitos adversos
Hiperidrose/tratamento farmacológico
Infliximab/administração & dosagem
Neurotoxinas/administração & dosagem
Uveíte/induzido quimicamente
[Mh] Termos MeSH secundário: Seres Humanos
Injeções Subcutâneas
Masculino
Meia-Idade
Tomografia de Coerência Óptica
Uveíte/diagnóstico por imagem
Uveíte/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); B72HH48FLU (Infliximab); EC 3.4.24.69 (Botulinum Toxins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s13256-017-1288-1


  4 / 11674 MEDLINE  
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[PMID]:27771241
[Au] Autor:Merino PS; Vera RE; Mariñas LG; Gómez de Liaño PS; Escribano JV
[Ad] Endereço:Ocular Motility Section, Department of Ophthalmology, Hospital General Universitario Gregorio Marañón, Madrid, Spain. Electronic address: pilimerino@gmail.com.
[Ti] Título:Botulinum toxin for treatment of restrictive strabismus.
[So] Source:J Optom;10(3):189-193, 2017 Jul - Sep.
[Is] ISSN:1989-1342
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To study the types of acquired restrictive strabismus treated in a tertiary hospital and the outcome of treatment with botulinum toxin. METHODS: We performed a 10-year retrospective study of patients with restrictive strabismus aged ≥18 years who were treated with botulinum toxin. Treatment was considered successful if the final vertical deviation was ≤5 PD, horizontal deviation ≤10 PD, with no head turn or diplopia. RESULTS: We included 27 cases (mean age, 61.9 years). Horizontal strabismus was diagnosed in 11.1%, vertical in 51.9%, and mixed in 37%. Strabismus was secondary to cataract surgery in 6 cases, high myopia in 6, orbital fractures in 5, retinal surgery in 5, Graves ophthalmopathy in 4, and repair of conjunctival injury in 1 case. Diplopia was diagnosed in all patients, head turn in 33.3%. The initial deviation was 14 PD (range, 2-40), the mean number of injections per patient was 1.6 (range, 1-3), and the mean dose was 9.5 IU (range, 2.5-22.5). At the end of follow-up, diplopia was recorded in 59.3%, head turn in 18.5%, surgical treatment in 51.9%, and need for prism glasses in 14.8%. Outcome was successful in 37% of patients (4 high myopia, 3 orbital fractures, 2 post-surgical retinal detachment, and 1 post-cataract surgery). Mean follow-up was 3±1.8 years. CONCLUSION: Vertical deviation was observed in half of the sample. The most frequent deviation was secondary to cataract surgery and high myopia. Treatment with botulinum toxin was successful in one-third of the patients at the end of follow-up.
[Mh] Termos MeSH primário: Toxinas Botulínicas/administração & dosagem
Movimentos Oculares/fisiologia
Previsões
Estrabismo/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seguimentos
Seres Humanos
Injeções Intramusculares
Masculino
Meia-Idade
Neurotoxinas/administração & dosagem
Músculos Oculomotores
Estudos Retrospectivos
Estrabismo/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); EC 3.4.24.69 (Botulinum Toxins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  5 / 11674 MEDLINE  
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[PMID]:29447689
[Au] Autor:Popoff MR
[Ad] Endereço:Bacterial Toxins, Institut Pasteur, Paris, France. Electronic address: mpopoff@pasteur.fr.
[Ti] Título:Botulinum Neurotoxins: Still a Privilege of Clostridia?
[So] Source:Cell Host Microbe;23(2):145-146, 2018 02 14.
[Is] ISSN:1934-6069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Botulinum neurotoxins (BoNTs) are potent bacterial toxins mostly produced by genetically diverse clostridial strains. Recently, BoNT variants have been reported in non-clostridial strains. In this issue of Cell Host & Microbe, Zhang et al. (2018) describe a novel BoNT in Entecoccus faecium.
[Mh] Termos MeSH primário: Toxinas Botulínicas
Neurotoxinas
[Mh] Termos MeSH secundário: Clostridium
Seres Humanos
Hidrolases
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Neurotoxins); EC 3.- (Hydrolases); EC 3.4.24.69 (Botulinum Toxins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180216
[St] Status:MEDLINE


  6 / 11674 MEDLINE  
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[PMID]:29258821
[Au] Autor:Masuda K; Tsutsuki H; Kasamatsu S; Ida T; Takata T; Sugiura K; Nishida M; Watanabe Y; Sawa T; Akaike T; Ihara H
[Ad] Endereço:Department of Biological Science, Graduate School of Science, Osaka Prefecture University, Osaka, Japan; Project Management Department, SHIONOGI & CO., LTD., Osaka, Japan.
[Ti] Título:Involvement of nitric oxide/reactive oxygen species signaling via 8-nitro-cGMP formation in 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in PC12 cells and rat cerebellar granule neurons.
[So] Source:Biochem Biophys Res Commun;495(3):2165-2170, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the role of nitric oxide (NO)/reactive oxygen species (ROS) redox signaling in Parkinson's disease-like neurotoxicity, we used 1-methyl-4-phenylpyridinium (MPP ) treatment (a model of Parkinson's disease). We show that MPP -induced neurotoxicity was dependent on ROS from neuronal NO synthase (nNOS) in nNOS-expressing PC12 cells (NPC12 cells) and rat cerebellar granule neurons (CGNs). Following MPP treatment, we found production of 8-nitroguanosine 3',5'-cyclic monophosphate (8-nitro-cGMP), a second messenger in the NO/ROS redox signaling pathway, in NPC12 cells and rat CGNs, that subsequently induced S-guanylation and activation of H-Ras. Additionally, following MPP treatment, extracellular signal-related kinase (ERK) phosphorylation was enhanced. Treatment with a mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) inhibitor attenuated MPP -induced ERK phosphorylation and neurotoxicity. In conclusion, we demonstrate for the first time that NO/ROS redox signaling via 8-nitro-cGMP is involved in MPP -induced neurotoxicity and that 8-nitro-cGMP activates H-Ras/ERK signaling. Our results indicate a novel mechanism underlying MPP -induced neurotoxicity, and therefore contribute novel insights to the mechanisms underlying Parkinson's disease.
[Mh] Termos MeSH primário: 1-Metil-4-fenilpiridínio
Cerebelo/metabolismo
GMP Cíclico/análogos & derivados
Neurônios/metabolismo
Óxido Nítrico/metabolismo
Transtornos Parkinsonianos/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Cerebelo/efeitos dos fármacos
Cerebelo/patologia
GMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Neurônios/efeitos dos fármacos
Neurônios/patologia
Neurotoxinas
Células PC12
Transtornos Parkinsonianos/induzido quimicamente
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (8-nitroguanosine 3',5'-cyclic monophosphate); 0 (Neurotoxins); 0 (Reactive Oxygen Species); 31C4KY9ESH (Nitric Oxide); H2D2X058MU (Cyclic GMP); R865A5OY8J (1-Methyl-4-phenylpyridinium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


  7 / 11674 MEDLINE  
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[PMID]:29225110
[Au] Autor:Bhattacharya D; Majrashi M; Ramesh S; Govindarajulu M; Bloemer J; Fujihashi A; Crump BR; Hightower H; Bhattacharya S; Moore T; Suppiramaniam V; Dhanasekaran M
[Ad] Endereço:Drug Discovery and Development, Harrison School of Pharmacy, Auburn University, USA.
[Ti] Título:Assessment of the cerebellar neurotoxic effects of nicotine in prenatal alcohol exposure in rats.
[So] Source:Life Sci;194:177-184, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The adverse effects of prenatal nicotine and alcohol exposure on human reproductive outcomes are a major scientific and public health concern. In the United States, substantial percentage of women (20-25%) of childbearing age currently smoke cigarettes and consume alcohol, and only a small percentage of these individuals quit after learning of their pregnancy. However, there are very few scientific reports on the effect of nicotine in prenatal alcohol exposure on the cerebellum of the offspring. Therefore, this study was conducted to investigate the cerebellar neurotoxic effects of nicotine in a rodent model of Fetal Alcohol Spectrum Disorder (FASD). In this study, we evaluated the behavioral changes, biochemical markers of oxidative stress and apoptosis, mitochondrial functions and the molecular mechanisms associated with nicotine in prenatal alcohol exposure on the cerebellum. Prenatal nicotine and alcohol exposure induced oxidative stress, did not affect the mitochondrial functions, increased the monoamine oxidase activity, increased caspase expression and decreased ILK, PSD-95 and GLUR1 expression without affecting the GSK-3ß. Thus, our current study of prenatal alcohol and nicotine exposure on cerebellar neurotoxicity may lead to new scientific perceptions and novel and suitable therapeutic actions in the future.
[Mh] Termos MeSH primário: Cerebelo/efeitos dos fármacos
Cerebelo/embriologia
Transtornos do Espectro Alcoólico Fetal/patologia
Neurotoxinas/toxicidade
Nicotina/toxicidade
Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Cerebelo/metabolismo
Cerebelo/patologia
Feminino
Transtornos do Espectro Alcoólico Fetal/metabolismo
Seres Humanos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/patologia
Estresse Oxidativo/efeitos dos fármacos
Gravidez
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Efeitos Tardios da Exposição Pré-Natal/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


  8 / 11674 MEDLINE  
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[PMID]:29237498
[Au] Autor:Lee DH; Han J; Han SH; Lee SC; Kim M
[Ad] Endereço:Institute of Vision Research, Department of Ophthalmology, Severance Eye and ENT Hospital, Yonsei University College of Medicine, Seoul, South Korea.
[Ti] Título:Vitreous hemorrhage and Rhegmatogenous retinal detachment that developed after botulinum toxin injection to the extraocular muscle: case report.
[So] Source:BMC Ophthalmol;17(1):249, 2017 Dec 13.
[Is] ISSN:1471-2415
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The authors report a case of a rare complication that occurred after botulinum toxin injection to the extraocular muscle, which was easily overlooked and successfully corrected by surgery. CASE PRESENTATION: A 34-year-old female patient visited our clinic for diplopia and ocular motility disorder after removal of an epidermoid tumor of the brain. At her initial visit, her best-corrected visual acuity (BCVA) was 20/20 for both eyes. An alternate cover test showed 45 prism-diopter esotropia and 3 prism-diopter hypertropia in the right eye. Following 6 months of observation, the deviation of the strabismus did not improve, and botulinum toxin was injected into the right medial rectus (RMR). After 6 days, she visited our clinic with decreased visual acuity of her right eye. The BCVA was found to be 20/50 for her right eye. Funduscopic examination presented a retinal tear inferonasal to the optic disc with preretinal hemorrhage. Subretinal fluid nasal to the fovea was seen on optical coherence tomography (OCT). Barrier laser photocoagulation was done around the retinal tear; however, her visual acuity continued to decrease, and vitreous hemorrhage and subretinal fluid at the lesion did not improve. In addition, a newly developed epiretinal membrane was seen on OCT. An alternate cover test presented 30 prism-diopter right esotropia. 19 weeks after RMR botulinum toxin injection, she received pars plana vitrectomy, membranectomy, endolaser barrier photocoagulation, and intravitreal bevacizumab (Avastin®) injection. After 4 months, her visual acuity improved to 20/20, and only 4 prism-diopter of right hypertropia and 3 prism-diopter of exotropia were noted. Vitreous opacity and the epiretinal membrane were completely removed, as confirmed by funduscopic and examination. CONCLUSIONS: Sudden loss of vision after injection of botulinum toxin into the extraocular muscle may suggest a serious complication, and a prompt, thorough ophthalmic examination should be performed. If improvements are not observed, rapid surgical intervention is recommended to prevent additional complications.
[Mh] Termos MeSH primário: Toxinas Botulínicas/efeitos adversos
Neurotoxinas/efeitos adversos
Descolamento Retiniano/induzido quimicamente
Hemorragia Vítrea/induzido quimicamente
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Injeções Intramusculares/efeitos adversos
Injeções Intraoculares/efeitos adversos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neurotoxins); EC 3.4.24.69 (Botulinum Toxins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1186/s12886-017-0649-2


  9 / 11674 MEDLINE  
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[PMID]:29180015
[Au] Autor:Tanaka KI; Shimoda M; Kawahara M
[Ad] Endereço:Department of Bio-Analytical Chemistry, Faculty of Pharmacy, Musashino University, 1-1-20 Shinmachi, Nishitokyo-shi, Tokyo 202-8585, Japan. Electronic address: k-tana@musashino-u.ac.jp.
[Ti] Título:Pyruvic acid prevents Cu /Zn -induced neurotoxicity by suppressing mitochondrial injury.
[So] Source:Biochem Biophys Res Commun;495(1):1335-1341, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Zinc (Zn) is known as a co-factor for over 300 metalloproteins or enzymes, and has essential roles in many physiological functions. However, excessively high Zn concentrations are induced in pathological conditions such as interruption of blood flow in stroke or transient global ischemia-induced neuronal cell death. Furthermore, we recently found that copper (Cu ) significantly exacerbates Zn neurotoxicity in mouse hypothalamic neuronal cells, suggesting that Zn interaction with Cu is important for the development of neurological disease. Meanwhile, organic acids such as pyruvic acid and citric acid are reported to prevent neuronal cell death induced by various stresses. Thus, in this study, we focused on organic acids and searched for compounds that inhibit Cu /Zn -induced neurotoxicity. Initially, we examined the protective effect of various organic acids on Cu /Zn -induced neurotoxicity, and found that pyruvic acid clearly suppresses Cu /Zn -induced neurotoxicity in GT1-7 cells. Next, we examined the protective mechanisms of pyruvic acid against Cu /Zn -induced neurotoxicity. Specifically, we examined the possibilities that pyruvic acid chelates Cu and Zn or suppresses the ER stress response, but found that neither was suppressed by pyruvic acid treatment. In contrast, pyruvic acid significantly suppressed cytochrome c release into cytoplasm, an index of mitochondrial injury, in a dose-dependent manner. These results suggest that pyruvic acid prevents Cu /Zn -induced neuronal cell death by suppressing mitochondrial injury. Based on our results, we assume that pyruvic acid may be therapeutically beneficial for neurological diseases involving neuronal cell death such as vascular dementia.
[Mh] Termos MeSH primário: Cobre/toxicidade
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Neurônios/efeitos dos fármacos
Neurônios/patologia
Ácido Pirúvico/administração & dosagem
Zinco/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Camundongos
Fármacos Neuroprotetores/administração & dosagem
Neurotoxinas/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuroprotective Agents); 0 (Neurotoxins); 789U1901C5 (Copper); 8558G7RUTR (Pyruvic Acid); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE


  10 / 11674 MEDLINE  
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[PMID]:28455330
[Au] Autor:Fredrick CM; Lin G; Johnson EA
[Ad] Endereço:Department of Bacteriology, University of Wisconsin-Madison, Madison, Wisconsin, USA.
[Ti] Título:Regulation of Botulinum Neurotoxin Synthesis and Toxin Complex Formation by Arginine and Glucose in Clostridium botulinum ATCC 3502.
[So] Source:Appl Environ Microbiol;83(13), 2017 Jul 01.
[Is] ISSN:1098-5336
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Botulinum neurotoxin (BoNT), produced by neurotoxigenic clostridia, is the most potent biological toxin known and the causative agent of the paralytic disease botulism. The nutritional, environmental, and genetic regulation of BoNT synthesis, activation, stability, and toxin complex (TC) formation is not well studied. Previous studies indicated that growth and BoNT formation were affected by arginine and glucose in types A and B. In the present study, ATCC 3502 was grown in toxin production medium (TPM) with different levels of arginine and glucose and of three products of arginine metabolism, citrulline, proline, and ornithine. Cultures were analyzed for growth (optical density at 600 nm [OD ]), spore formation, and BoNT and TC formation by Western blotting and immunoprecipitation and for BoNT activity by mouse bioassay. A high level of arginine (20 g/liter) repressed BoNT production approximately 1,000-fold, enhanced growth, slowed lysis, and reduced endospore production by greater than 1,000-fold. Similar effects on toxin production were seen with equivalent levels of citrulline but not ornithine or proline. In TPM lacking glucose, levels of formation of BoNT/A1 and TC were significantly decreased, and extracellular BoNT and TC proteins were partially inactivated after the first day of culture. An understanding of the regulation of growth and BoNT and TC formation should be valuable in defining requirements for BoNT formation in foods and clinical samples, improving the quality of BoNT for pharmaceutical preparations, and elucidating the biological functions of BoNTs for the bacterium. Botulinum neurotoxin (BoNT) is a major food safety and bioterrorism concern and is also an important pharmaceutical, and yet the regulation of its synthesis, activation, and stability in culture media, foods, and clinical samples is not well understood. This paper provides insights into the effects of critical nutrients on growth, lysis, spore formation, BoNT and TC production, and stability of BoNTs of We show that for ATCC 3502 cultured in a complex medium, a high level of arginine repressed BoNT expression by ca. 1,000-fold and also strongly reduced sporulation. Arginine stimulated growth and compensated for a lack of glucose. BoNT and toxin complex proteins were partially inactivated in a complex medium lacking glucose. This work should aid in optimizing BoNT production for pharmaceutical uses, and furthermore, an understanding of the nutritional regulation of growth and BoNT formation may provide insights into growth and BoNT formation in foods and clinical samples and into the enigmatic function of BoNTs in nature.
[Mh] Termos MeSH primário: Arginina/metabolismo
Toxinas Botulínicas/biossíntese
Botulismo/microbiologia
Clostridium botulinum/genética
Regulação Bacteriana da Expressão Gênica
Glucose/metabolismo
Neurotoxinas/biossíntese
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Toxinas Botulínicas/genética
Clostridium botulinum/crescimento & desenvolvimento
Clostridium botulinum/metabolismo
Seres Humanos
Neurotoxinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Neurotoxins); 94ZLA3W45F (Arginine); EC 3.4.24.69 (Botulinum Toxins); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171225
[Lr] Data última revisão:
171225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE



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