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[PMID]:29059204
[Au] Autor:Potthast AB; Heuer T; Warneke SJ; Das AM
[Ad] Endereço:Clinic for Paediatric Kidney-, Liver-, and Metabolic Diseases, Hannover Medical School, Hannover, Germany.
[Ti] Título:Alterations of sirtuins in mitochondrial cytochrome c-oxidase deficiency.
[So] Source:PLoS One;12(10):e0186517, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sirtuins are NAD+ dependent deacetylases, which regulate mitochondrial energy metabolism as well as cellular response to stress. The NAD/NADH-system plays a crucial role in oxidative phosphorylation linking sirtuins and the mitochondrial respiratory chain. Furthermore, sirtuins are able to directly deacetylate and activate different complexes of the respiratory chain. This prompted us to analyse sirtuin levels in skin fibroblasts from patients with cytochrome c-oxidase (COX) deficiency and to test the impact of different pharmaceutical activators of sirtuins (SRT1720, paeonol) to modulate sirtuins and possibly respiratory chain enzymes in patient cells in vitro. METHODS: We assayed intracellular levels of sirtuin 1 and the mitochondrial sirtuins SIRT3 and SIRT4 in human fibroblasts from patients with COX- deficiency. Furthermore, sirtuins were measured after inhibiting complex IV in healthy control fibroblasts by cyanide and after incubation with activators SRT1720 and paeonol. To determine the effect of sirtuin inhibition at the cellular level we measured total cellular acetylation (control and patient cells, with and without treatment) by Western blot. RESULTS: We observed a significant decrease in cellular levels of all three sirtuins at the activity, protein and transcriptional level (by 15% to 50%) in COX-deficient cells. Additionally, the intracellular concentration of NAD+ was reduced in patient cells. We mimicked the biochemical phenotype of COX- deficiency by incubating healthy fibroblasts with cyanide and observed reduced sirtuin levels. A pharmacological activation of sirtuins resulted in normalized sirtuin levels in patient cells. Hyper acetylation was also reversible after treatment with sirtuin activators. Pharmacological modulation of sirtuins resulted in altered respiratory chain complex activities. CONCLUSIONS: We found inhibition of situins 1, 3 and 4 at activity, protein and transcriptional levels in fibroblasts from patient with COX-deficiency. Pharmacological activators were able to restore reduced sirtuin levels and thereby modulate respiratory chain activities.
[Mh] Termos MeSH primário: Complexo IV da Cadeia de Transporte de Elétrons/genética
Mitocôndrias/metabolismo
Sirtuínas/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Transporte de Elétrons/efeitos dos fármacos
Seres Humanos
Mitocôndrias/enzimologia
Espécies Reativas de Oxigênio/metabolismo
Cianeto de Sódio/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); EC 1.9.3.1 (Electron Transport Complex IV); EC 3.5.1.- (Sirtuins); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186517


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[PMID]:28533325
[Au] Autor:Lall VK; Bruce G; Voytenko L; Drinkhill M; Wellershaus K; Willecke K; Deuchars J; Deuchars SA
[Ad] Endereço:Faculty of Biological Sciences, School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom.
[Ti] Título:Physiologic regulation of heart rate and blood pressure involves connexin 36-containing gap junctions.
[So] Source:FASEB J;31(9):3966-3977, 2017 Sep.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronically elevated sympathetic nervous activity underlies many cardiovascular diseases. Elucidating the mechanisms contributing to sympathetic nervous system output may reveal new avenues of treatment. The contribution of the gap junctional protein connexin 36 (Cx36) to the regulation of sympathetic activity and thus blood pressure and heart rate was determined using a mouse with specific genetic deletion of Cx36. Ablation of the Cx36 protein was confirmed in sympathetic preganglionic neurons of Cx36-knockout (KO) mice. Telemetric analysis from conscious Cx36 KO mice revealed higher variance in heart rate and blood pressure during rest and activity compared to wild-type (WT) mice, and smaller responses to chemoreceptor activation when anesthetized. In the working heart-brain stem preparation of the Cx36-KO mouse, respiratory-coupled sympathetic nerve discharge was attenuated and responses to chemoreceptor stimulation and noxious stimulation were blunted compared to WT mice. Using whole cell patch recordings, sympathetic preganglionic neurons in spinal cord slices of Cx36-KO mice displayed lower levels of spikelet activity compared to WT mice, indicating reduced gap junction coupling between neurons. Cx36 deletion therefore disrupts normal regulation of sympathetic outflow with effects on cardiovascular parameters.-Lall, V. K., Bruce, G., Voytenko, L., Drinkhill, M., Wellershaus, K., Willecke, K., Deuchars, J., Deuchars, S. A. Physiologic regulation of heart rate and blood pressure involves connexin 36-containing gap junctions.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Conexinas/metabolismo
Junções Comunicantes/fisiologia
Frequência Cardíaca/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Quimiorreceptoras/efeitos dos fármacos
Conexinas/genética
Fenômenos Eletrofisiológicos
Feminino
Masculino
Camundongos
Camundongos Knockout
Cianeto de Sódio/farmacologia
Sistema Nervoso Simpático/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexins); 0 (connexin 36); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600919RR


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[PMID]:28110076
[Au] Autor:Takagi S; Kono Y; Nagase M; Mochio S; Kato F
[Ad] Endereço:Department of Neurology, The Jikei University School of Medicine, Japan; Department of Neuroscience, The Jikei University School of Medicine, Japan.
[Ti] Título:Facilitation of distinct inhibitory synaptic inputs by chemical anoxia in neurons in the oculomotor, facial and hypoglossal motor nuclei of the rat.
[So] Source:Exp Neurol;290:95-105, 2017 Apr.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective loss of motor neurons in the brainstem and spinal cord. Clinical studies have indicated that there is a distinct region-dependent difference in the vulnerability of motor neurons. For example, the motor neurons in the facial and hypoglossal nuclei are more susceptible to neuronal death than those in the oculomotor nucleus. To understand the mechanism underlying the differential susceptibility to cell death of the neurons in different motor nuclei, we compared the effects of chemical anoxia on the membrane currents and postsynaptic currents in different motor nuclei. The membrane currents were recorded from neurons in the oculomotor, facial and hypoglossal nuclei in brain slices of juvenile Wistar rats by using whole-cell recording in the presence of tetrodotoxin that prevents action potential-dependent synaptic transmission. NaCN consistently induced an inward current and a significant increase in the frequency of spontaneous synaptic inputs in neurons from these three nuclei. However, this increase in the synaptic input frequency was abolished by strychnine, a glycine receptor antagonist, but not by picrotoxin in neurons from the hypoglossal and facial nuclei, whereas that in neurons from the oculomotor nucleus was abolished by picrotoxin, but not by strychnine. Blocking ionotropic glutamate receptors did not significantly affect the NaCN-induced release facilitation in any of the three motor nuclei. These results suggest that anoxia selectively facilitates glycine release in the hypoglossal and facial nuclei and GABA release in the oculomotor nucleus. The region-dependent differences in the neurotransmitters involved in the anoxia-triggered release facilitation might provide a basis for the selective vulnerability of motor neurons in the neurodegeneration associated with ALS.
[Mh] Termos MeSH primário: Nervo Facial/patologia
Nervo Hipoglosso/patologia
Hipóxia/induzido quimicamente
Hipóxia/patologia
Neurônios/patologia
Nervo Oculomotor/patologia
Sinapses/patologia
[Mh] Termos MeSH secundário: Esclerose Amiotrófica Lateral/patologia
Animais
Morte Celular/efeitos dos fármacos
Modelos Animais de Doenças
Técnicas de Patch-Clamp
Ratos
Ratos Wistar
Cianeto de Sódio
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170123
[St] Status:MEDLINE


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[PMID]:28013061
[Au] Autor:Wang J; Hogan JO; Kim D
[Ad] Endereço:Department of Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL 60064, USA.
[Ti] Título:Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells.
[So] Source:Respir Physiol Neurobiol;237:13-21, 2017 Mar.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:A recent study showed that hypoxia activates a Ca -sensitive, Na -permeable non-selective cation channel (NSC) in carotid body glomus cells. We studied the effects of mitochondrial inhibitors that increase Ca influx via Ca channel (Ca ), and receptor agonists that release Ca from endoplasmic reticulum (ER) on NSC. Mitochondrial inhibitors (NaCN, FCCP, H S, NO) elevated [Ca ] and activated NSC. Angiotensin II and acetylcholine that elevate [Ca ] via the Gq-IP pathway activated NSC. However, endothelin-1 (Gq) and 5-HT (Gq) showed little or no effect on [Ca ] and did not activate NSC. Adenosine (Gs) caused a weak rise in [Ca ] but did not activate NSC. Dopamine (Gs) and γ-aminobytyric acid (Gi) were ineffective in raising [Ca ] and failed to activate NSC. Store-operated Ca entry (SOCE) produced by depletion of Ca stores with cyclopiazonic acid activated NSC. Our results show that Ca entry via Ca , ER Ca release and SOCE can activate NSC. Thus, NSC contributes to both voltage- and receptor-mediated excitation of glomus cells.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Corpo Carotídeo/citologia
Células Quimiorreceptoras/fisiologia
Canais Iônicos/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Angiotensina II/farmacologia
Anilidas/farmacologia
Animais
Animais Recém-Nascidos
Cafeína/farmacologia
Cálcio/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Carbonil Cianeto p-Trifluormetoxifenil Hidrazona/farmacologia
Células Quimiorreceptoras/efeitos dos fármacos
Relação Dose-Resposta a Droga
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/metabolismo
Inibidores Enzimáticos/farmacologia
Hipóxia/fisiopatologia
Ionóforos de Próton/farmacologia
Ratos
Ratos Sprague-Dawley
S-Nitroso-N-Acetilpenicilamina/farmacologia
Cianeto de Sódio/farmacologia
Tiadiazóis/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-methyl-4'-(3,5-bis(trifluoromethyl)-1H-pyrazol-1-yl)-1,2,3-thiadiazole-5-carboxanilide); 0 (Anilides); 0 (Calcium Channel Blockers); 0 (Enzyme Inhibitors); 0 (Ion Channels); 0 (Proton Ionophores); 0 (Thiadiazoles); 11128-99-7 (Angiotensin II); 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone); 3G6A5W338E (Caffeine); 79032-48-7 (S-Nitroso-N-Acetylpenicillamine); O5DDB9Z95G (Sodium Cyanide); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161226
[St] Status:MEDLINE


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[PMID]:27611087
[Au] Autor:Naseri NN; Bonica J; Xu H; Park LC; Arjomand J; Chen Z; Gibson GE
[Ad] Endereço:Weill Cornell Medical College, Brain and Mind Research Institute, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605, United States of America.
[Ti] Título:Novel Metabolic Abnormalities in the Tricarboxylic Acid Cycle in Peripheral Cells From Huntington's Disease Patients.
[So] Source:PLoS One;11(9):e0160384, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic dysfunction is well-documented in Huntington's disease (HD). However, the link between the mutant huntingtin (mHTT) gene and the pathology is unknown. The tricarboxylic acid (TCA) cycle is the main metabolic pathway for the production of NADH for conversion to ATP via the electron transport chain (ETC). The objective of this study was to test for differences in enzyme activities, mRNAs and protein levels related to the TCA cycle between lymphoblasts from healthy subjects and from patients with HD. The experiments utilize the advantages of lymphoblasts to reveal new insights about HD. The large quantity of homogeneous cell populations permits multiple dynamic measures to be made on exactly comparable tissues. The activities of nine enzymes related to the TCA cycle and the expression of twenty-nine mRNAs encoding for these enzymes and enzyme complexes were measured. Cells were studied under baseline conditions and during metabolic stress. The results support our recent findings that the activities of the pyruvate dehydrogenase complex (PDHC) and succinate dehydrogenase (SDH) are elevated in HD. The data also show a large unexpected depression in MDH activities. Furthermore, message levels for isocitrate dehydrogenase 1 (IDH1) were markedly increased in in HD lymphoblasts and were responsive to treatments. The use of lymphoblasts allowed us to clarify that the reported decrease in aconitase activity in HD autopsy brains is likely due to secondary hypoxic effects. These results demonstrate the mRNA and enzymes of the TCA cycle are critical therapeutic targets that have been understudied in HD.
[Mh] Termos MeSH primário: Ciclo do Ácido Cítrico
Metabolismo Energético
Doença de Huntington/metabolismo
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Morte Celular/efeitos dos fármacos
Morte Celular/genética
Linhagem Celular
Feminino
Expressão Gênica
Regulação Enzimológica da Expressão Gênica
Seres Humanos
Doença de Huntington/genética
Masculino
Meia-Idade
Mitocôndrias/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/genética
Complexo Piruvato Desidrogenase/genética
Complexo Piruvato Desidrogenase/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Cianeto de Sódio/farmacologia
Estresse Fisiológico
Repetições de Trinucleotídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyruvate Dehydrogenase Complex); 0 (RNA, Messenger); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0160384


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[PMID]:27506577
[Au] Autor:Kanda H; Kaneda T; Kato A; Yogo T; Harada Y; Hara Y; Urakawa N; Shimizu K
[Ad] Endereço:Laboratory of Veterinary Pharmacology, Nippon Veterinary and Life Science University, Kyonan-cho 1-chome, Musashino, Tokyo 180-862 Japan.
[Ti] Título:Aerobic metabolism on muscle contraction in porcine iris sphincter.
[So] Source:J Vet Med Sci;78(11):1673-1676, 2016 Dec 01.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Eyes are supplied O through the cornea and vessels of the retina and iris, which are tissues characterized by aerobic metabolism. Meanwhile, there are no reports on the association between iris sphincter contraction and aerobic metabolism. In this paper, we studied the aforementioned association. Eyes from adult pigs of either sex were obtained from a local abattoir. A muscle strip was connected to a transducer to isometrically record the tension. O consumption was measured using a Clark-type polarograph connected to a biological oxygen monitor. Creatine phosphate (PCr) and adenosine triphosphate (ATP) contents were measured in the muscle strips by high-performance liquid chromatography (HPLC). Iris sphincter muscles were measured in resting, contractile or hypoxic phases. Contraction was induced by hyperosmotic 65 mM KCl (H-65K ) or carbachol (CCh), and hypoxia was induced by aeration with N instead of O or by addition of sodium cyanide (NaCN). H-65K - and CCh-induced muscle contraction, involved increasing O consumption. Hypoxia and NaCN significantly decreased H-65K - and CCh-induced muscle contraction and/or O consumption and PCr contents. Our results suggest that the contractile behavior in porcine iris sphincter highly depends on mitogen oxidative metabolism.
[Mh] Termos MeSH primário: Iris/metabolismo
Músculo Liso/metabolismo
Consumo de Oxigênio/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Carbacol/farmacologia
Hipóxia Celular
Feminino
Iris/efeitos dos fármacos
Masculino
Contração Muscular/efeitos dos fármacos
Contração Muscular/fisiologia
Músculo Liso/efeitos dos fármacos
Fosfocreatina/metabolismo
Cloreto de Potássio/farmacologia
Cianeto de Sódio/farmacologia
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
020IUV4N33 (Phosphocreatine); 660YQ98I10 (Potassium Chloride); 8L70Q75FXE (Adenosine Triphosphate); 8Y164V895Y (Carbachol); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160811
[St] Status:MEDLINE


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[PMID]:26840837
[Au] Autor:Dhingra RR; Dutschmann M; Dick TE
[Ad] Endereço:Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, USA; Department of Neurosciences, Case Western Reserve University, Cleveland, OH, USA.
[Ti] Título:Blockade of dorsolateral pontine 5HT1A receptors destabilizes the respiratory rhythm in C57BL6/J wild-type mice.
[So] Source:Respir Physiol Neurobiol;226:110-4, 2016 Jun.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The neurotransmitter serotonin (5HT) acting via 5HT1a receptors (5HT1aR) is a potent determinant of respiratory rhythm variability. Here, we address the 5HT1aR-dependent control of respiratory rhythm variability in C57BL6/J mice. Using the in situ perfused preparation, we compared the effects of systemic versus focal blockade of 5HT1aRs. Blocking 5HT1aRs in the Kölliker-Fuse nucleus (KFn) increased the occurrence of spontaneous apneas and accounted for the systemic effects of 5HT1aR antagonists. Further, 5HT1aRs of the KFn stabilized the respiratory rhythm's response to arterial chemoreflex perturbations; reducing the recovering time, e.g., the latency to return to the baseline pattern. Together, these results suggest that the KFn regulates both intrinsic and sensory determinants of respiratory rhythm variability.
[Mh] Termos MeSH primário: Cicloexanos/farmacologia
Núcleo de Kölliker-Fuse/efeitos dos fármacos
Núcleo de Kölliker-Fuse/metabolismo
Piperazinas/farmacologia
Receptor 5-HT1A de Serotonina/metabolismo
Respiração/efeitos dos fármacos
Antagonistas do Receptor 5-HT1 de Serotonina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apneia/induzido quimicamente
Apneia/metabolismo
Células Quimiorreceptoras/efeitos dos fármacos
Células Quimiorreceptoras/fisiologia
Feminino
Potenciais da Membrana/efeitos dos fármacos
Camundongos da Linhagem 129
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Fármacos do Sistema Nervoso Periférico/farmacologia
Nervo Frênico/efeitos dos fármacos
Nervo Frênico/fisiologia
Reflexo/efeitos dos fármacos
Reflexo/fisiologia
Cianeto de Sódio/farmacologia
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclohexanes); 0 (Peripheral Nervous System Agents); 0 (Piperazines); 0 (Serotonin 5-HT1 Receptor Antagonists); 0 (WAY 101363); 112692-38-3 (Receptor, Serotonin, 5-HT1A); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160204
[St] Status:MEDLINE


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[PMID]:26335525
[Au] Autor:David M; Kartheek RM
[Ad] Endereço:Environmental Toxicology and Molecular Biology Laboratory, Department of PG Studies and Research in Zoology, Karnatak University, Dharwad, 580003, India. mdavid.kud@gmail.com.
[Ti] Título:In vivo studies on hepato-renal impairments in freshwater fish Cyprinus carpio following exposure to sublethal concentrations of sodium cyanide.
[So] Source:Environ Sci Pollut Res Int;23(1):722-33, 2016 Jan.
[Is] ISSN:1614-7499
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Reactive oxygen species is an inevitable composite of aerobic systems that could channelize their lethality by imparting oxidative stress under a stressful environment. Cyanide is an important environmental toxicant that could be responsible in the resulting detrimental health issues of aquatic fauna. The present effort investigates the possibilities of hepato-renal damage in freshwater fish Cyprinus carpio following exposure to sublethal concentrations of sodium cyanide (NaCN). Fish were exposed to 0.1 mg/L of NaCN for 10 days (E1) and 20 days (E2) and were further subjected to recovery for 14 days (R) in NaCN-free medium. Liver tissue exhibited a significant decline in activity of catalase, superoxide dismutase, glutathione peroxidase, and glutathione S-transferase enzymes in exposed fish, unlike in control (C). Subsequent levels of lipid peroxidation elevation at 'E1' and 'E2' suggested oxidative damage to hepatocytes. This was further confirmed through a histopathological evaluation which indicated important findings like lymphocytic infiltration and necrosis in liver and tubular and glomerular degeneration in renal organ. The investigation suggests biochemical and histopathological alterations in fish following exposure to NaCN. Nevertheless, fish upon the recovery period were known to exhibit incomplete recuperation which was indicated by partial restoration tendencies under biochemical and histopathological factions. The study clearly implicated the role of NaCN in emphasizing its toxicity to C. carpio, further suggesting lack of recovery transition at a limited tenure of 14 days. The study might contribute in the course of regulatory surveillance and monitoring of aquatic bodies and may also reflect the possibilities of NaCN contamination during aquaculture practices. Graphical Abstract á…Ÿ.
[Mh] Termos MeSH primário: Carpas
Rim/efeitos dos fármacos
Fígado/efeitos dos fármacos
Cianeto de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Carpas/metabolismo
Catalase/metabolismo
Água Doce
Glutationa Peroxidase/metabolismo
Glutationa Transferase/metabolismo
Rim/metabolismo
Rim/fisiopatologia
Peroxidação de Lipídeos
Fígado/metabolismo
Fígado/fisiopatologia
Oxirredução
Estresse Oxidativo
Espécies Reativas de Oxigênio/metabolismo
Silimarina
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Reactive Oxygen Species); 0 (Silymarin); 4RKY41TBTF (silybin); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); EC 2.5.1.18 (Glutathione Transferase); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150904
[St] Status:MEDLINE
[do] DOI:10.1007/s11356-015-5286-9


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[PMID]:26254869
[Au] Autor:Bautista TG; Dutschmann M
[Ad] Endereço:Systems Neurophysiology division, Florey Institute of Neuroscience and Mental Health, Gate 11 Royal Parade, University of Melbourne, VIC 3010, Australia. Electronic address: tara.bautista@florey.edu.au.
[Ti] Título:The role of the Kölliker-Fuse nuclei in the determination of abdominal motor output in a perfused brainstem preparation of juvenile rat.
[So] Source:Respir Physiol Neurobiol;226:102-9, 2016 Jun.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The abdominal muscles are largely quiescent during normal breathing but may exhibit tonic activity or subtle respiratory modulation. The origin of baseline abdominal motor nerve activity (AbNA) if present remains uncharacterised. The contribution of the Kölliker-Fuse nucleus (KF) in the dorsolateral pons in the patterning and amplitude of AbNA was investigated using in situ perfused brainstem preparations of juvenile rats (n=12). Two types of AbNA were observed: Type I - expiratory-modulated (n=7), and Type II - weakly inspiratory/post-inspiratory-modulated (n=5). Despite this, all preparations exhibited the same bi-phasic late expiratory/postinspiratory bursts upon elicitation of the peripheral chemoreflex. Interestingly, the type of AbNA exhibited correlated with postinspiratory duration. Targeted microinjections of GABA-A receptor agonist isoguvacine (10mM; 70nl) into KF however did not significantly modify pattern or amplitude of baseline AbNA in either Type besides the selective abolition of the postinspiratory phase and, consequently, postinspiratory modulation in AbNAwhen present. In sum, the KF is not a major contributorin setting baseline abdominal motor output.
[Mh] Termos MeSH primário: Abdome/fisiologia
Núcleo de Kölliker-Fuse/fisiologia
Movimento/fisiologia
Respiração
[Mh] Termos MeSH secundário: Abdome/inervação
Animais
Animais Recém-Nascidos
Geradores de Padrão Central/efeitos dos fármacos
Geradores de Padrão Central/fisiologia
Células Quimiorreceptoras/efeitos dos fármacos
Células Quimiorreceptoras/fisiologia
Agonistas de Receptores de GABA-A/farmacologia
Ácidos Isonicotínicos/farmacologia
Núcleo de Kölliker-Fuse/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Fármacos do Sistema Nervoso Periférico/farmacologia
Nervo Frênico/fisiologia
Ratos Sprague-Dawley
Receptores de GABA-A/metabolismo
Respiração/efeitos dos fármacos
Músculos Respiratórios/fisiologia
Cianeto de Sódio/farmacologia
Taquipneia/fisiopatologia
Técnicas de Cultura de Tecidos
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Agonists); 0 (Isonicotinic Acids); 0 (Peripheral Nervous System Agents); 0 (Receptors, GABA-A); O5DDB9Z95G (Sodium Cyanide); YTF580771Y (isoguvacine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150810
[St] Status:MEDLINE


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[PMID]:26501107
[Au] Autor:Kishi S; Campanholle G; Gohil VM; Perocchi F; Brooks CR; Morizane R; Sabbisetti V; Ichimura T; Mootha VK; Bonventre JV
[Ad] Endereço:Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:Meclizine Preconditioning Protects the Kidney Against Ischemia-Reperfusion Injury.
[So] Source:EBioMedicine;2(9):1090-101, 2015 Sep.
[Is] ISSN:2352-3964
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a 'nutrient-sensitized' chemical screen. Pretreatment with 100 mg/kg of meclizine, 17 h prior to ischemia protected mice from IRI. Serum creatinine levels at 24 h after IRI were 0.13 ± 0.06 mg/dl (sham, n = 3), 1.59 ± 0.10 mg/dl (vehicle, n = 8) and 0.89 ± 0.11 mg/dl (meclizine, n = 8). Kidney injury was significantly decreased in meclizine treated mice compared with vehicle group (p < 0.001). Protection was also seen when meclizine was administered 24 h prior to ischemia. Meclizine reduced inflammation, mitochondrial oxygen consumption, oxidative stress, mitochondrial fragmentation, and tubular injury. Meclizine preconditioned kidney tubular epithelial cells, exposed to blockade of glycolytic and oxidative metabolism with 2-deoxyglucose and NaCN, had reduced LDH and cytochrome c release. Meclizine upregulated glycolysis in glucose-containing media and reduced cellular ATP levels in galactose-containing media. Meclizine inhibited the Kennedy pathway and caused rapid accumulation of phosphoethanolamine. Phosphoethanolamine recapitulated meclizine-induced protection both in vitro and in vivo.
[Mh] Termos MeSH primário: Precondicionamento Isquêmico
Rim/irrigação sanguínea
Rim/patologia
Meclizina/uso terapêutico
Substâncias Protetoras/uso terapêutico
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/complicações
Lesão Renal Aguda/tratamento farmacológico
Lesão Renal Aguda/patologia
Trifosfato de Adenosina/metabolismo
Animais
Respiração Celular/efeitos dos fármacos
Citocromos c/metabolismo
Desoxiglucose/farmacologia
Modelos Animais de Doenças
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/patologia
Etanolaminas/metabolismo
Galactose/farmacologia
Glicólise/efeitos dos fármacos
Seres Humanos
Inflamação/complicações
Inflamação/patologia
Rim/efeitos dos fármacos
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/metabolismo
Túbulos Renais/patologia
L-Lactato Desidrogenase/metabolismo
Células LLC-PK1
Masculino
Meclizina/farmacologia
Meclizina/toxicidade
Camundongos Endogâmicos C57BL
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/ultraestrutura
Substâncias Protetoras/farmacologia
Traumatismo por Reperfusão/complicações
Traumatismo por Reperfusão/patologia
Cianeto de Sódio/farmacologia
Suínos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ethanolamines); 0 (Protective Agents); 3L5TQ84570 (Meclizine); 78A2BX7AEU (phosphorylethanolamine); 8L70Q75FXE (Adenosine Triphosphate); 9007-43-6 (Cytochromes c); 9G2MP84A8W (Deoxyglucose); EC 1.1.1.27 (L-Lactate Dehydrogenase); O5DDB9Z95G (Sodium Cyanide); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170615
[Lr] Data última revisão:
170615
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151027
[St] Status:MEDLINE
[do] DOI:10.1016/j.ebiom.2015.07.035



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