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[PMID]:28250271
[Au] Autor:Ishida K; Kotake Y; Sanoh S; Ohta S
[Ad] Endereço:Graduate School of Biomedical and Health Sciences, Hiroshima University.
[Ti] Título:Lead-Induced ERK Activation Is Mediated by GluR2 Non-containing AMPA Receptor in Cortical Neurons.
[So] Source:Biol Pharm Bull;40(3):303-309, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Lead is a persistent environmental pollutant and exposure to high environmental levels causes various deleterious toxicities, especially to the central nervous system (CNS). The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor that is devoid of the glutamate receptor 2 (GluR2) subunit is Ca -permeable, which increases the neuronal vulnerability to excitotoxicity. We have previously reported that long-term exposure of rat cortical neurons to lead acetate induces decrease of GluR2 expression. However, it is not clarified whether lead-induced GluR2 decrease is involved in neurotoxicity. Therefore, we investigated the contribution of GluR2 non-containing AMPA receptor to lead-induced neurotoxic events. Although the expression of four AMPA receptor subunits (GluR1, GluR2, GluR3, and GluR4) was decreased by lead exposure, the decrease in GluR2 expression was remarkable among four subunits. Lead-induced neuronal cell death was rescued by three glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, a non-selective AMPA receptor blocker), MK-801 (N-methyl-D-aspartate (NMDA) receptor blocker), and 1-naphthyl acetyl spermine (NAS, a specific Ca -permeable AMPA receptor blocker). Lead exposure activated extracellular signal-regulated protein kinase (ERK) 1/2, which was significantly ameliorated by CNQX. In addition, lead exposure activated p38 mitogen-activated protein kinase (MAPK p38), and protein kinase C (PKC), which was partially ameliorated by CNQX. Our findings indicate that Ca -permeable AMPA receptors resulting from GluR2 decrease may be involved in lead-induced neurotoxicity.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Ácido Glutâmico/metabolismo
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Chumbo/efeitos adversos
Receptores de AMPA/metabolismo
Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiônico/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Encéfalo/citologia
Cálcio/metabolismo
Células Cultivadas
Poluentes Ambientais/efeitos adversos
Antagonistas de Aminoácidos Excitatórios/farmacologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Proteína Quinase C/metabolismo
Subunidades Proteicas
Ratos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Excitatory Amino Acid Antagonists); 0 (Protein Subunits); 0 (Receptors, AMPA); 0 (glutamate receptor ionotropic, AMPA 2); 2P299V784P (Lead); 3KX376GY7L (Glutamic Acid); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 77521-29-0 (alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid); EC 2.7.11.13 (Protein Kinase C); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00784


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Vassallo, Dalton Valentim
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[PMID]:27272938
[Au] Autor:Simões MR; Preti SC; Azevedo BF; Fiorim J; Freire DD; Covre EP; Vassallo DV; Dos Santos L
[Ad] Endereço:Department of Physiological Sciences, Federal University of Espirito Santo, Avenida Marechal Campos, 1468, Maruípe, Vitoria, ES, 29043-900, Brazil. yllars@hotmail.com.
[Ti] Título:Low-level Chronic Lead Exposure Impairs Neural Control of Blood Pressure and Heart Rate in Rats.
[So] Source:Cardiovasc Toxicol;17(2):190-199, 2017 Apr.
[Is] ISSN:1559-0259
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lead (Pb) induces adverse effects when it chronically accumulates in the body, including effects on the nervous and cardiovascular systems. Wistar rats were exposed to lead acetate for 30 days (first dose 4 µg/100 g followed by 0.05 µg/100 g/day, i.m.) to investigate the cardiovascular system impact on the autonomic control. The femoral artery and vein were catheterised to perform hemodynamic evaluations in awake rats: heart rate variability (HRV), baroreflex sensitivity, cardiopulmonary reflex and hemodynamic responses to vagal and sympathetic pharmacological blockade. Rats exposed to Pb exhibited a higher blood pressure and reduced HRV in the time domain when compared to the saline-injected group. Spectral analysis of the HRV in the frequency-domain showed an augmented low-frequency component of the spectrum. Methylatropine and atenolol administration suggest increased sympathetic tone and reduced vagal tone on the control of heart rate. Chronic Pb exposure decreased the sensitivity of the baroreflex without significantly changing the cardiopulmonary reflex. This study demonstrated for the first time in an animal model of a controlled, low-dose chronic lead exposure that cardiovascular changes, such as arterial hypertension, are accompanied by impaired autonomic control of the cardiovascular system, as characterised by reduced baroreflex sensitivity and a sympathovagal imbalance.
[Mh] Termos MeSH primário: Barorreflexo
Pressão Sanguínea
Sistema Cardiovascular/inervação
Frequência Cardíaca
Intoxicação do Sistema Nervoso por Chumbo/fisiopatologia
Compostos Organometálicos
Sistema Nervoso Simpático/fisiopatologia
Nervo Vago/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Intoxicação do Sistema Nervoso por Chumbo/etiologia
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Organometallic Compounds); RX077P88RY (lead acetate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160609
[St] Status:MEDLINE
[do] DOI:10.1007/s12012-016-9374-y


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[PMID]:27230353
[Au] Autor:Wu Y; Wang Y; Wang M; Sun N; Li C
[Ad] Endereço:1 Wuxi Medical School, Jiangnan University, Wuxi, China.
[Ti] Título:GRIN2A polymorphisms and expression levels are associated with lead-induced neurotoxicity.
[So] Source:Toxicol Ind Health;33(4):332-339, 2017 Apr.
[Is] ISSN:1477-0393
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lead acts as an antagonist of the N-methyl-d-aspartate receptor (NMDAR). GRIN2A encodes an important subunit of NMDARs and may be a critical factor in the mechanism of lead neurotoxicity. Changes in GRIN2A expression levels or gene variants may be mechanisms of lead-induced neurotoxicity. In this study, we hypothesized that GRIN2A might contribute to lead-induced neurotoxicity. A preliminary HEK293 cell experiment was performed to analyze the association between GRIN2A expression and lead exposure. In addition, in a population-based study, serum GRIN2A levels were measured in both lead-exposed and control populations. To detect further the influence of GRIN2A gene single nucleotide polymorphisms (SNPs) in lead-induced neurotoxicity, 3 tag SNPs (rs2650429, rs6497540, and rs9302415) were genotyped in a case-control study that included 399 lead-exposed subjects and 398 controls. Lead exposure decreased GRIN2A expression levels in HEK293 cells ( p < 0.001) compared with lead-free cells. Lead-exposed individuals had lower serum GRIN2A levels compared with controls ( p < 0.001), and we found a trend of decreasing GRIN2A level with an increase in blood lead level ( p < 0.001). In addition, we found a significant association between rs2650429 CT and TT genotypes and risk of lead poisoning compared with the rs2650429 CC genotype (adjusted odds ratio = 1.42, 95% confidence interval = 1.01-2.00]. Therefore, changes in GRIN2A expression levels and variants may be important mechanisms in the development of lead-induced neurotoxicity.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/efeitos dos fármacos
Predisposição Genética para Doença
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Chumbo/toxicidade
Doenças Profissionais/metabolismo
Polimorfismo de Nucleotídeo Único
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Adulto
Alelos
Estudos de Casos e Controles
China
Poluentes Ambientais/toxicidade
Feminino
Frequência do Gene
Estudos de Associação Genética
Células HEK293
Seres Humanos
Chumbo/sangue
Intoxicação do Sistema Nervoso por Chumbo/sangue
Intoxicação do Sistema Nervoso por Chumbo/genética
Masculino
Meia-Idade
Doenças Profissionais/sangue
Doenças Profissionais/genética
Exposição Ocupacional/efeitos adversos
RNA Mensageiro/metabolismo
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/sangue
Receptores de N-Metil-D-Aspartato/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (N-methyl D-aspartate receptor subtype 2A); 0 (RNA, Messenger); 0 (Receptors, N-Methyl-D-Aspartate); 2P299V784P (Lead)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160528
[St] Status:MEDLINE
[do] DOI:10.1177/0748233716647636


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[PMID]:27190262
[Au] Autor:Li N; Li X; Li L; Zhang P; Qiao M; Zhao Q; Song L; Yu Z
[Ad] Endereço:Food Science and Technology College, Henan Agriculture University, Zhengzhou 450002, China ln8028@163.com.
[Ti] Título:Original Research: The expression of MMP2 and MMP9 in the hippocampus and cerebral cortex of newborn mice under maternal lead exposure.
[So] Source:Exp Biol Med (Maywood);241(16):1811-8, 2016 Oct.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The current study focused on the MMP2 and MMP9 expression in cerebral cortex and hippocampus of newborn mice under maternal lead exposure. Lead exposure was initiated from gestation to weaning. Lead acetate was dissolved in deionized water with concentration of 0.1, 0.2, and 0.5% and was absorbed through daily drinking. On day 21 after birth, lead in blood and tissue levels was examined by Graphite Furnace Atomic Absorption Spectrum (GFAAS). The protein expressions of MMP2 and MMP9 in hippocampus and cerebral cortex tissues were tested by western blotting and immunohistochemistry. Compared to the control group, blood, cerebral cortex, and hippocampus lead levels of newborn mice in 0.1, 0.2, and 0.5% lead exposure groups were markedly high (P < 0.05), and mice within the 0.2 and 0.5% lead exposure groups performed much worse than that of the control group in Water Maze test (P < 0.05). Compared with the control group, MMP2 and MMP9 expressions in hippocampus were up-regulated in the lead exposure groups (P < 0.05), and the MMP2 and MMP9 expressions in cerebral cortex were also higher (P < 0.05). The increased expression of MMP2 and MMP9 in the hippocampus and cerebral cortex may lead to the neurotoxicity in the context of maternal lead exposure.
[Mh] Termos MeSH primário: Córtex Cerebral/química
Hipocampo/química
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Efeitos Tardios da Exposição Pré-Natal/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos/metabolismo
Western Blotting
Feminino
Masculino
Metaloproteinase 2 da Matriz/análise
Metaloproteinase 9 da Matriz/análise
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Gravidez
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160519
[St] Status:MEDLINE
[do] DOI:10.1177/1535370216647808


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[PMID]:26836461
[Au] Autor:Benammi H; El Hiba O; Gamrani H
[Ad] Endereço:Neurosciences, Pharmacology and Environment Unit, Department of Biology, Faculty of Sciences Semlalia, Cadi Ayyad University, Marrakesh, Morocco.
[Ti] Título:Evidence of a subcommissural organ involvement in the brain response to lead exposure and a modulatory potential of curcumin.
[So] Source:Neuroreport;27(4):264-71, 2016 Mar 02.
[Is] ISSN:1473-558X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Substantial evidence supports the neurochemical vulnerability to lead (Pb) as one of the most potent neurotoxic heavy metals. In the present study, we aimed to assess: (i) The subcommissural organ (SCO) responsiveness as a secretory circumventricular organ to chronic and acute Pb intoxication together with its serotoninergic innervation. (ii) The possible restorative effect of curcumin against Pb intoxication under the same pathological conditions. We used immunohistochemistry with antibodies against Reissner's fiber and serotonin [5-hydroxytryptophan (5-HT)] in Wistar rats following chronic as well as acute Pb administration, respectively, at 25 mg/kg intraperitoneally for 3 days and 0.3% in drinking water from the intrauterine stage until 2 months of adult age. Our data showed a significant decrease in Reissner's fiber material immunoreactivity concomitant with an overall increased 5-HT innervation of the SCO and the ventricular borders. Coadministration of curcumin (50 mg/kg body weight) restores this impairment by reversing the effect of chronic and acute Pb on the secretory activity and the 5-HTergic innervation of the SCO. The investigation showed, on the one hand, the involvement of the SCO in the response to heavy metals, especially Pb, and on the other, the beneficial corrector role of curcumin. As a part of the circumventricular organ, known as a privileged area of brain-blood exchanges, the SCO may play a key role in the mechanism of brain defense against heavy metal neurotoxicity in rats.
[Mh] Termos MeSH primário: Curcumina/farmacologia
Intoxicação do Sistema Nervoso por Chumbo/tratamento farmacológico
Intoxicação do Sistema Nervoso por Chumbo/patologia
Fármacos Neuroprotetores/farmacologia
Órgão Subcomissural/efeitos dos fármacos
Órgão Subcomissural/patologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Doença Crônica
Modelos Animais de Doenças
Feminino
Imuno-Histoquímica
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Masculino
Ratos Wistar
Serotonina/metabolismo
Órgão Subcomissural/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuroprotective Agents); 333DO1RDJY (Serotonin); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1097/WNR.0000000000000531


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[PMID]:26562488
[Au] Autor:Hu F; Ge MM; Chen WH
[Ad] Endereço:School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei, Anhui, 230009, People's Republic of China.
[Ti] Título:Effects of lead exposure on dendrite and spine development in hippocampal dentate gyrus areas of rats.
[So] Source:Synapse;70(3):87-97, 2016 Mar.
[Is] ISSN:1098-2396
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lead exposure has been implicated in the impairment of synaptic plasticity in the hippocampal dentate gyrus (DG) areas of rats. However, whether the degradation of physiological properties is based on the morphological alteration of granule neurons in DG areas remains elusive. Here, we examined the dendritic branch extension and spine formation of granule neurons after lead exposure during development in rats. Dendritic morphology was studied using Golgi-Cox stain method, which was followed by Sholl analysis at postnatal days 14 and 21. Our results indicated that, for both ages, lead exposure significantly decreased the total dendritic length and spine density of granule neurons in the DG of the rat hippocampus. Further branch order analysis revealed that the decrease of dendritic length was observed only at the second branch order. Moreover, there were obvious deficits in the proportion and size of mushroom-type spines. These deficits in spine formation and maturity were accompanied by a decrease in Arc/Arg3.1 expression. Our present findings are the first to show that developmental lead exposure disturbs branch and spine formation in hippocampal DG areas. Arc/Arg3.1 may have a critical role in the disruption of neuronal morphology and synaptic plasticity in lead-exposed rats.
[Mh] Termos MeSH primário: Dendritos/patologia
Giro Denteado/patologia
Intoxicação do Sistema Nervoso por Chumbo/patologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Proteínas do Citoesqueleto/metabolismo
Dendritos/efeitos dos fármacos
Dendritos/fisiologia
Giro Denteado/efeitos dos fármacos
Giro Denteado/crescimento & desenvolvimento
Giro Denteado/fisiopatologia
Modelos Animais de Doenças
Chumbo/toxicidade
Intoxicação do Sistema Nervoso por Chumbo/fisiopatologia
Proteínas do Tecido Nervoso/metabolismo
Plasticidade Neuronal/efeitos dos fármacos
Plasticidade Neuronal/fisiologia
Distribuição Aleatória
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Sinapses/efeitos dos fármacos
Sinapses/patologia
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (Nerve Tissue Proteins); 0 (activity regulated cytoskeletal-associated protein); 2P299V784P (Lead)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151113
[St] Status:MEDLINE
[do] DOI:10.1002/syn.21873


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[PMID]:26435406
[Au] Autor:Abdulmajeed WI; Sulieman HB; Zubayr MO; Imam A; Amin A; Biliaminu SA; Oyewole LA; Owoyele BV
[Ad] Endereço:Department of Physiology Faculty of Basic Medical Sciences, University of Ilorin, Ilorin, Nigeria. abdulmajeed.w@unilorin.edu.ng.
[Ti] Título:Honey prevents neurobehavioural deficit and oxidative stress induced by lead acetate exposure in male Wistar rats- a preliminary study.
[So] Source:Metab Brain Dis;31(1):37-44, 2016 Feb.
[Is] ISSN:1573-7365
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This research sought to investigate the possible neuroprotective effects of honey against lead (Pb)-induced neurotoxicity. Twenty four male Wistar rats were divided into four groups: Control group that received 1 ml/kg distilled orally for 28 days; while groups II-IV received 0.2% lead in drinking water and 1 ml/kg of distilled water, 1 ml/kg of honey, 1.5 ml/kg of honey respectively for 28 days. Anxiety and exploratory activities were determined in the open field test. Memory function was determined using Morris water maze after which the animals were sacrificed. The brains were then excised, homogenized and Lipid peroxidation (MDA), Superoxide dismutase (SOD), Catalase, Glutathione (GSH) and Glutathione -S- Transferase (GST) activities were determined in the brains. Results showed that lead exposure causes decrease in locomotor and exploratory activities; increase anxiety, memory impairment, lipid peroxidation and decrease antioxidant activities. However, co-administration of honey with lead inhibited neurotoxicity as indicated by the improvement in memory function as evidenced by decreased latency period and increased in time spent in target quadrant in honey-fed rats compared to the lead-exposed animals. Furthermore, honey increased locomotion, exploration and decreased anxiety in lead-exposed rats as indicated by the frequency of rearing, freezing duration and the number of line crossed by animals. Also administration of honey improves antioxidant activities as shown by increased brain SOD, GST and GSH activities compared to the lead-treated groups but no significant effect on MDA level. It can be concluded that honey has neuroprotective effects against lead-induced cognitive deficit probably by enhancing antioxidant activities.
[Mh] Termos MeSH primário: Mel
Intoxicação do Sistema Nervoso por Chumbo/prevenção & controle
Intoxicação do Sistema Nervoso por Chumbo/psicologia
Compostos Organometálicos/toxicidade
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Comportamento Animal/efeitos dos fármacos
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Transtornos da Memória/induzido quimicamente
Transtornos da Memória/psicologia
Atividade Motora/efeitos dos fármacos
Proteínas do Tecido Nervoso/metabolismo
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Nerve Tissue Proteins); 0 (Organometallic Compounds); RX077P88RY (lead acetate)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151006
[St] Status:MEDLINE
[do] DOI:10.1007/s11011-015-9733-6


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[PMID]:26005885
[Au] Autor:Singh PK; Nath R; Ahmad MK; Rawat A; Babu S; Dixit RK
[Ad] Endereço:a Department of Pharmacology and Therapeutics , King George's Medical University , Lucknow 226003 , India.
[Ti] Título:Attenuation of lead neurotoxicity by supplementation of polyunsaturated fatty acid in Wistar rats.
[So] Source:Nutr Neurosci;19(9):396-405, 2016 Nov.
[Is] ISSN:1476-8305
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Among various types of polyunsaturated fatty acid (PUFA), omega-3 fatty acids play a crucial role in development and function of the brain. This study was undertaken to investigate the possible neuroprotective efficacy of omega-3 fatty acid on lead-induced neurotoxicity in rats. MATERIAL AND METHODS: The experiment was carried out on 32 male Wistar rats divided into four groups. The first group (control) was treated with distilled water and second group with lead acetate at the doses of 3 mg/kg b.wt. (body weight)/oral, whereas third and fourth groups were simultaneously treated with lead acetate (3 mg/kg b.wt.) plus omega-3 fatty acid (300 mg/kg b.wt./oral) and lead acetate (3 mg/kg b.wt.) plus vitamin E (100 mg/kg b.wt./oral), respectively, for a period of 90 days. Their biochemical and histopathological investigations have been carried out. RESULTS: The level of lead was markedly elevated in brain (4.71-fold) and blood (5.65-fold), also increased levels of ROS, GSH, LPO with concomitant reduction in the activities of delta-ALAD, CAT, SOD, and GPx. In addition, lead-induced brain damage was indicated by histopathological changes. Omega-3 fatty acid resulted in marked improvement in most of the biochemical parameters as well as histopathological changes in rats. The results obtained were compared with vitamin E as the standard antioxidant agents. DISCUSSION: Omega-3 fatty acid significantly (P < 0.05) decreased the effect of lead-induced brain damage as well as biochemical changes similar to that of standard drug, vitamin E. So, our result suggested that omega-3 fatty acid may play a protective role in lead-induced neurotoxicity and associated human health risk.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Suplementos Nutricionais
Ácidos Graxos Ômega-3/uso terapêutico
Intoxicação do Sistema Nervoso por Chumbo/prevenção & controle
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/uso terapêutico
Biomarcadores/sangue
Biomarcadores/metabolismo
Barreira Hematoencefálica
Encéfalo/metabolismo
Encéfalo/patologia
Óleos de Peixe/uso terapêutico
Chumbo/sangue
Chumbo/metabolismo
Chumbo/toxicidade
Intoxicação do Sistema Nervoso por Chumbo/sangue
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Intoxicação do Sistema Nervoso por Chumbo/patologia
Masculino
Neurônios/metabolismo
Neurônios/patologia
Compostos Organometálicos/administração & dosagem
Distribuição Aleatória
Ratos Wistar
Distribuição Tecidual
Toxicocinética
Vitamina E/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (Fatty Acids, Omega-3); 0 (Fish Oils); 0 (Neuroprotective Agents); 0 (Organometallic Compounds); 1406-18-4 (Vitamin E); 2P299V784P (Lead); RX077P88RY (lead acetate)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150526
[St] Status:MEDLINE


  9 / 124 MEDLINE  
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[PMID]:26363853
[Au] Autor:Dabrowska A; Venero JL; Iwasawa R; Hankir MK; Rahman S; Boobis A; Hajji N
[Ad] Endereço:Imperial College London, Centre for Pharmacology and Therapeutics, Department of Medicine, London, United Kingdom.
[Ti] Título:PGC-1α controls mitochondrial biogenesis and dynamics in lead-induced neurotoxicity.
[So] Source:Aging (Albany NY);7(9):629-47, 2015 Sep.
[Is] ISSN:1945-4589
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Due to its role in regulation of mitochondrial function, PGC1α is emerging as an important player in ageing and neurodegenerative disorders. PGC1α exerts its neuroprotective effects by promoting mitochondrial biogenesis (MB) and functioning. However, the precise regulatory role of PGC1α in the control of mitochondrial dynamics (MD) and neurotoxicity is still unknown. Here we elucidate the role of PGC1αin vitro and in vivo in the regulatory context of MB and MD in response to lead (II) acetate as a relevant model of neurotoxicity. We show that there is an adaptive response (AR) to lead, orchestrated by the BAP31-calcium signalling system operating between the ER and mitochondria. We find that this hormetic response is controlled by a cell-tolerated increase of PGC1α expression, which in turn induces a balanced expression of fusion/fission genes by binding to their promoters and implying its direct role in regulation of MD. However, dysregulation of PGC1α expression through either stable downregulation or overexpression, renders cells more susceptible to lead insult leading to mitochondrial fragmentation and cell death. Our data provide novel evidence that PGC1α expression is a key regulator of MD and the maintenance of tolerated PGC1α expression may offer a promising strategy for neuroprotective therapies.
[Mh] Termos MeSH primário: Intoxicação do Sistema Nervoso por Chumbo/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Envelhecimento/genética
Animais
Apoptose/efeitos dos fármacos
Morte Celular/efeitos dos fármacos
Linhagem Celular
Neurônios Dopaminérgicos/efeitos dos fármacos
Retículo Endoplasmático/efeitos dos fármacos
Intoxicação do Sistema Nervoso por Chumbo/fisiopatologia
Proteínas de Membrana/genética
Dinâmica Mitocondrial/genética
Fármacos Neuroprotetores/farmacologia
Biogênese de Organelas
Compostos Organometálicos/toxicidade
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo
Ratos
Transdução de Sinais/efeitos dos fármacos
Fatores de Transcrição/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BAP31 protein, rat); 0 (Membrane Proteins); 0 (Neuroprotective Agents); 0 (Organometallic Compounds); 0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Transcription Factors); RX077P88RY (lead acetate)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150914
[St] Status:MEDLINE


  10 / 124 MEDLINE  
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[PMID]:25845299
[Au] Autor:Venkareddy LK; Muralidhara
[Ad] Endereço:Department of Biochemistry and Nutrition, CSIR-Central Food Technological Research Institute (CFTRI), Mysore 570020, India.
[Ti] Título:Potential of casein as a nutrient intervention to alleviate lead (Pb) acetate-mediated oxidative stress and neurotoxicity: First evidence in Drosophila melanogaster.
[So] Source:Neurotoxicology;48:142-51, 2015 May.
[Is] ISSN:1872-9711
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Understanding the interaction between dietary protein deficits and neurotoxicants such as lead (Pb) is critical since oxidative stress is a common denominator under such conditions. The Drosophila system is an extensively used model to investigate the interaction between nutrients and environmental toxicants. Accordingly, we have examined the hypothesis that casein (CSN) enrichment has the propensity to attenuate Pb-associated phenotype, oxidative stress and neurotoxicity in Drosophila melanogaster. Exposure of young (2-3 d) and adult flies (10-12 d old) to Pb acetate (0-20 mM, 7 d) in the medium resulted in a concentration dependent mortality and the survivors exhibited a hyperactive phenotype. While males showed higher susceptibility to Pb among both age groups, young flies were relatively more susceptible than adults. Pb exposure (5-10 mM, 5 d) among young flies caused robust oxidative stress as evidenced by markedly elevated levels of reactive oxygen species with concomitant perturbations in the activities of antioxidant enzymes (diminished SOD and elevated thioredoxin reductase) and altered redox state. Further, Pb caused significant elevation in the activity of acetylcholinesterase and dopamine levels. In a satellite study, we assessed the modulatory effect of CSN-enriched diet (1-2%) on Pb intoxication in terms of lethality, hyperactivity, oxidative stress and neurotoxicity. CSN markedly offset Pb-induced lethality and diminished the hyperactivity response. While CSN enrichment among Pb (5 mM) treated flies caused further elevation in ROS levels and thioredoxin reductase activity, the SOD levels were restored to normalcy. Further, CSN improved the activity levels of complex I-III and restored the dopamine levels. Our data suggest that Pb-induced toxicity in the Drosophila system may be predominantly mediated through oxidative stress mechanisms and the propensity of casein-enriched diet to abrogate such responses. Hence, we propose that enrichment of diet with protein such as casein may be a useful approach to alleviate Pb associated adverse effects in children.
[Mh] Termos MeSH primário: Caseínas/administração & dosagem
Dieta
Drosophila melanogaster/efeitos dos fármacos
Intoxicação do Sistema Nervoso por Chumbo/prevenção & controle
Sistema Nervoso/efeitos dos fármacos
Compostos Organometálicos/toxicidade
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Fatores Etários
Animais
Antioxidantes/metabolismo
Comportamento Animal/efeitos dos fármacos
Biomarcadores/metabolismo
Dopamina/metabolismo
Relação Dose-Resposta a Droga
Drosophila melanogaster/metabolismo
Enzimas/metabolismo
Feminino
Voo Animal/efeitos dos fármacos
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Intoxicação do Sistema Nervoso por Chumbo/patologia
Masculino
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Sistema Nervoso/metabolismo
Sistema Nervoso/patologia
Estresse Oxidativo
Fatores Sexuais
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (Caseins); 0 (Enzymes); 0 (Organometallic Compounds); EC 3.1.1.7 (Acetylcholinesterase); RX077P88RY (lead acetate); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150525
[Lr] Data última revisão:
150525
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150408
[St] Status:MEDLINE



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