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Pesquisa : D02.705.400.550 [Categoria DeCS]
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[PMID]:28479505
[Au] Autor:Zhang X; Li S; Wang C; Tian H; Wang W; Ru S
[Ad] Endereço:College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China.
[Ti] Título:Effects of monocrotophos pesticide on cholinergic and dopaminergic neurotransmitter systems during early development in the sea urchin Hemicentrotus pulcherrimus.
[So] Source:Toxicol Appl Pharmacol;328:46-53, 2017 Aug 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During early development in sea urchins, classical neurotransmitters, including acetylcholine (ACh), dopamine (DA), and serotonin (5-HT), play important roles in the regulation of morphogenesis and swimming behavior. However, the underlying mechanisms of how organophosphate pesticides cause developmental neurotoxicity by interfering with different neurotransmitter systems are unclear. In this study, we investigated the effects of 0.01, 0.10, and 1.00mg/L monocrotophos (MCP) pesticide on the activity of acetyltransferase (ChAT), acetylcholinesterase (AChE), monoamine oxidase, the concentration of DA, dopamine transporter, and the transcription activity of DA receptor D and tyrosine hydroxylase, during critical periods in cholinergic and dopaminergic nervous system development in sea urchin (Hemicentrotus pulcherrimus) embryos and larvae. At the blastula stages, MCP disrupted DA metabolism but not 5-HT metabolism, resulting in abnormal development. High ChAT and AChE activity were observed at the gastrulation-completed stage and the two-armed pluteus stage, respectively, MCP inhibited ChAT activity and AChE activity/distribution and resulted in developmental defects of the plutei. From the gastrula stage to the two-armed pluteus stage, we found ubiquitous disrupting effects of MCP on ACh, DA, and 5-HT metabolism, particularly at critical periods during the development of these neurotransmitter systems. Therefore, we propose that this disruption is one of the main mechanisms of MCP-related developmental neurotoxicity, which would contribute better understanding insight into the mechanism of MCP pesticide's toxic effects.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Hemicentrotus
Inseticidas/toxicidade
Monocrotofós/toxicidade
Síndromes Neurotóxicas/metabolismo
Neurotransmissores/metabolismo
Sistema Nervoso Parassimpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Colina O-Acetiltransferase/metabolismo
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Gastrulação
Hemicentrotus/crescimento & desenvolvimento
Monoaminoxidase/metabolismo
Síndromes Neurotóxicas/patologia
Receptores de Dopamina D1/biossíntese
Receptores de Dopamina D1/genética
Serotonina/metabolismo
Natação
Tirosina 3-Mono-Oxigenase/biossíntese
Tirosina 3-Mono-Oxigenase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Plasma Membrane Transport Proteins); 0 (Insecticides); 0 (Neurotransmitter Agents); 0 (Receptors, Dopamine D1); 333DO1RDJY (Serotonin); 6923-22-4 (Monocrotophos); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.4.3.4 (Monoamine Oxidase); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 3.1.1.7 (Acetylcholinesterase); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


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[PMID]:27810534
[Au] Autor:Narra MR; Rajender K; Reddy RR; Murty US; Begum G
[Ad] Endereço:Department of Zoology, College of Science, Osmania University, Hyderabad, 500 007, India.
[Ti] Título:Insecticides induced stress response and recuperation in fish: Biomarkers in blood and tissues related to oxidative damage.
[So] Source:Chemosphere;168:350-357, 2017 Feb.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The present research investigated the growth, blood, antioxidant response (liver), AChE (brain and muscle) and Na+/K + ATPase in gills of Clarias batrachus exposed to 0 (control), two insecticides, 1.65 mg L chlorpyrifos (CPF) and 2.14 mg L monocrotophos (MCP) for a fixed interval time of 3, 6, 9, 12 and 15 days and follow up depuration process in fresh water for 30 days (at an interval of 7, 15 and 30 days). The toxicants exposed fish indicated significantly (P < 0.05) lower weight gain and HSI. The RBC, Hb, Hct, plasma total protein, glucose, albumin, globulin and respiratory burst activity was reduced. However, WBC, plasma glucose, serum creatinine, and triglycerides were enhanced. The weight gain, HSI and all haematological parameters were reversed following depuration of CPF and MCP exposed fish. Hepatic superoxide dismutase, catalase, lipid peroxidation, reduced glutathione, and glutathione S-transferase activities were significantly activated whereas glutathione peroxidase was inhibited in both tested groups. All the antioxidant enzymes were reversed on day 15 in MCP concentration, whereas CPF on day 30 of depuration process. The inhibition of acetylcholinesterase (brain, muscle) and gill Na+/K + ATPase activities were more in CPF exposure and early recovery in MCP. The results indicated that depuration process might help in detoxification of fish and improve growth, haematological conditions, oxidative stress and AChE, Na+/K + ATPase activity. However, further studies are needed in different fish species with different toxicants to support this strategy of depuration process in order to detoxify polluted fish.
[Mh] Termos MeSH primário: Biomarcadores/metabolismo
Peixes-Gato/metabolismo
Clorpirifos/toxicidade
Inseticidas/toxicidade
Monocrotofós/toxicidade
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Antioxidantes/metabolismo
Encéfalo/efeitos dos fármacos
Catalase/metabolismo
Água Doce
Brânquias/efeitos dos fármacos
Brânquias/metabolismo
Glutationa/metabolismo
Glutationa Peroxidase/metabolismo
Glutationa Transferase/metabolismo
Peroxidação de Lipídeos
Fígado/efeitos dos fármacos
Músculos/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
ATPase Trocadora de Sódio-Potássio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Biomarkers); 0 (Insecticides); 0 (Water Pollutants, Chemical); 6923-22-4 (Monocrotophos); 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); EC 3.1.1.7 (Acetylcholinesterase); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); GAN16C9B8O (Glutathione); JCS58I644W (Chlorpyrifos)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:27914538
[Au] Autor:Nagaraju R; Rajini PS
[Ad] Endereço:Food Protectants and Infestation Control Department, CSIR- Central Food Technological Research Institute, Mysuru 570 020, India.
[Ti] Título:Adaptive response of rat pancreatic ß-cells to insulin resistance induced by monocrotophos: Biochemical evidence.
[So] Source:Pestic Biochem Physiol;134:39-48, 2016 Nov.
[Is] ISSN:1095-9939
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our previous findings clearly suggested the role of duration of exposure to monocrotophos (MCP) in the development of insulin resistance. Rats exposed chronically to MCP developed insulin resistance with hyperinsulinemia without overt diabetes. In continuation of this vital observation, we sought to delineate the biochemical mechanisms that mediate heightened pancreatic ß-cell response in the wake of MCP-induced insulin resistance in rats. Adult rats were orally administered (0.9 and 1.8mg/kgb.w/d) MCP for 180days. Terminally, MCP-treated rats exhibited glucose intolerance, hyperinsulinemia, and potentiation of glucose-induced insulin secretion along with elevated levels of circulating IGF1, free fatty acids, corticosterone, and paraoxonase activity. Biochemical analysis of islet extracts revealed increased levels of insulin, malate, pyruvate and ATP with a concomitant increase in activities of cytosolic and mitochondrial enzymes that are known to facilitate insulin secretion and enhanced shuttle activities. Interestingly, islets from MCP-treated rats exhibited increased insulin secretory potential ex vivo compared to those isolated from control rats. Further, MCP-induced islet hypertrophy was associated with increased insulin-positive cells. Our study demonstrates the impact of the biological interaction between MCP and components of metabolic homeostasis on pancreatic beta cell function/s. We speculate that the heightened pancreatic beta cell function evidenced may be mediated by increased IGF1 and paraoxonase activity, which effectively counters insulin resistance induced by chronic exposure to MCP. Our findings emphasize the need for focused research to understand the confounding environmental risk factors which may modulate heightened beta cell functions in the case of organophosphorus insecticide-induced insulin resistance. Such an approach may help us to explain the sharp increase in the prevalence of type II diabetes worldwide.
[Mh] Termos MeSH primário: Inseticidas/toxicidade
Resistência à Insulina
Células Secretoras de Insulina/efeitos dos fármacos
Monocrotofós/toxicidade
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Difosfato de Adenosina/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Glicemia/análise
Insulina/sangue
Insulina/metabolismo
Células Secretoras de Insulina/metabolismo
Células Secretoras de Insulina/patologia
Malatos/metabolismo
Masculino
Ácido Pirúvico/metabolismo
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insecticides); 0 (Insulin); 0 (Malates); 61D2G4IYVH (Adenosine Diphosphate); 6923-22-4 (Monocrotophos); 817L1N4CKP (malic acid); 8558G7RUTR (Pyruvic Acid); 8L70Q75FXE (Adenosine Triphosphate)
[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:161205
[St] Status:MEDLINE


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[PMID]:26980114
[Au] Autor:Wang J; Zhang X; Shan R; Ma S; Tian H; Wang W; Ru S
[Ad] Endereço:Marine Life Science College, Ocean University of China, Qingdao 266003, China.
[Ti] Título:Lipovitellin as an antigen to improve the precision of sandwich ELISA for quantifying zebrafish (Danio rerio) vitellogenin.
[So] Source:Comp Biochem Physiol C Toxicol Pharmacol;185-186:87-93, 2016 Jul-Aug.
[Is] ISSN:1532-0456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vitellogenin (Vtg) in zebrafish (Danio rerio) is a core biomarker for screening environmental estrogens in test guidelines of the Organization for Economic Cooperation and Development. To accurately quantify zebrafish Vtg, lipovitellin (Lv), the main Vtg-derived yolk protein, was used as the antigen to establish a sandwich enzyme-linked immunosorbent assay (ELISA). The purified Lv was a phospholipoglycoprotein with apparent molecular weight of ~445kDa, and separated into three polypeptides corresponding to ~117, ~102, and ~23.8kDa by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Immunological analysis confirmed the specificity of the anti-Lv antibody for Vtg and the immunological similarity between Vtg and Lv. Using the purified Lv and anti-Lv antibody, a sandwich ELISA with a detection limit of 4.3ng/mL and a detection range from 7.8 to 250ng/mL was developed. The intra- and inter-assay coefficients of variation were both below 10%. Moreover, the Lv standard curve was nearly identical to the Vtg standard curve, and paralleled serial whole-body homogenate dilutions of male zebrafish exposed to 17ß-estradiol, demonstrating that the Lv-based ELISA could be used for quantification of zebrafish Vtg. Zebrafish Lv showed high stability during purification process, heat treatment, -80°C storage, and repeated freeze/thaw cycles. Additionally, the standard curve of Lv stored at -80°C for 3months exhibited higher robustness than that of Vtg stored under the same conditions. Finally, the usefulness of the ELISA for detecting estrogenic activity was verified by quantifying Vtg inductions in zebrafish exposed to monocrotophos.
[Mh] Termos MeSH primário: Anticorpos/imunologia
Antígenos
Proteínas do Ovo/imunologia
Ensaio de Imunoadsorção Enzimática/métodos
Vitelogeninas/imunologia
Proteínas de Peixe-Zebra/imunologia
Peixe-Zebra/imunologia
[Mh] Termos MeSH secundário: Animais
Especificidade de Anticorpos
Biomarcadores/metabolismo
Calibragem
Proteínas do Ovo/química
Proteínas do Ovo/isolamento & purificação
Proteínas do Ovo/metabolismo
Disruptores Endócrinos/toxicidade
Ensaio de Imunoadsorção Enzimática/normas
Estrogênios/toxicidade
Feminino
Masculino
Peso Molecular
Monocrotofós/toxicidade
Estabilidade Proteica
Padrões de Referência
Reprodutibilidade dos Testes
Vitelogeninas/metabolismo
Peixe-Zebra/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Antibodies); 0 (Antigens); 0 (Biomarkers); 0 (Egg Proteins); 0 (Endocrine Disruptors); 0 (Estrogens); 0 (Vitellogenins); 0 (Zebrafish Proteins); 0 (Zvtg1 protein, zebrafish); 6923-22-4 (Monocrotophos); 9088-43-1 (lipovitellin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170804
[Lr] Data última revisão:
170804
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160317
[St] Status:MEDLINE


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[PMID]:26720809
[Au] Autor:Majumder SP; Das AC
[Ad] Endereço:Department of Agricultural Chemistry and Soil Science, Bidhan Chandra Krishi Viswavidyalaya, Mohanpur 741252, India.
[Ti] Título:Phosphate-solubility and phosphatase activity in Gangetic alluvial soil as influenced by organophosphate insecticide residues.
[So] Source:Ecotoxicol Environ Saf;126:56-61, 2016 Apr.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:An experiment was conducted under laboratory conditions to investigate the effect of four organophosphate insecticides, viz. monocrotophos, profenophos, quinalphos and triazophos at their field application rates (0.75, 1.0, 0.5 and 0.6 kg a.i.ha(-1), respectively), on the growth and activities of phosphate solubilizing microorganisms in relation to availability of insoluble phosphates in the Gangetic alluvial soil of West Bengal, India. The proliferation of phosphate solubilizing microorganisms was highly induced with profenophos (38.3%), while monocrotophos exerted maximum stimulation (20.8%) towards the solubility of insoluble phosphates in soil. The phosphatase activities of the soil (both acid phosphatase and alkaline phosphatase) were significantly increased due to the incorporation of the insecticides in general, and the augmentation was more pronounced with quinalphos (43.1%) followed by profenophos (27.6%) for acid phosphatase, and with monocrotophos (25.2%) followed by profenophos (16.1%) for alkaline phosphatase activity in soil. The total phosphorus was highly retained by triazophos (19.9%) followed by monocrotophos (16.5%), while incorporation of triazophos and quinalphos manifested greater availability of water soluble phosphorus in soil.
[Mh] Termos MeSH primário: Bactérias/efeitos dos fármacos
Inseticidas/farmacologia
Organofosfatos/toxicidade
Fosfatos/química
Monoéster Fosfórico Hidrolases/metabolismo
Microbiologia do Solo
Poluentes do Solo/toxicidade
Solo/química
[Mh] Termos MeSH secundário: Análise de Variância
Bactérias/crescimento & desenvolvimento
Bactérias/metabolismo
Índia
Inseticidas/metabolismo
Inseticidas/toxicidade
Monocrotofós/farmacologia
Compostos Organotiofosforados/farmacologia
Resíduos de Praguicidas/farmacologia
Fosfatos/metabolismo
Fósforo/metabolismo
Solubilidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insecticides); 0 (Organophosphates); 0 (Organothiophosphorus Compounds); 0 (Pesticide Residues); 0 (Phosphates); 0 (Soil); 0 (Soil Pollutants); 26S837727Y (quinalphos); 27YLU75U4W (Phosphorus); 6923-22-4 (Monocrotophos); EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160101
[St] Status:MEDLINE


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[PMID]:26498809
[Au] Autor:Sun L; Zhu S; Yang Z; Chen Q; Liu H; Zhang J; Hu G; Li S; Hong Q
[Ad] Endereço:Key Laboratory of Agricultural Environmental Microbiology, Ministry of Agriculture, College of Life Sciences, Nanjing Agricultural University, Nanjing, 210095, China.
[Ti] Título:Degradation of monocrotophos by Starkeya novella YW6 isolated from paddy soil.
[So] Source:Environ Sci Pollut Res Int;23(4):3727-35, 2016 Feb.
[Is] ISSN:1614-7499
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A bacteria strain, YW6, capable of utilizing monocrotophos (MCP) as the sole carbon and nitrogen sources for growth was isolated from paddy soil and identified as Starkeya novella. Strain YW6 completely degraded 0.2 mM MCP within 36 h without any lag period. Addition of carbon source resulted in slowing down of the initial rate of degradation of MCP, while the presence of a more favorable source of nitrogen enhanced the degradation of MCP. In addition to the degradation of MCP, strain YW6 was also able to degrade a wide range of organophosphorus pesticides (OPs) containing P-O-C bond, but not dimethoate, which has P-S-C bond. A MCP degradation pathway was proposed on the basis of metabolite production patterns and identification of the metabolites. MCP is hydrolyzed at the P-O-C bond to form N-methylacetoacetamide and dimethyl phosphate; N-methylacetoacetamide is transformed to N-methyl-4-oxo-pentanamide, which was subsequently converted to 5-(methylamino)-5-oxo-pentanoic acid, and 5-(methylamino)-5-oxo-pentanoic acid is cleaved to glutaric acid and methylamine. These findings provide new insights into the microbial metabolism of MCP. To the best of our knowledge, this is the first report on the degradation of MCP by Starkeya bacteria.
[Mh] Termos MeSH primário: Alphaproteobacteria/crescimento & desenvolvimento
Monocrotofós/análise
Praguicidas/análise
Poluentes do Solo/análise
[Mh] Termos MeSH secundário: Alphaproteobacteria/isolamento & purificação
Alphaproteobacteria/metabolismo
Biodegradação Ambiental
Hidrólise
Monocrotofós/química
Praguicidas/química
Solo/química
Microbiologia do Solo
Poluentes do Solo/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Pesticides); 0 (Soil); 0 (Soil Pollutants); 6923-22-4 (Monocrotophos)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151027
[St] Status:MEDLINE
[do] DOI:10.1007/s11356-015-5606-0


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[PMID]:26453861
[Au] Autor:Nidheesh T; Salim C; Rajini PS; Suresh PV
[Ad] Endereço:Academy of Scientific and Innovative Research, CSIR - Central Food Technological Research Institute, Mysuru 570 020, India; Department of Meat and Marine Sciences, CSIR - Central Food Technological Research Institute, Mysuru 570 020, India.
[Ti] Título:Antioxidant and neuroprotective potential of chitooligomers in Caenorhabditis elegans exposed to Monocrotophos.
[So] Source:Carbohydr Polym;135:138-44, 2016 Jan 01.
[Is] ISSN:1879-1344
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objectives of this investigation were to establish the propensity of the chitooligomers (COS) to ameliorate neurodegeneration and oxidative stress in Caenorhabditis elegans induced by an organophosphorus insecticide, Monocrotophos (MCP). COS was prepared from α-chitosan by the enzymatic method using chitosanase and characterized by HPLC and electron spray ionization-TOF-(ESI-TOF)-MS. We exposed age synchronized L4 C. elegans worms (both wild type N2 and transgenic strain BZ555 (Pdat-1:GFP) to sublethal concentration of MCP (0.75mM) for 24h in the presence or absence of COS (0.2mM). The neuroprotective effect of COS was examined in N2 worms in terms of brood size, lifespan, egg laying, dopamine content, acetylcholinesterase and carboxylesterase activity and by direct visualization and quantification of degeneration of dopaminergic neurons in BZ555. Exposure to COS extended lifespan, normalized egg laying, increased brood size, decreased the dopaminergic neurodegeneration, increased the dopamine content and increased AChE and carboxylesterase activity in C. elegans treated with MCP. COS induced a significant decrease in reactive oxygen species and increased the reduced glutathione level as well as increased superoxide dismutase and catalase activity. Our findings demonstrate that COS significantly inhibits the dopaminergic neurodegeneration and associated physiological alterations induced by MCP in C. elegans by attenuating the oxidative stress as well.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Caenorhabditis elegans/efeitos dos fármacos
Quitosana/análogos & derivados
Quitosana/farmacologia
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Animais Geneticamente Modificados
Antioxidantes/química
Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/fisiologia
Carboxilesterase/metabolismo
Catalase/metabolismo
Quitosana/química
Inibidores da Colinesterase/toxicidade
Dopamina/metabolismo
Glutationa/metabolismo
Inseticidas/toxicidade
Monocrotofós/toxicidade
Fármacos Neuroprotetores/química
Espécies Reativas de Oxigênio/metabolismo
Reprodução/efeitos dos fármacos
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cholinesterase Inhibitors); 0 (Insecticides); 0 (Neuroprotective Agents); 0 (Reactive Oxygen Species); 6923-22-4 (Monocrotophos); 9012-76-4 (Chitosan); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); EC 3.1.1.1 (Carboxylesterase); EC 3.1.1.7 (Acetylcholinesterase); GAN16C9B8O (Glutathione); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151011
[Lr] Data última revisão:
151011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE


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[PMID]:25227224
[Au] Autor:Ali SJ; Rajini PS
[Ad] Endereço:Department of Food Protectants and Infestation Control, Council of Scientific and Industrial Research (CSIR)-Central Food Technological Research Institute, Mysore, Karnataka, India.
[Ti] Título:Effect of monocrotophos, an organophosphorus insecticide, on the striatal dopaminergic system in a mouse model of Parkinson's disease.
[So] Source:Toxicol Ind Health;32(7):1153-65, 2016 Jul.
[Is] ISSN:1477-0393
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Our earlier study had shown that low concentrations of monocrotophos (MCP) elicited dopaminergic features of Parkinson's disease (PD) in the nematode Caenorhabditis elegans In the present study, the effect of low doses of MCP on the striatal dopaminergic neurons was investigated using the mouse model system. MCP was initially screened for its ability to cause any neurobehavioral deficits and alterations in the dopaminergic system in Swiss albino mice, aged 8 weeks and weighing 25-30 g, with repeated doses at 0.3 and 0.6 mg/kg body weight (b.w.)/day for 7 days and 30 days. Mice were treated with four intraperitoneal injections for every 2 h with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) at the dosage of 14 mg/kg b.w. MCP was administered to these mice at the above-mentioned doses for 7 days. Mice administered with MCP alone revealed a significant (p < 0.05) reduction in the dopamine (DA) content at both 7 and 30 days and showed a significant (p < 0.05) increase in neurobehavioral deficits. Interestingly, when MCP was administered for 7 days to MPTP-treated mice, further significant decrease in both DA content and increase in neurobehavioral deficits were apparent. The extent of reactive oxygen species and lipid peroxidation were markedly increased, while the ratio of reduced to oxidized glutathione levels were significantly decreased (p < 0.05) in the treated mice as compared to the control. Significant histopathological alterations and a marked reduction in the number of tyrosine hydroxylase positive cells were evident in striatum of mice treated with higher doses of MCP. These changes were comparable to that seen in mice treated with MPTP and post-administered lower doses of MCP. Our findings suggest that MCP per se has the propensity to induce pathological changes in the dopaminergic neurons as well as augment the degeneration in a compromised nigrostriatal system such as that in PD.
[Mh] Termos MeSH primário: Corpo Estriado/efeitos dos fármacos
Inseticidas/toxicidade
Monocrotofós/toxicidade
Doença de Parkinson/patologia
[Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina/administração & dosagem
Animais
Comportamento Animal/efeitos dos fármacos
Modelos Animais de Doenças
Dopamina/metabolismo
Relação Dose-Resposta a Droga
Dissulfeto de Glutationa/metabolismo
Injeções Intraperitoneais
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Camundongos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Neurotoxinas/toxicidade
Doença de Parkinson/etiologia
Espécies Reativas de Oxigênio/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insecticides); 0 (Neurotoxins); 0 (Reactive Oxygen Species); 6923-22-4 (Monocrotophos); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); ULW86O013H (Glutathione Disulfide); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170413
[Lr] Data última revisão:
170413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140918
[St] Status:MEDLINE
[do] DOI:10.1177/0748233714547733


  9 / 280 MEDLINE  
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[PMID]:24105069
[Au] Autor:Sankhwar ML; Yadav RS; Shukla RK; Singh D; Ansari RW; Pant AB; Parmar D; Khanna VK
[Ad] Endereço:Council of Scientific and Industrial Research, Indian Institute of Toxicology Research, Lucknow, Uttar Pradesh, India.
[Ti] Título:Monocrotophos induced oxidative stress and alterations in brain dopamine and serotonin receptors in young rats.
[So] Source:Toxicol Ind Health;32(3):422-36, 2016 Mar.
[Is] ISSN:1477-0393
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human exposure to monocrotophos, an organophosphate pesticide, could occur due to its high use in agriculture to protect crops. Recently, we found that postlactational exposure to monocrotophos impaired cholinergic mechanisms in young rats and such changes persisted even after withdrawal of monocrotophos exposure. In continuation to this, the effect of monocrotophos on noncholinergic targets and role of oxidative stress in its neurotoxicity has been studied. Exposure of rats from postnatal day (PD)22 to PD49 to monocrotophos (0.50 or 1.0 mg kg(-1) body weight, perorally) significantly impaired motor activity and motor coordination on PD50 as compared to controls. A significant decrease in the binding of (3)H-spiperone to striatal membrane (26%, p < 0.01; 30%, p < 0.05) in rats exposed to monocrotophos at both the doses and increase in the binding of (3)H-ketanserin to frontocortical membrane (14%, p > 0.05; 37%, p < 0.05) in those exposed at a higher dose, respectively, was observed on PD50 compared with the controls. Alterations in the binding persisted even after withdrawal of monocrotophos exposure on PD65. Increased oxidative stress in brain regions following exposure of rats to monocrotophos was also observed on PD50 that persisted 15 days after withdrawal of exposure on PD65. The results suggest that monocrotophos exerts its neurobehavioral toxicity by affecting noncholinergic functions involving dopaminergic and serotonergic systems associated with enhanced oxidative stress. The results also exhibit vulnerability of developing brain to monocrotophos as most of the changes persisted even after withdrawal of its exposure.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Monocrotofós/toxicidade
Estresse Oxidativo/efeitos dos fármacos
Receptores Dopaminérgicos/efeitos dos fármacos
Receptores de Serotonina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Feminino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Dopamine); 0 (Receptors, Serotonin); 6923-22-4 (Monocrotophos)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131010
[St] Status:MEDLINE
[do] DOI:10.1177/0748233713500834


  10 / 280 MEDLINE  
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[PMID]:26370177
[Au] Autor:Kumar V; Gupta AK; Shukla RK; Tripathi VK; Jahan S; Pandey A; Srivastava A; Agrawal M; Yadav S; Khanna VK; Pant AB
[Ad] Endereço:CSIR-Indian Institute of Toxicology Research, Lucknow-226001, India.
[Ti] Título:Molecular Mechanism of Switching of TrkA/p75(NTR) Signaling in Monocrotophos Induced Neurotoxicity.
[So] Source:Sci Rep;5:14038, 2015 Sep 15.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We demonstrate the role of molecular switching of TrkA/p75(NTR) signaling cascade in organophosphate pesticide-Monocrotophos (MCP) induced neurotoxicity in stem cell derived cholinergic neurons and in rat brain. Our in-silico studies reveal that MCP followed the similar pattern of binding as staurosporine and AG-879 (known inhibitors of TrkA) with TrkA protein (PDB ID: 4AOJ) at the ATP binding sites. This binding of MCP to TrkA led to the conformational change in this protein and triggers the cell death cascades. The in-silico findings are validated by observing the down regulated levels of phosphorylated TrkA and its downstream molecules viz., pERK1/2, pAkt and pCREB in MCP-exposed cells. We observe that these MCP induced alterations in pTrkA and downstream signaling molecules are found to be associated with apoptosis and injury to neurons. The down-regulation of TrkA could be linked to increased p75(NTR). The in-vitro studies could be correlated in the rat model. The switching of TrkA/p75(NTR) signaling plays a central role in MCP-induced neural injury in rBNSCs and behavioral changes in exposed rats. Our studies significantly advance the understanding of the switching of TrkA/p75(NTR) that may pave the way for the application of TrkA inducer/p75(NTR) inhibitor for potential therapeutic intervention in various neurodegenerative disorders.
[Mh] Termos MeSH primário: Inibidores da Colinesterase/farmacologia
Inseticidas/farmacologia
Monocrotofós/farmacologia
Receptor trkA/metabolismo
Receptores de Fator de Crescimento Neural/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Encéfalo/metabolismo
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Inibidores da Colinesterase/química
Inibidores da Colinesterase/toxicidade
Inseticidas/química
Inseticidas/toxicidade
Modelos Moleculares
Conformação Molecular
Simulação de Acoplamento Molecular
Monocrotofós/química
Monocrotofós/toxicidade
Células-Tronco Neurais/citologia
Células-Tronco Neurais/efeitos dos fármacos
Células-Tronco Neurais/metabolismo
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Ratos
Receptor trkA/antagonistas & inibidores
Receptor trkA/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (Insecticides); 0 (Receptors, Nerve Growth Factor); 0 (TNFRSF16 protein, rat); 6923-22-4 (Monocrotophos); EC 2.7.10.1 (Receptor, trkA)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150916
[St] Status:MEDLINE
[do] DOI:10.1038/srep14038



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