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[PMID]:27773359
[Au] Autor:van Wendel de Joode B; Mora AM; Lindh CH; Hernández-Bonilla D; Córdoba L; Wesseling C; Hoppin JA; Mergler D
[Ad] Endereço:Central American Institute for Studies on Toxic Substances (IRET), Universidad Nacional, Heredia, Costa Rica. Electronic address: bernavanwendel@una.cr.
[Ti] Título:Pesticide exposure and neurodevelopment in children aged 6-9 years from Talamanca, Costa Rica.
[So] Source:Cortex;85:137-150, 2016 12.
[Is] ISSN:1973-8102
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Certain pesticides may affect children's neurodevelopment. We assessed whether pesticide exposure was associated with impaired neurobehavioral outcomes in children aged 6-9 years. We conducted a cross-sectional study in 140 children living near banana plantations and plantain farms in the Talamanca County, Costa Rica and assessed their neurobehavioral performance. Exposure was determined by analyzing urinary metabolites of chlorpyrifos (3,5,6-trichloro-2-pyridinol, TCPy), mancozeb (ethylenethiourea, ETU), and pyrethroids (3-phenoxybenzoic acid, 3-PBA). Repeated urine samples were obtained for 36 children. We estimated associations of pesticide concentrations with neurobehavioral outcomes using multivariable linear and logistic regression models. Median (25th-75th percentiles) TCPy, ETU, and 3-PBA concentrations were 1.4 (.7-3.1), 1.2 (.7-3.0), and .8 (.5-1.5) µg/L, respectively. Intraclass correlation coefficients (ICC) ranged between .32 and .67. After adjustment for potential confounders, higher urinary TCPy concentrations were associated with poorer working memory in boys (n = 59) (ß per 10-fold increase in TCPy concentrations = -7.5, 95% CI: -14.4, -.7); poorer visual motor coordination (ß = -1.4, 95% CI: -2.7, -.1); increased prevalence of parent-reported cognitive problems/inattention (adjusted OR per 10-fold increase in urinary concentrations = 5.8, 95% CI: 1.6, 22.9), oppositional disorders (aOR = 3.9, 95% CI: 1.0, 16.0), and ADHD (aOR = 6.8, 95% CI: 1.8, 28.6), and; decreased ability to discriminate colors (aOR = 6.6, 95% CI: 1.6, 30.3; the higher the score the worse). Higher ETU concentrations were associated with poorer verbal learning outcomes (ß = -7.0, 95% CI: -12.7, -1.3). Higher 3-PBA concentrations were associated with poorer processing speed scores, particularly in girls (ß = -8.8, 95% CI: -16.1, -1.4). Our findings indicate that children living near banana and plantain plantations are exposed to pesticides that may affect their neurodevelopment, which for certain domains may differ between boys and girls. We recommend the implementation of measures to reduce pesticide exposure in children living nearby banana plantations.
[Mh] Termos MeSH primário: Benzoatos/urina
Sistema Nervoso Central/efeitos dos fármacos
Sistema Nervoso Central/crescimento & desenvolvimento
Clorpirifos/urina
Maneb/urina
Praguicidas/urina
Zineb/urina
[Mh] Termos MeSH secundário: Criança
Comportamento Infantil
Costa Rica
Estudos Transversais
Feminino
Seres Humanos
Masculino
Piridonas/urina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzoates); 0 (Pesticides); 0 (Pyridones); 12427-38-2 (Maneb); 6515-38-4 (3,5,6-trichloro-2-pyridinol); 69DC2655VH (3-phenoxybenzoic acid); JCS58I644W (Chlorpyrifos); R0HY55EB9E (mancozeb); X1FSB1OZPT (Zineb)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:28330765
[Au] Autor:Zizza M; Di Lorenzo M; Laforgia V; Furia E; Sindona G; Canonaco M; Facciolo RM
[Ad] Endereço:Comparative Neuroanatomy Laboratory, Biology, Ecology and Earth Science Department (DiBEST), University of Calabria, Arcavacata of Rende, 87036, CS, Italy.
[Ti] Título:HSP90 and pCREB alterations are linked to mancozeb-dependent behavioral and neurodegenerative effects in a marine teleost.
[So] Source:Toxicol Appl Pharmacol;323:26-35, 2017 May 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pesticide mancozeb (mz) is recognized as a potent inducer of oxidative stress due to its ability to catalyze the production of reactive oxygen species plus inhibiting mitochondrial respiration thus becoming an environmental risk for neurodegenerative diseases. Despite numerous toxicological studies on mz have been directed to mammals, attention on marine fish is still lacking. Thus, it was our intention to evaluate neurobehavioral activities of ornate wrasses (Thalassoma pavo) exposed to 0.2mg/l of mz after a preliminary screening test (0.07-0.3mg/l). Treated fish exhibited an evident (p<0.001) latency to reach T-maze arms (>1000%) while exploratory attitudes (total arm entries) diminished (-50%; p<0.05) versus controls during spontaneous exploration tests. Moreover, they showed evident enhancements (+111%) of immobility in the cylinder test. Contextually, strong (-88%; p<0.01) reductions of permanence in light zone of the Light/Dark apparatus along with diminished crossings (-65%) were also detected. Conversely, wrasses displayed evident enhancements (160%) of risk assessment consisting of fast entries in the dark side of this apparatus. From a molecular point of view, a notable activation (p<0.005) of the brain transcription factor pCREB occurred during mz-exposure. Similarly, in situ hybridization supplied increased HSP90 mRNAs in most brain areas such as the lateral part of the dorsal telencephalon (Dl; +68%) and valvula of the cerebellum (VCe; +35%) that also revealed evident argyrophilic signals. Overall, these first indications suggest a possible protective role of the early biomarkers pCREB and HSP90 against fish toxicity.
[Mh] Termos MeSH primário: Comportamento Animal/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Proteínas de Peixes/metabolismo
Peixes/metabolismo
Fungicidas Industriais/toxicidade
Proteínas de Choque Térmico HSP90/metabolismo
Maneb/toxicidade
Degeneração Neural
Síndromes Neurotóxicas/etiologia
Poluentes Químicos da Água/toxicidade
Zineb/toxicidade
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Comportamento Exploratório/efeitos dos fármacos
Feminino
Proteínas de Peixes/genética
Peixes/genética
Proteínas de Choque Térmico HSP90/genética
Atividade Motora/efeitos dos fármacos
Síndromes Neurotóxicas/metabolismo
Síndromes Neurotóxicas/patologia
Síndromes Neurotóxicas/psicologia
Tempo de Reação/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Fish Proteins); 0 (Fungicides, Industrial); 0 (HSP90 Heat-Shock Proteins); 0 (Water Pollutants, Chemical); 12427-38-2 (Maneb); R0HY55EB9E (mancozeb); X1FSB1OZPT (Zineb)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE


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[PMID]:28322069
[Au] Autor:Jaballi I; Ben Saad H; Bkhairia I; Kammoun I; Droguet M; Magné C; Boudawara T; Kallel C; Nasri M; Hakim A; Ben Amara I
[Ad] Endereço:a Laboratory of Pharmacology, Faculty of Medicine , University of Sfax , Sfax , Tunisia.
[Ti] Título:Increasing maneb doses induces reactive oxygen species overproduction and nephrotoxicity in adult mice.
[So] Source:Toxicol Mech Methods;27(5):382-393, 2017 Jun.
[Is] ISSN:1537-6524
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: The aim of this study was to elucidate the biochemical, molecular and histopathological aspects of the kidney injuries as well as the hematological perturbations induced after adult mice exposure to increasing doses of maneb (MB). MATERIAL AND METHOD: Adult mice were intraperitoneally treated for seven days with four graded doses of MB, corresponding to 1/8, 1/6, 1/4 and 1/2 of its lethal dose (LD =1500 mg/kg body weight). RESULTS: Hematological analysis revealed a significant disruption in total white blood cells and platelets and a significant decrease in the plasmatic levels of ferrozine in mice treated with 1/8, 1/6 and 1/4 of MB LD . However, the ferrozine levels increased significantly in the group treated with 1/2 of MB LD . Evenly, our results showed a significant increase in the levels of malondialdehyde, lipid hydroperoxides, hydrogen peroxide and advanced oxidation protein products in all treated groups. The activities of catalase and glutathione peroxidase decreased significantly in all MB treated mice. Additionally, all treated groups exhibited strong nephrotoxicity signs, including increases in plasma urea, creatinine and albumin levels and lactate dehydrogenase activity, as well as a significant decrease in uric acid levels. Electrophoresis analysis revealed nucleic acid degradation, testifying the genotoxicity of MB. Moreover, the histopathological observations showed severe renal injuries, which could be related to the above mentioned data. CONCLUSIONS: Our data showed, for the first time, that the MB tested doses led to oxidative stress installation causing renal cell damages and lowering all defense systems capacities.
[Mh] Termos MeSH primário: Dano ao DNA
Fungicidas Industriais/toxicidade
Rim/efeitos dos fármacos
Maneb/toxicidade
Nefrite/induzido quimicamente
Espécies Reativas de Oxigênio/sangue
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Relação Dose-Resposta a Droga
Feminino
Rim/metabolismo
Rim/patologia
Camundongos
Nefrite/sangue
Nefrite/genética
Nefrite/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fungicides, Industrial); 0 (Reactive Oxygen Species); 12427-38-2 (Maneb)
[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:170322
[St] Status:MEDLINE
[do] DOI:10.1080/15376516.2017.1300617


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[PMID]:28202386
[Au] Autor:Hou L; Zhang C; Wang K; Liu X; Wang H; Che Y; Sun F; Zhou X; Zhao X; Wang Q
[Ad] Endereço:Department of Occupational and Environmental Health, School of Public Health, Dalian Medical University, No. 9 W. Lvshun South Road, Dalian 116044, China.
[Ti] Título:Paraquat and maneb co-exposure induces noradrenergic locus coeruleus neurodegeneration through NADPH oxidase-mediated microglial activation.
[So] Source:Toxicology;380:1-10, 2017 Apr 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Co-exposure to paraquat (PQ) and maneb (Mb) has been shown to increase the risk of Parkinson's disease (PD) and dopaminergic (DA) neurodegeneration in the substantia nigra pars compacta (SNpc) is observed in PQ and Mb-treated experimental animals. The loss of noradrenergic locus coeruleus (LC/NE) neurons in brainstem is a common feature shared by multiple neurodegenerative diseases, including PD. However, whether PQ and Mb is able to damage LC/NE neurons remains undefined. In this study, mice treated with combined PQ and Mb displayed progressive LC/NE neurodegeneration. Time course studies revealed that the activation of microglia preceded LC/NE neurodegeneration. Mechanistically, the activation of NADPH oxidase contributed to microglial activation and subsequent LC/NE neurodegeneration. We found that PQ and Mb co-exposure induced activation of NADPH oxidase as shown by increased superoxide production and membrane translocation of p47 , a cytosolic subunit of NADPH oxidase. Inhibition of NADPH oxidase by apocynin, a widely used NADPH oxidase inhibitor, suppressed microglial activation and gene expressions of proinflammatory factors. Furthermore, reduced activation of nuclear factor-κB (NF-κB) pathway was observed in apocynin-treated mice. More importantly, inhibition of NADPH oxidase by apocynin afforded LC/NE neuroprotection against PQ and Mb-induced neurotoxicity. Thus, our findings revealed the critical role NADPH oxidase-mediated microglial activation in driving LC/NE neurodegeneration induced by PQ and Mb, providing new insights into the pathogenesis of environmental toxins-induced PD.
[Mh] Termos MeSH primário: Neurônios Adrenérgicos/efeitos dos fármacos
Locus Cerúleo/efeitos dos fármacos
Maneb/toxicidade
Microglia/efeitos dos fármacos
NADPH Oxidases/metabolismo
Paraquat/toxicidade
[Mh] Termos MeSH secundário: Acetofenonas/farmacologia
Neurônios Adrenérgicos/metabolismo
Animais
Modelos Animais de Doenças
Inibidores Enzimáticos/farmacologia
Locus Cerúleo/patologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microglia/metabolismo
NADPH Oxidases/antagonistas & inibidores
NF-kappa B/genética
NF-kappa B/metabolismo
Degeneração Neural/induzido quimicamente
Degeneração Neural/prevenção & controle
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/prevenção & controle
Doença de Parkinson/etiologia
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Enzyme Inhibitors); 0 (NF-kappa B); 12427-38-2 (Maneb); B6J7B9UDTR (acetovanillone); EC 1.6.3.- (NADPH Oxidases); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE


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[PMID]:28110212
[Au] Autor:López-Fernández O; Pose-Juan E; Rial-Otero R; Simal-Gándara J
[Ad] Endereço:Nutrition and Bromatology Group, Analytical and Food Chemistry Department. Faculty of Food Science and Technology, University of Vigo, Ourense Campus, E-32004 Ourense, Spain.
[Ti] Título:Effects of hydrochemistry variables on the half-life of mancozeb and on the hazard index associated to the sum of mancozeb and ethylenethiourea.
[So] Source:Environ Res;154:253-260, 2017 04.
[Is] ISSN:1096-0953
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mancozeb is a dithiocarbamate non-systemic agricultural fungicide with multi-site, protective action. It helps to control many fungal diseases in a wide range of field crops, fruits, nuts, vegetables, and ornamental plants. We have investigated the stability profiles of mancozeb in aqueous solutions to determine the effect of pH, temperature and light on the degradation process of mancozeb. In addition, the toxicological risk for humans associated with the joint intake of mancoze7b and its final degradation product, ethylenethiourea (ETU), was calculated and modelled as a function of the experimental conditions. Stability study results showed a very low stability profile of mancozeb in all the aqueous solutions with rapid degradation that varied with experimental conditions. The process followed first order kinetics. The study of the degradation kinetics showed a significant effect of pH*temperature interaction on the degradation process. The results also expressed that light has a greater impact on the stability of mancozeb and the formation of ETU. The current study concludes that mancozeb is unstable in aqueous solutions, particularly at an acid pH, in addition to presenting both severe light and lower temperature sensitivity. The toxicological risk associated with mancozeb degradation increases with time and temperature, being higher at basic pH and in absence of light.
[Mh] Termos MeSH primário: Etilenotioureia/química
Etilenotioureia/metabolismo
Fungicidas Industriais/química
Fungicidas Industriais/metabolismo
Maneb/química
Maneb/metabolismo
Zineb/química
Zineb/metabolismo
[Mh] Termos MeSH secundário: Meia-Vida
Concentração de Íons de Hidrogênio
Hidrólise
Cinética
Luz
Fotólise
Temperatura Ambiente
Fatores de Tempo
Água
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fungicides, Industrial); 059QF0KO0R (Water); 12427-38-2 (Maneb); 24FOJ4N18S (Ethylenethiourea); R0HY55EB9E (mancozeb); X1FSB1OZPT (Zineb)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170123
[St] Status:MEDLINE


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[PMID]:28073049
[Au] Autor:Medda E; Santini F; De Angelis S; Franzellin F; Fiumalbi C; Perico A; Gilardi E; Mechi MT; Marsili A; Citroni A; Leandri A; Mantovani A; Vitti P; Olivieri A
[Ad] Endereço:National Centre for Epidemiology Surveillance and Health Promotion, Italian National Institute of Health, Viale Regina Elena 299, 00161 Rome, Italy.
[Ti] Título:Iodine nutritional status and thyroid effects of exposure to ethylenebisdithiocarbamates.
[So] Source:Environ Res;154:152-159, 2017 04.
[Is] ISSN:1096-0953
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Italy is still characterized by a mild iodine deficiency and is among the most intensive users of chemical products for agriculture in Europe. The aim of this study was i) to evaluate thyroid effects of exposure to mancozeb, a fungicide widely used in agriculture, in a sample of Italian grapevine workers, and ii) to verify whether the iodine intake may modulate the risk of thyroid disruption due to the mancozeb metabolite ethylenthiourea (ETU). METHODS: One hundred seventy-seven occupationally exposed male workers (29 from Chianti, a mild iodine deficient area, and 148 from Bolzano an iodine sufficient province) and 74 non-occupationally exposed male controls (34 from Chianti and 40 from Bolzano) were enrolled in the study. Serum biomarkers of thyroid function, as well as urinary iodine and ETU concentrations were assessed. Moreover all the recruited subjects underwent clinical examination and thyroid ultrasound. RESULTS: Multivariate comparisons showed lower mean serum levels of FT4 in Chianti-workers as compared to Bolzano-workers. Moreover, an increased urinary iodine excretion (>250µg/L) was more frequently found among more exposed workers (ETU>20µg/L) than among less exposed ones and this effect was more pronounced in Chianti- than in Bolzano-workers. Chianti-workers also showed a significantly higher frequency of very low thyroid volume (≤6.0ml) as compared to controls. CONCLUSIONS: These findings showed a mild thyroid disrupting effect due to occupational exposure to mancozeb, more pronounced in workers residing in an area characterized by a mild to moderate iodine deficiency as compared to workers residing in an area covered by a long-lasting iodine prophylaxis program.
[Mh] Termos MeSH primário: Fungicidas Industriais/toxicidade
Iodo/administração & dosagem
Maneb/toxicidade
Doenças da Glândula Tireoide/prevenção & controle
Zineb/toxicidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Doenças dos Trabalhadores Agrícolas/induzido quimicamente
Doenças dos Trabalhadores Agrícolas/prevenção & controle
Estudos de Casos e Controles
Etilenotioureia/análise
Fazendeiros
Seres Humanos
Iodo/deficiência
Itália
Masculino
Meia-Idade
Estado Nutricional
Exposição Ocupacional/efeitos adversos
Doenças da Glândula Tireoide/induzido quimicamente
Testes de Função Tireóidea
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fungicides, Industrial); 12427-38-2 (Maneb); 24FOJ4N18S (Ethylenethiourea); 9679TC07X4 (Iodine); R0HY55EB9E (mancozeb); X1FSB1OZPT (Zineb)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE


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[PMID]:28038352
[Au] Autor:Richter F; Gabby L; McDowell KA; Mulligan CK; De La Rosa K; Sioshansi PC; Mortazavi F; Cely I; Ackerson LC; Tsan L; Murphy NP; Maidment NT; Chesselet MF
[Ad] Endereço:Department of Neurology, UCLA, Los Angeles, CA, USA. Electronic address: franziska.richter@vmf.uni-leipzig.de.
[Ti] Título:Effects of decreased dopamine transporter levels on nigrostriatal neurons and paraquat/maneb toxicity in mice.
[So] Source:Neurobiol Aging;51:54-66, 2017 Mar.
[Is] ISSN:1558-1497
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:How genetic variations in the dopamine transporter (DAT) combined with exposure to environmental toxins modulate the risk of Parkinson's disease remains unclear. Using unbiased stereology in DAT knock-down mice (DAT-KD) and wild-type (WT) littermates, we found that decreased DAT caused a loss of tyrosine hydroxylase-positive (dopaminergic) neurons in subregions of the substantia nigra pars compacta at 3-4 days, 5 weeks, and 18 months of age. Both genotypes lost dopaminergic neurons with age and remaining neurons at 11 months were resilient to paraquat/maneb. In 5-week-old mice, the toxins decreased substantia nigra pars compacta dopaminergic neurons in both genotypes but less in DAT-KD. Regional analysis revealed striking differences in the subsets of neurons affected by low DAT, paraquat/maneb, and aging. In particular, we show that a potentially protective effect of low DAT against toxin exposure is not sufficient to reduce death of all nigrostriatal dopaminergic neurons. Thus, different regional vulnerability of nigrostriatal dopaminergic neurons may contribute to an increased risk of developing Parkinson's disease when multiple factors are combined.
[Mh] Termos MeSH primário: Envelhecimento/patologia
Proteínas da Membrana Plasmática de Transporte de Dopamina/deficiência
Proteínas da Membrana Plasmática de Transporte de Dopamina/genética
Neurônios Dopaminérgicos/patologia
Variação Genética
Maneb/toxicidade
Paraquat/toxicidade
Doença de Parkinson/etiologia
Parte Compacta da Substância Negra/patologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Masculino
Camundongos Knockout
Camundongos Mutantes
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dopamine Plasma Membrane Transport Proteins); 12427-38-2 (Maneb); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161231
[St] Status:MEDLINE


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[PMID]:28025796
[Au] Autor:Singh D; Kumar V; Singh C
[Ad] Endereço:Developmental Toxicology Laboratory, Systems Toxicology and Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow, Uttar Pradesh, 226 001, India.
[Ti] Título:IFN-γ regulates xanthine oxidase-mediated iNOS-independent oxidative stress in maneb- and paraquat-treated rat polymorphonuclear leukocytes.
[So] Source:Mol Cell Biochem;427(1-2):133-143, 2017 Mar.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Maneb (MB) and paraquat (PQ) provoke oxidative stress-mediated cell damage. Role of xanthine oxidase (XO) in oxidative stress and its association with nitric oxide (NO)/NO synthase (NOS) have been widely reported. While inducible NOS (iNOS) is implicated in MB+PQ-induced toxicity in rat polymorphonuclear leukocytes (PMNs), role of XO and its alliance with iNOS have not yet been established. The study investigated the role of XO in MB+PQ-induced oxidative stress in rat PMNs and its regulation by iNOS and inflammatory cytokines. MB+PQ-augmented reactive oxygen species (ROS), superoxide, nitro-tyrosine, lipid peroxidation (LPO), and nitrite levels along with the catalytic activity of iNOS, superoxide dismutase (SOD), and XO. XO inhibitor, allopurinol (AP), alleviated MB+PQ-induced changes except nitrite content and iNOS activity. Conversely, an iNOS inhibitor, aminoguanidine, mitigated MB+PQ-induced LPO, nitrite, iNOS, and nitro-tyrosine levels; however, no change was observed in ROS, SOD, and XO. Nuclear factor-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), tumor necrosis factor-alpha (TNF-α) inhibitor, pentoxyfylline, and an anti-inflammatory agent, dexamethasone, attenuated MB+PQ-induced increase in XO, superoxide, and ROS with parallel reduction in the expression of interferon-gamma (IFN-γ), TNF-α, and interleukin-1ß (IL-1ß) in rat PMNs. Exogenous IFN-γ, TNF-α, and IL-1ß enhanced superoxide, ROS, and XO in the PMNs of control and MB+PQ-treated rats; however, IFN- γ was found to be the most potent inducer. Moreover, AP ameliorated cytokine-induced free radical generation and restored XO activity towards normalcy. The results thus demonstrate that XO mediates oxidative stress in MB+PQ-treated rat PMNs via iNOS-independent but cytokine (predominantly IFN-γ)-dependent mechanism.
[Mh] Termos MeSH primário: Interferon gama/metabolismo
Maneb/farmacologia
Neutrófilos/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Paraquat/farmacologia
Xantina Oxidase/metabolismo
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
12427-38-2 (Maneb); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, rat); EC 1.17.3.2 (Xanthine Oxidase); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161228
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-016-2905-9


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[PMID]:27884192
[Au] Autor:Kumar A; Ganini D; Mason RP
[Ad] Endereço:Free Radical Biology Group, Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, 111 T.W. Alexander Dr., Research Triangle Park, Durham, NC, 27709, USA. kumara10@niehs.nih.gov.
[Ti] Título:Role of cytochrome c in α-synuclein radical formation: implications of α-synuclein in neuronal death in Maneb- and paraquat-induced model of Parkinson's disease.
[So] Source:Mol Neurodegener;11(1):70, 2016 Nov 24.
[Is] ISSN:1750-1326
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The pathological features of Parkinson's disease (PD) include an abnormal accumulation of α-synuclein in the surviving dopaminergic neurons. Though PD is multifactorial, several epidemiological reports show an increased incidence of PD with co-exposure to pesticides such as Maneb and paraquat (MP). In pesticide-related PD, mitochondrial dysfunction and α-synuclein oligomers have been strongly implicated, but the link between the two has not yet been understood. Similarly, the biological effects of α-synuclein or its radical chemistry in PD is largely unknown. Mitochondrial dysfunction during PD pathogenesis leads to release of cytochrome c in the cytosol. Once in the cytosol, cytochrome c has one of two fates: It either binds to apaf1 and initiates apoptosis or can act as a peroxidase. We hypothesized that as a peroxidase, cytochrome c leaked out from mitochondria can form radicals on α-synuclein and initiate its oligomerization. METHOD: Samples from controls, and MP co-exposed wild-type and α-synuclein knockout mice were studied using immuno-spin trapping, confocal microscopy, immunohistochemistry, and microarray experiments. RESULTS: Experiments with MP co-exposed mice showed cytochrome c release in cytosol and its co-localization with α-synuclein. Subsequently, we used immuno-spin trapping method to detect the formation of α-synuclein radical in samples from an in vitro reaction mixture consisting of cytochrome c, α-synuclein, and hydrogen peroxide. These experiments indicated that cytochrome c plays a role in α-synuclein radical formation and oligomerization. Experiments with MP co-exposed α-synuclein knockout mice, in which cytochrome c-α synuclein co-localization and interaction cannot occur, mice showed diminished protein radical formation and neuronal death, compared to wild-type MP co-exposed mice. Microarray data from MP co-exposed wild-type and α-synuclein knockout mice further showed that the absence of α-synuclein per se or its co-localization with cytochrome c confers protection from MP co-exposure, as several important pathways were unaffected in α-synuclein knockout mice. CONCLUSIONS: Altogether, these results show that peroxidase activity of cytochrome c contributes to α-synuclein radical formation and oligomerization, and that α-synuclein, through its co-localization with cytochrome c or on its own, affects several biological pathways which contribute to increased neuronal death in an MP-induced model of PD.
[Mh] Termos MeSH primário: Citocromos c/metabolismo
Radicais Livres/metabolismo
Neurônios/patologia
Transtornos Parkinsonianos/patologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Animais
Morte Celular
Imuno-Histoquímica
Masculino
Maneb/toxicidade
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia Confocal
Neurônios/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
Estresse Oxidativo/fisiologia
Paraquat/toxicidade
Transtornos Parkinsonianos/induzido quimicamente
Transtornos Parkinsonianos/metabolismo
Praguicidas/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radicals); 0 (Pesticides); 0 (alpha-Synuclein); 12427-38-2 (Maneb); 9007-43-6 (Cytochromes c); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE


  10 / 441 MEDLINE  
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[PMID]:27742361
[Au] Autor:Marques A; Rego A; Guilherme S; Gaivão I; Santos MA; Pacheco M
[Ad] Endereço:Department of Biology and CESAM, University of Aveiro, 3810-193 Aveiro, Portugal. Electronic address: anammarques@ua.pt.
[Ti] Título:Evidences of DNA and chromosomal damage induced by the mancozeb-based fungicide Mancozan in fish (Anguilla anguilla L.).
[So] Source:Pestic Biochem Physiol;133:52-58, 2016 Oct.
[Is] ISSN:1095-9939
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The formulation Mancozan , containing mancozeb as active ingredient, is among the most widely used fungicides. Although mancozeb has been detected in surface waters, studies addressing the genotoxic risk to fish arising from the use of this formulation, testing environmentally realistic concentrations, are absent from the literature. Hence, this work aimed to investigate the DNA and chromosome damaging potential of Mancozan (0.29 and 2.9µgL ) in the European eel (Anguilla anguilla L.), after a short-term exposure (3days), through the adoption of the comet and the erythrocytic nuclear abnormality (ENA) assays. In addition, it was intended to elucidate the subjacent damage mechanisms, improving the comet assay with the adoption of the endonucleases formamidopyrimidine DNA glycosylase (FPG) and endonuclease III (EndoIII), which detect oxidized bases. The highest Mancozan concentration was able to affect the DNA integrity (comet assay), while the adoption of endonucleases pointed out an oxidative cause to the damage. Regarding the chromosomal damage (ENA assay), both concentrations displayed significant effects, revealing the clastogenic and/or aneugenic properties of Mancozan . Furthermore, the two genotoxic endpoints were significantly correlated. Overall, the results revealed a genetic hazard to fish inhabiting aquatic systems contaminated by Mancozan and strongly recommend the development of biomonitoring and regulatory policies regarding the utilization of this agrochemical.
[Mh] Termos MeSH primário: Anguilla/genética
Dano ao DNA
Fungicidas Industriais/toxicidade
Maneb/toxicidade
Poluentes Químicos da Água/toxicidade
Zineb/toxicidade
[Mh] Termos MeSH secundário: Animais
Cromossomos/efeitos dos fármacos
Ensaio Cometa
DNA-Formamidopirimidina Glicosilase/metabolismo
Endodesoxirribonucleases/metabolismo
Eritrócitos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fungicides, Industrial); 0 (Water Pollutants, Chemical); 12427-38-2 (Maneb); EC 3.1.- (Endodeoxyribonucleases); EC 3.2.2.23 (DNA-Formamidopyrimidine Glycosylase); R0HY55EB9E (mancozeb); X1FSB1OZPT (Zineb)
[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:161016
[St] Status:MEDLINE



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