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Oliveira, Jennifer Kelly Silva de, Jociele Moreira de Carvalho, Camila Alexandre Silva, Mateus Barbosa de Lima, Paulo Matheus Freitas Cavalcante, and Daniel Felipe Fernandes Paiva. "Relação entre a exposição ao pesticida Rotenona e o desenvolvimento de sintomas motores e não-motores da doença de Parkinson." Research, Society and Development 9, no. 9 (September 4, 2020): e706997917. http://dx.doi.org/10.33448/rsd-v9i9.7917.
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Introdução: A doença de Parkinson (DP) é conhecida por seus sintomas motores debilitantes e pela dependência que sua progressão ocasiona. Apesar de clássica, essa condição ainda não possui seus fatores causais totalmente elucidados e, portanto, a predição se torna, por vezes, ineficaz. Na busca pela melhor compreensão da doença, pesquisadores encontraram uma íntima relação de sua sintomatologia com populações que tinham contato com o pesticida Rotenona, muito usada nos processos agrícolas e que pode ser fator auxiliar no desenvolvimento da enfermidade na população agrícola. Objetivo: Elucidar com base na literatura a interrelação da DP com a Rotenona. Metodologia: Revisão integrativa da literatura que utilizou os descritores: “Parkinson Disease”, “Rotenone”, “Synucleins”, “Gastrointestinal Tract”, “Vagus Nerve” e “Microbiota” nos buscadores: PubMed, ScienceDirect, SCIELO e BVS onde foram selecionados 13 documentos para análise que elucidavam em seu texto a relação entre a enfermidade com a substancia estudada. Resultados: Os trabalhos retratam uma íntima relação da exposição a Rotenona com os sintomas não-motores da DP. Ademais, tais sintomas acometem principalmente sinais no trato gastrointestinal que, por vezes, podem auxiliar na predição da doença muito antes da manifestação dos sintomas clássicos. Considerações Finais: A Rotenona possui relação bem elucidada no desenvolvimento da DP, ademais, tal relação possibilita uma melhor compreensão da conexão entre cérebro e trato gastrointestinal através do nervo vago. Assim, tais achados podem servir de base para uma melhor compreensão e prevenção do diagnóstico e tratamento da DP.
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Gómez-Chavarín, Margarita, Rosalinda Díaz-Pérez, Rosario Morales-Espinosa, Juan Fernández-Ruiz, Gabriel Roldán-Roldán, and Carlos Torner. "Efecto de la exposición al pesticida rotenona sobre el desarrollo del sistema dopaminérgico nigro-estriatal en ratas." Salud Mental 36, no. 1 (January 1, 2013): 1. http://dx.doi.org/10.17711/sm.0185-3325.2013.001.
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La rotenona es un pesticida utilizado en México a pesar de que se ha demostrado experimentalmente que produce una degeneración de las neuronas dopaminérgicas, y puede derivar en deterioro psicomotor. Sin embargo, no existen estudios de la exposición indirecta a rotenona a través de las madres en el efecto que produzca sobre su descendencia. Nosotros administramos rotenona a ratas durante la gestación y la lactancia para evaluar las alteraciones producidas sobre las neuronas dopaminérgicas y la coordinación motora de sus crias, a los 30 o 60 días posnatales. Para cuantificar las neuronas inmunorreactivas a tirosina hidroxilasa de la sustancia nigra, se inyectaron subcutaneamente seis grupos de hembras Wistar: intactas (control), con solvente de rotenona (vehículo) y cuatro grupos con rotenona en dosis: 0.2, 0.4, 0.6 y 1.0 mg/kg/dia. En un experimento paralelo, las crías de otros grupos de hembras tratadas con rotenona 1 mg/kg/dia o controles fueron evaluados en la prueba de coordinación motora a los 30 y 60 dias posnatales. Las madres tratadas con 1 mg/kg de rotenona tuvieron menos neuronas dopaminérgicas en la sustancia nigra. Dicho efecto se observo también en las crías, pero con todas las dosis de rotenona utilizadas, tanto a los 30 como a los 60 días posnatales. Además, la exposición indirecta a rotenona aumento significativamente el tiempo que requirieron las crías para ejecutar la prueba de coordinación motora. Estos datos indican que la rotenona es capaz de inducir daño en las neuronas dopaminérgicas de las crías cuando son expuestas a través de sus madres. Este efecto en las crías se observa con dosis menores de rotenona que en ratas adultas. Por lo tanto, los individuos indirectamente expuestos a rotenona podrían tener menos neuronas dopaminérgicas desde etapas tempranas de la vida, lo que aumenta el riesgo de desarrollar trastornos relacionados con el sistema dopaminérgico.
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COSTA, José Paulo Chaves da, Sérgio de Mello ALVES, and Muracy BÉLO. "Teores de rotenona em Clones de Timbó (Derris Spp. Fabaceae) de diferentes regiões da Amazônia e os seus efeitos na emergência de Imagos em Musca Domestica L." Acta Amazonica 29, no. 4 (December 1999): 563–73. http://dx.doi.org/10.1590/1809-43921999294573.
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A análise dos teores de rotenona, em clones de três espécies de timbó, permitiram a classificação destas plantas de acordo com as suas eficiências no controle de larvas de Musca domestica. Os resultados evidenciaram correlações significativas entre os teores de rotenona apresentados pelos clones de Derris urucu e de Derris nicou, com relação a capacidade de controle das larvas. As plantas com os maiores teores de rotenona foram as mais eficientes. O conteúdo de rotenona, os efeitos dos clones das espécies de Derris nas moscas, além dos locais de origem das plantas, mostraram que deve ter ocorrido entre estes timbós, a existência de isolamento populacional, durante a época do pleistoceno na Amazônia. Em Derris sp., que apresentou menor teor de rotenona, sendo ineficiente no controle das larvas, estas diferenças não foram assinaladas.
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Fajardo Vélez, Adriana Elizabeth, Joaquín Teodoro Morán Bajaña, Paulo Humberto Centanaro Quiroz, María Isabel Cartagena Faytong, Colon Eusebio Cruz Romero, and Pedro José Andrade Alvarado. "Efecto biocida del fruto del barbasco (Lonchocarpus nicou) en el control del caracol (Pomacea canaliculata) en el arroz en Naranjal-Ecuador." Pro Sciences 3, no. 20 (March 29, 2019): 1–4. http://dx.doi.org/10.29018/issn.2588-1000vol3iss20.2019pp1-4.
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La presente investigación tuvo como objetivo, evaluar el bioplaguicida de origen botánico en el control del caracol (Pomácea canaliculata) en el cultivo del arroz (Oryza sativa) en el cantón Naranjal, provincia del Guayas, se determinó la dosis de rotenona que mejor controló la presencia del caracol y se realizó económicamente la dosis de los tratamientos estudiados. La valoración estadística de los datos se realizó mediante el análisis de varianza, y los promedios de tratamientos se los realizó con la prueba de TUKEY, al 5% de probabilidad, en la variable promedios de número de macollos por planta, se observó una pareja puntuación tanto en (rotenona 60 ml y 120 ml en 20 litros de agua), siendo 31.50 m/p; en el control de masas de huevos por planta, se controló con las dosis (rotenona 80 ml a 120 ml en 20 litros de agua) con un promedio de 1 mh/p, que no difiere significativamente con el testigo absoluto; la población de ninfas y adultos obtenidos, que se observó mediante trampas, ayuda a controlar la presencia del caracol manzano.
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Spletozer, Aline Gonçalves, Cleiton Rosa dos Santos, Laura Araujo Sanches, and Juliana Garlet. "Plantas com potencial inseticida: enfoque em espécies amazônicas." Ciência Florestal 31, no. 2 (June 1, 2021): 974–97. http://dx.doi.org/10.5902/1980509832244.
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Um imenso potencial para a produção de compostos secundários e potencial inseticida vem sendo estudado dentro da ampla diversidade que a flora brasileira apresenta. Dessa forma, o presente estudo objetivou apresentar informações sobre o potencial das plantas no controle de insetos, através de uma revisão bibliográfica. Os primeiros inseticidas botânicos utilizados foram a nicotina, a piretrina, a rotenona, a sabadilla e a rianodina. A partir de então foram estudados vários compostos e espécies, como a azadiractina, extraída do nim, alcaloides das Anonaceaes, rotenona em Derris urucu, Piperaceae com as amidas, entre outros registros com as espécies amazônicas. Observa-se então que as espécies amazônicas compõem uma rica fonte de pesquisa e muitos dos exemplares estudados mostraram-se promissores para o desenvolvimento de inseticidas. Entretanto, novas pesquisas, principalmente em campo, devem ser realizadas para prospecção de novas espécies, buscando compostos seletivos e consequentemente com menor contaminação ambiental, para utilização tanto direta, quanto para o desenvolvimento de novos inseticidas comerciais.
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Azevedo, Francisco Roberto de, Maria Andréia Rodrigues de Moura, Silvério De Paiva Freitas Júnior, Tamiris Pereira da Silva, and Antônio Ismael Silva de Oliveira. "Ação de inseticidas vegetais associados a variedades de milho resistentes a Spodoptera frugiperda (Lepidoptera: Noctuidae) em campo." REVISTA AGRO@MBIENTE ON-LINE 7, no. 3 (December 31, 2013): 345. http://dx.doi.org/10.18227/1982-8470ragro.v7i3.1117.
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A cultura do milho (Zea mays L.) é extremamente rica em conhecimentos técnico-científicos, possuindo grande valor econômico e bom potencial para gerar renda a muitas famílias, principalmente a pequenos produtores. Objetivando avaliar a ação de inseticidas vegetais associados a variedades de milhos resistentes a Spodoptera frugiperda, realizaram-se duas pesquisas em condições de campo em Juazeiro do Norte. A condução da primeira pesquisa deu-se no período de18 de março a 07 de abril de 2011, com dezesseis variedades de milhos: Cateto Sete Lagoas Flint; Central MexDent; Maya; Catingueira; Asteca; BR 106; Composto Flint; Asteca Dent; Jose Lucena; Neuton Pequeno; Maria Firmino; Milho Pão; Armazém; José Geraldo; ACB Várzea Alegre e Francisco de Assis. Avaliaram-se os danos das lagartas baseados em uma escala visual de notas. Após detectar os milhos mais resistentes, realizou-se a segunda pesquisa no mesmo local, de 18 de maio a 01 de junho de 2011, submetendo-os a três aplicações semanais de Natuneem® (azadiractina) e Rotenat® (rotenona), utilizando-se a mesma escala de notas. A variedade José Lucena é mais resistente ao ataque da praga, enquanto que ACB Várzea Alegre e Francisco de Assis são as mais suscetíveis. As demais expressam resistência intermediária. A ação da azadiractina e rotenona associada a variedade José Lucena reduz os danos das lagartas de Spodoptera frugiperda em condições de campo.
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Jiménez, Erika V., Jennifer Tovar, Oscar M. Mosquera, and Fernando Cardozo. "Actividad neuroprotectora de Solanum ovalifolium (Solanaceae) contra la toxicidad inducida por rotenona en Drosophila melanogaster." Revista Facultad de Ciencias Básicas 13, no. 1 (February 7, 2017): 26–34. http://dx.doi.org/10.18359/rfcb.2751.
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Los objetivos de este trabajo fueron evidenciar la presencia de flavonoides en el extracto metanólico de Solanum ovalifolium por cromatografía líquida de alta eficiencia (HPLC-UV), analizar la actividad antioxidante por los métodos de 1,1-difenil-2-picrilhidrazilo (DPPH•) y ácido 2,2'-azinobis-(3-etilbenzotiazolina)-6-sulfónico (ABTS•+), cuantificar el glutatión (GSH), las unidades de enzima antioxidante superóxido dismutasa (SOD) y determinar el efecto neuroprotector contra la toxicidad inducida por rotenona (100 µM) con el modelo in vivo de Drosophila melanogaster mediante geotaxis negativa y cuantificación de la dopamina (DA) de las células cerebrales por (HPLC-UV). A través del perfil fitoquímico por cromatografía líquida de alta eficiencia (HPLC-UV) se evidenció un alto contenido de flavonoides, principalmente dihidroxiflavona (83.33%) y flavona-flavonol (16.66%), el extracto presentó una concentración media inhibitoria para los radicales DPPH• y ABTS•+de 179.8 µg/mL y 34.4 µg/mL respectivamente. En el extracto de S. ovalifolium a 1000 mg/L se cuantificó 4.28 nmol de GSH/ mL de extracto y 1.43 unidades SOD/mL del extracto. En la evaluación del efecto neuroprotector, las moscas macho variedad silvestre (75) co-expuestas a 7 días de tratamiento con el extracto metanólico de S. ovalifolium 0.1% presentaron un menor efecto tóxico y una protección completa contra el estrés oxidativo inducido por rotenona. El contenido de dopamina fue de 61-65 µg/L. Adicionalmente, este trabajo confirma la utilidad del modelo in vivo de D. melanogaster como una etapa en la evaluación de posibles medicamentos neuroprotectores.
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Jesus, F. G., L. A. de Paiva, V. C. Gonçalves, M. A. Marques, and A. L. Boiça Junior. "EFEITO DE PLANTAS INSETICIDAS NO COMPORTAMENTO E BIOLOGIA DE PLUTELLA XYLOSTELLA (LEPIDOPTERA: PLUTELLIDAE)." Arquivos do Instituto Biológico 78, no. 2 (June 2011): 279–85. http://dx.doi.org/10.1590/1808-1657v78p2792011.
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RESUMO Avaliou-se o efeito de Azadirachta indica A. Juss. (Nim), Sapindus saponaria L. (Sabão de soldado), Nim + Piretro + Rotenona, Dimorphandra mollis (Faveira) e Stryphnodendron adstringens (Mart) Coville (Barbatimão) em relação a não-preferência para oviposição e alimentação, atratividade e biologia de Plutella xylostella. Discos foliares de couve (Brassica oleracea var. acephala) cultivar Manteiga foram imersos em cada extrato à concentração de 10% (massa/volume) por 30 segundos para realização dos experimentos. Para o teste sem chance de escolha, os tratamentos que apresentaram menores atratividades foram os extratos de A. indica e D. mollis, e o menor consumo foi em A. indica. Os extratos de A. indica, S. saponaria D. mollis e S. adstringens proporcionaram efeito deterrente na oviposição de P. xylostella. Os tratamentos A. indica, S. saponaria e S. adstringens influênciaram negativamente os parâmetros biológicos da praga.
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Mascaro, U. C. P., L. A. Rodrigues, J. K. Bastos, E. Santos, and J. P. Chaves da Costa. "Valores de DL50 em peixes e no rato tratados com pó de raízes de Derris spp e suas implicações ecotoxicológicas." Pesquisa Veterinária Brasileira 18, no. 2 (April 1998): 53–56. http://dx.doi.org/10.1590/s0100-736x1998000200002.
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Os "timbós verdadeiros" (plantas do gênero Derris), originários da Amazônia Brasileira, tem demonstrado importância crescente por produzirem uma classe de compostos flavonoídicos relacionados à rotenona, que possuem atividade tóxica para peixes e mamíferos. Neste estudo foi determinado a dose letal 50% (DL50) do extrato alcoólico do pó de Derris spp para três espécies de peixes filogeneticamente diferentes e um mamífero roedor (rato). As DL50 de 2,6 microgramas/ml para Collosoma macropomum (tambaqui), 4,8 microgramas/ml para Oreochromis niloticus (tilápia), 14,2 microgramas/ml para Plecostomus sp (cascudo) e DL50 de 100,0 mg/kg para Rattus norvegicus (rato) denotam acentuadas diferenças entre os valores de DL50, principalmente entre os peixes e o rato. Isto possivelmente é devido a fatores farmaco-cinéticos que se relacionam com as diferentes barreiras teciduais encontradas pelos rotenóides quando administrados pela via oral em mamíferos.
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Zahara, Evi, Een Nuraenah, Tri Yuliyani, Darwitri Darwitri, Husnul Khotimah, Umi Kalsum, I. Wayan Arsana Wiyasa, Nurlaili Ramli, Agus Hendra Al Rahmad, and Mohammad Muljohadi Ali. "Ekstrak ethanol pegagan (Centella asiatica) meningkatkan osifikasi tulang dan panjang badan larva zebrafish (Danio rerio) model stunting usia 9 hari pasca fertilisasi." AcTion: Aceh Nutrition Journal 3, no. 2 (November 30, 2018): 95. http://dx.doi.org/10.30867/action.v3i2.87.
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Centella Asiatica (Linn) Urban is known as Gotu Kola. Centella Asiatica (CA) is rich in micro and macronutrients. The aim of this study was to investigate the effect of ethanol extract of CA on bone ossification and body length in zebrafish larva stunting model at 9 dpf. This study used zebrafish at 2 hpf (hour post-fertilization) - 9 dpf (day post-fertilization). The population of 300 larvae divided into 5 groups consisting of control group, rotenone group (exposed by 12.5 ppb of rotenone) and 3 rotenone+CA groups that exposed to CA extract for 4, 5 and 6 days, respectively. The CA extract was obtained by maceration method with ethanol solvent. The results showed that rotenone 12,5 ppb able to inhibit the growth of larvae >2SD of body length and decrease bone ossification at rotenone group, were significantly different from the control group. Administration of CA extract was increased expression of cartilage at rotenone+CA5 as well rotenone+CA6 group and increase expression of bone at the rotenone+CA5 group and also increase body length rotenone+CA groups significantly different from rotenone group. It can be concluded that the period of CA extract exposure can correct the length of the body reaching 99.6% at 9 dpf and increased bone ossification in a time-dependent manner.Centella asiatica (Linn) Urban dikenal dengan nama pegagan. Centella Asiatica (CA) kaya akan mikro maupun makro nutrisi yang diperlukan bagi tubuh terutama masa pertumbuhan. Penelitian ini bertujuan mengetahui efek ekstrak etanol CA terhadap osifikasi tulang dan panjang badan larva zebrafish model stunting yang diinduksi rotenone pada 9 hari post fertilisasi. Penelitian ini menggunakan zebrafish mulai 2 hpf (hour post fertilisation) - 9 dpf (day post fertilisation), populasi larva sejumlah 300 yang dibagi 5 kelompok yang terdiri dari kelompok kontrol, kelompok rotenon (dipapar rotenone 12,5 ppb) dan 3 kelompok rotenone+CA yang diberikan pegagan selama 4, 5 dan 6 hari secara berurutan. Ekstrak CA diperoleh melalui metode maserasi dengan pelarut etanol. Hasil penelitian menunjukkan bahwa rotenone dapat menghambat pertumbuhan panjang larva >2SD dan menurunkan osifikasi tulang pada kelompok rotenon secara signifikan dibanding kontrol. Pemberian ekstrak CA dapat meningkatkan ekspresi tulang rawan kelompok rotenone+CA5 maupun rotenone+CA6 dan meningkatkan ekspresi tulang keras kelompok rotenone+CA5 serta meningkatkan panjang badan kelompok rotenone_CA secara signifikan dibanding kelompok rotenone. Dapat disimpulkan bahwa lamanya pemberian ekstrak CA dapat meningkatkan osifikasi tulang dan meningkatkan panjang badan mencapai 99.6% pada 9 dpf.
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Catto, J. B., I. Bianchin, J. M. Santurio, G. L. D. Feijó, A. N. Kichel, and J. M. da Silva. "Sistema de pastejo, rotenona e controle de parasitas em bovinos cruzados: efeito no ganho de peso e no parasitismo." Revista Brasileira de Parasitologia Veterinária 18, no. 04 (2009): 37–43. http://dx.doi.org/10.4322/rbpv.01804007.
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Khotimah, Husnul, Darwitri Darwitri, Tri Yuliyani, Een Nuraenah, Evi Zahara, Umi Kalsum, Nurdiana Nurdiana, and Mohammad Muljohadi Ali. "Centella Asiatica Increased the Body Length Through the Modulation of Antioxidant in Rotenone-Induced Zebrafish Larvae." Biomedical and Pharmacology Journal 11, no. 2 (June 8, 2018): 827–33. http://dx.doi.org/10.13005/bpj/1438.
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Centella asiatica (CA) is herbal medicine that used as traditional medicine including ayurvedic theraphy since hundreds years ago. This herb containa of pentacyclic triterpenoids such as asiaticoside, madecassoside, Asiatic acid and brahmoside that proved had anti-oxidant and anti-inflammatory properties. This research aims to know the effect of ethanolic extract of CA extract against the length of rotenone-induced zebrafish larvae through the free radicals.mechanism. This research used zebrafish larvae until 6 dpf that consists of 5 groups (controls, rotenon 12.5 ppb on 2 hpf-3 dpf, and group treatment given rotenone 12.5 ppb 2 hpf-3 dpf and 5 µg/mL extract with long exposure to start 2 hpf to 4, 5 and 6 dpf respectively). The body length measured on 3-6 dpf using software Image Raster v 3.0 from optilab v 2.0. Malondialdehyde (MDA), superoxide Dismutase (SOD), catalase were measured by ELISA on 6 dpf. The results showed rotenon can inhibit the growth of length > 2 standard deviation (SD) and CA extract may increased ithe body in 6 dpf which correction value was 99.6%. CA extract significantly decreased the levels of MDA, and increased the level of SOD and catalase (p=0.000). Ethanol extract of Centella asiatica may increase in length through the modulation of oxidative stress.
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Mezzalira, Éder Júnior, André Luiz Piva, Gilmar Antônio Nava, Dalva Paulus, and Anderson Santin. "Controle da ferrugem e da broca-dos-ramos da figueira com diferentes fungicidas e inseticidas." Revista Ceres 62, no. 1 (February 2015): 44–51. http://dx.doi.org/10.1590/0034-737x201562010006.
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Temperaturas e precipitações elevadas favorecem a incidência da ferrugem (Cerotelium fici(Cast.)) e da broca-dos-ramos (Azochis gripusalis (Walker, 1859) (Lepidoptera: Pyralidae)), limitando a produção comercial de figos. O objetivo deste trabalho foi comparar a eficiência de fungicidas e inseticidas alternativos em relação à de produtos convencionais registrados para a cultura. Foram realizados dois experimentos, no delineamento de blocos inteiramente casualizados, com quatro repetições, no setor de fruticultura da Universidade Tecnológica Federal do Paraná, Campus Dois Vizinhos. Para controle da ferrugem, foram utilizados, em 100 L de água, azoxistrobin (10 g), calda bordalesa (1.500 g de cal virgem + 1.500 g de sulfato de cobre) e testemunha (água). No controle da broca-dos-ramos utilizaram-se, em 100 L de água, azadiractina (1.000 mL P.C.), alho (Allium sativum L.) (100 mL P.C.), cinza (20.000 g), extrato de fumo (nicotina) (10.000 mL do preparado), deltametrina (50 mL P.C.), Bacillus thuringiensis Berliner (100 g P.C.), rotenona (1.000 mL P.C.), sabão de coco (1.000 g) e testemunha (água). A calda bordalesa foi o tratamento mais efetivo no controle da ferrugem, promovendo aumento da produtividade e da qualidade dos frutos. A deltametrina promoveu o melhor controle da broca-dos-ramos da figueira. Entre os produtos alternativos testados, o alho foi o mais efetivo no controle dessa praga.
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Hebling-Beraldo, Maria J. A., and Regina C. Vicelli-Zanão. "Toxicidade de nicotina e rotenona e efeitos respiratórios em Atta laevigata (F. Smith , 1858) e Atta sexdens rubropilosa Forel, 1908 (Hymenoptera: Formicidae)." Anais da Sociedade Entomológica do Brasil 15, no. 2 (November 28, 1986): 219–29. http://dx.doi.org/10.37486/0301-8059.v15i2.423.
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Diéguez-Campa, Carlos, and Iván Pérez-Neri. "De los orígenes de la parálisis agitante al desarrollo de un modelo experimental para su estudio." Archivos de Neurociencias 22, no. 3 (September 1, 2017): 73–77. http://dx.doi.org/10.31157/archneurosciencesmex.v22i3.162.
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La importancia de mirar al pasado de la enfermedad de Parkinson (EP) radica en entender sus primeras descripciones y clasificación para dirigirnos hacia su tratamiento. En documentos de hace 4,000 años se encuentran signos clínicos de la enfermedad, en 1817 James Parkinson la caracterizó e integró como un trastorno neurológico llamándolo "parálisis agitante"; Martin Charcot completó su espectro sindrómico, en donde identificó la bradicinesia, discriminó los distintos tipos de temblor, signos no motores y sugirió el término "enfermedad de Parkinson". Brissaud propuso que el daño en la substantia nigra es la base anatómica de la EP. A partir de la comprensión de su fisiopatología y el desarrollo de modelos experimentales que logran mimetizar las características de la enfermedad, se ha logrado plantear estrategias de tratamiento. Existen distintos modelos con alcances y limitaciones, como la 6-hidroxidopamina, la 1-metil-4-fenil-1,2,3,6-tetrahidropiridina (MPTP), el paraquat y la rotenona. La MPTP fue descubierta por casualidad en usuarios de drogas intravenosas. Aun cuando ningún modelo reproduce completamente la enfermedad, por su fácil reproducibilidad, de signos motores y no motores, la presencia de cuerpos de Lewy y, sobre todo, por lesionar selectivamente a la substantia nigra, el modelo de la neurotoxina MPTP en monos se considera el estándar de oro, convirtiéndolo en un hallazgo fortuito y en una herramienta científica de gran valor.
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Alecio, Márcio Rodrigo, Murilo Fazolin, Rosalee Albuquerque Coelho Netto, Valdomiro Catani, Joelma Lima Vidal Estrela, Suziane Barros Alves, Raquel da Silva Correa, Romeu de Carvalho Andrade Neto, and Adriana Dantas Gonzaga. "Ação inseticida do extrato de Derris amazonica Killip para Cerotoma arcuatus Olivier (Coleoptera: Chrysomelidae." Acta Amazonica 40, no. 4 (December 2010): 719–28. http://dx.doi.org/10.1590/s0044-59672010000400012.
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A abundância e o potencial inseticida de Derris amazonica e a necessidade de controle de Cerotoma arcuatus Olivier (Coleoptera: Chrysomelidae) na cultura do feijão-caupi (Vigna unguiculata L. Walp) estimularam a realização desta pesquisa, que objetivou avaliar a ação inseticida do extrato de D. amazonica a adultos de C. arcuatus em condições de laboratório. Os bioensaios testaram as vias de intoxicação por ingestão de folhas contaminadas, contato com superfície contaminada e aplicação tópica, com delineamento experimental inteiramente casualizado, com quatro repetições. Os valores de mortalidade e consumo foliar dos insetos foram submetidos à análise de regressão, sendo utilizada a análise de Probit para determinação das CL50, da DL50 e dos TL50. O extrato de D. amazonica, contendo 3,7% de rotenona, foi tóxico para adultos de C. arcuatus via ingestão de folhas contaminadas (CL50=15,14 µL do extrato.mL-1 de água), superfície contaminada (CL50=0,45 µL do extrato.cm-2) e aplicação tópica (DL50=1,44 µL do extrato.g-1 do inseto). Mortalidades de adultos de C. arcuatus superiores a 80% e os menores tempos letais médios foram obtidos na concentração de 5% (v v-1) do extrato em todos os bioensaios. O consumo foliar de adultos de C. arcuatus foi inversamente proporcional a concentração do extrato quando expostos por via de ingestão foliar ou aplicação tópica, sendo inclusive observada inibição da alimentação dos indivíduos. O extrato de D. amazonica é tóxico para C. arcuatus e inibe a alimentação dos insetos a partir da concentração de 1% (v v-1).
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Ortega, Alfredo R., Nury Pérez-Hernández, and Pedro Joseph-Nathan. "Piscicartone, a Rotenoid From Piscidia carthagenensis." Natural Product Communications 14, no. 5 (May 2019): 1934578X1984979. http://dx.doi.org/10.1177/1934578x19849799.
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The bark of the roots of Piscidia carthagenensis afforded the known insecticides rotenone (1) and millettone (2), as well as the new rotenoid piscicartone (3). The structure of 3 followed from nuclear magnetic resonance studies, while its absolute configuration (AC) was determined by vibrational circular dichroism (VCD) measurements in comparison with discrete Fourier transform B3LYP/DGDZVPcalculated spectra using the Compare VOA software. In addition, the AC of 1 and 2 was verified using the same VCD methodology.
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Gonçalves, Alexandre Henrique Costa, Noély Dantas Araújo, Pablo Ferlon, Thazia Katianne de Oliveira Cunha, Milena Nunes Alves de Sousa, and Patrício Borges Maracajá. "Efeitos da apitoxina e da geleia real sobre o sistema nervoso central." Revista Brasileira de Educação e Saúde 8, no. 4 (October 1, 2018): 25. http://dx.doi.org/10.18378/rebes.v8i4.6322.
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Propôs-se avaliar os benefícios do veneno de abelha e a geleia real no sistema nervoso central. Foi realizada uma Revisão Integrativa da Literatura, selecionando artigos na base de dados Science Direct que abordassem o tema de pesquisa. Foram escolhidos artigos com informações relevantes de pesquisas realizadas entre os anos de 2012 a 2018 para a apresentação de dados e informações relacionados com o presente estudo. O uso do veneno de abelha pode atuar como adjuvante no tratamento para Parkinson, fornecendo efeito neuroprotetor. Acupuntura com veneno de abelha pode reduzir neuroinflamação e induzir recuperação na lesão de medula espinhal. Também, a terapia com veneno de abelha restaurou a neuroquímica do cérebro após administração de rotenona. Em longo prazo, a utilização da geleia real pode diminuir a concentração de GABA estriatal e hipotalâmica. Ainda, possui efeitos antiestresse e neuroprotetores sob condições de estresse. A geleia real fornece proteção suficiente contra os efeitos danosos da tartrazina na função e estrutura do tecido cerebral de filhotes de ratos. Também, seu uso resultou em melhorias na neurotransmissão em idades avançadas, trazendo benefícios à memória e o tratamento com geleia real diminuiu de maneira significativa o número de células apoptóticas induzidas por lesão na medula espinal. A partir dos resultados obtidos nesse presente estudo, constaram-se os principais benefícios do veneno de abelha e da geleia real para o sistema nervoso central, dentre os quais se destacam: adjuvante para o tratamento de Parkinson, melhora da memória em idades avançadas, redução significativa do número de células apoptóticas em lesões espinhais, como também normalizou marcadores neuroinflamatórios e apoptóticos.
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Vats, Sharad, and Preeti Mehra. "Insecticidal Active Rotenoids from Plant Parts and Callus Culture of Medicago sativa L. from a Semiarid Region of India (Rajasthan)." Current Bioactive Compounds 16, no. 6 (October 2, 2020): 937–41. http://dx.doi.org/10.2174/1573407215666190628145149.
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Background: Vector-borne diseases are quite prevalent globally and are one of the major causes of deaths due to infectious diseases. There is an availability of synthetic insecticides, however, their excessive and indiscriminate use have resulted in the emergence of resistant varieties of insects. Thus, a search for novel biopesticide has become inevitable. Methods: Rotenoids were isolated and identified from different parts of Medicago sativa L. This group of metabolites was also identified in the callus culture, and the rotenoid content was monitored during subculturing for a period of 10 months. Enhancement of the rotenoid content was evaluated by feeding precursors in a tissue culture medium. Results: Four rotenoids (elliptone, deguelin, rotenone and Dehydrorotenone) were identified, which were confirmed using spectral and chromatographic techniques. The maximum rotenoid content was found in the seeds (0.33±0.01%), followed by roots (0.31±0.01%) and minimum in the aerial parts (0.20±0.05%). A gradual decrease in the rotenoid content was observed with the ageing of subcultured tissue maintained for 10 months. The production of rotenoids was enhanced up to 2 folds in the callus culture using amino acids, Phenylalanine and Methionine as precursors as compared to the control. The LC50 value of the rotenoids was found to be 91 ppm and 162 ppm against disease vectors of malaria and Dracunculiasis, respectively. Conclusion: The study projects M. sativa as a novel source of biopesticide against the disease vectors of malaria and Dracunculiasis. The use of precursors to enhance the rotenoid content in vitro can be an effective venture from a commercial point of view.
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ALCANTARA-BOCANEGRA, Fernando, and Humberto GUERRA-FLORES. "ALGUNAS CONSIDERACIONES BIOLOGICAS DEL TUCUNARE, Cichla ocellaris Schneider." Folia Amazónica 1, no. 1-2 (January 1, 2006): 13. http://dx.doi.org/10.24841/fa.v1i1-2.93.
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Durante la ejecución del crucero 8508 (**) del BIC “Rosendo Melo”, se efectuaron registros de longitud, peso, grado de llenura del estómago y estadio de madurez sexual de 65 ejemplares de tucunaré, Cichla ocellaris Schneider, capturados en el área de la Reserva Nacional Pacaya-Samiria, por el método de remoción total con rotenona. La relación peso-longitud de la población estudiada responde a la ecuación W = aLn , siendo el crecimiento de tipo alométrico, de acuerdo a Rickér 3(1975), y diferencial para cada sexo a longitudes mayores de 32 cm. La distribución de frecuencias del factor de condición muestra que al estado adulto, los machos presentan una mejor condición que las hembras. El tamaño mínimo de primera maduración, determinado según SANTOS (1978) y VAZZOLER (1981), es hembras 36 cm. y machos 42 cm. El tamaño al cual el 100% de individuos alcanzan la madurez, determinado según los investigadores antes citados, es: hembras 44 cm. y machos 50 cm. Se observó una proporción de sexos de 2: 1 a favor de los machos, verificándose mediante el test del ji cuadrado, a un nivel de probabilidad mayor que 0.5. Sin embargo, la proporción observada puede ser también el resultado de un sesgo introducido en el muestreo. El 54% de la población muestreada presentó estómago vacío y el 31% estomago semi vacío, siendo el 15% restante semilleno y lleno. El 45% de la población muestreada presentó estadio de madurez sexual III o maduro y el 38% II o en maduración, perteneciendo el 17% restante al 1 o inmaduro. Palabras claves: Relación peso-longitud. Factor de condición.Tamaño mínimo de primera maduración. Tucunaré, Cichla ocellaris.
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Ingham, John L., Satoshi Tahara, Seiji Shibaki, and Junya Mizutani. "Isoflavonoids from the Root Bark of Piscidia erythrina and a Note on the Structure of Piscidone." Zeitschrift für Naturforschung C 44, no. 11-12 (December 1, 1989): 905–13. http://dx.doi.org/10.1515/znc-1989-11-1205.
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Abstract A methanolic extract of Piscidia erythrina root bark has been found to contain various isofla-vonoids including rotenone (rotenoid), lisetin (coum aronochrom one) and six known isoflavones (ichthynone, piscidone, piscerythrone, 2′-deoxypiscerythrone, 6′-prenylpiscerythrone and 3′,5′-diprenylgenistein). The extract additionally yielded three new 5-hydroxyisoflavones (piscery-thrinetin, 2′-hydroxypiscerythrinetin and isow ighteone) and a previously unreported coum arono chrom one (8-prenyl-lisetin). All four com pounds were identified using a com bination of spectro scopic (UV , MS, 1H NMR) and chemical methods. Although several other 5-hydroxyisoflavones were also isolated from the root bark extract, the quantities of each were sufficient only to permit their partial characterization. Structure 2 for piscidone has been confirmed by 1H NMR spectros copy.
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Redman, Zachary C., Joshua Wesolowski, and Patrick L. Tomco. "Photochemical Pathways of Rotenone and Deguelin Degradation: Implications for Rotenoid Attenuation and Persistence in High-Latitude Lakes." Environmental Science & Technology 55, no. 8 (March 16, 2021): 4974–83. http://dx.doi.org/10.1021/acs.est.1c00129.
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Miyazaki, Ikuko, Nami Isooka, Fuminori Imafuku, Jin Sun, Ryo Kikuoka, Chieko Furukawa, and Masato Asanuma. "Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson’s Disease." International Journal of Molecular Sciences 21, no. 9 (May 4, 2020): 3254. http://dx.doi.org/10.3390/ijms21093254.
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Epidemiological studies demonstrated that pesticide exposure, such as rotenone and paraquat, increases the risk of Parkinson’s disease (PD). Chronic systemic exposure to rotenone, a mitochondrial complex I inhibitor, could reproduce many features of PD. However, the adoption of the models is limiting because of variability in animal sensitivity and the inability of other investigators to consistently reproduce the PD neuropathology. In addition, most of rotenone models were produced in rats. Here, we tried to establish a high-reproducible rotenone model using C57BL/6J mice. The rotenone mouse model was produced by chronic systemic exposure to a low dose of rotenone (2.5 mg/kg/day) for 4 weeks by subcutaneous implantation of rotenone-filled osmotic mini pump. The rotenone-treated mice exhibited motor deficits assessed by open field, rotarod and cylinder test and gastrointestinal dysfunction. Rotenone treatment decreased the number of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) and lesioned nerve terminal in the striatum. In addition, we observed significant reduction of cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and the intestinal myenteric plexus. Moreover, α-synuclein was accumulated in neuronal soma in the SNpc, DMV and intestinal myenteric plexus in rotenone-treated mice. These data suggest that the low-dose rotenone mouse model could reproduce behavioral and central and peripheral neurodegenerative features of PD and be a useful model for investigation of PD pathogenesis.
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Terzi, Alpaslan, Mustafa Iraz, Semsettin Sahin, Atilla Ilhan, Nuri Idiz, and Ersin Fadillioglu. "Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue." Toxicology and Industrial Health 20, no. 6-10 (July 2004): 141–47. http://dx.doi.org/10.1191/0748233704th208oa.
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Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. This study was undertaken to determine whether rotenone-induced liver oxidant injury is prevented by erdosteine, a mucolytic agent showing antioxidant properties. There were four groups of Male Wistar Albino rats: group one was untreated as control; the other groups were treated with erdosteine (50 mg/kg per day, orally), rotenone (2.5 mg/mL once and 1 mL/kg per day for 60 days, i.p.) or rotenone plus erdosteine, respectively. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue P < 0.05). The rats treated with rotenone plus erdosteine produced a significant decrease in lipid peroxidation and XO activities in comparison with rotenone group PB / 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group PB / 0.05). There was no significant difference in nitric oxide (NO) level between groups. There were negative correlations between CAT activity and malondialdehyde (MDA) level (r= -0.934, P <0.05) with between CAT and SOD activities (r= -0.714, P <0.05), and a positive correlation between SOD activity and MDA level (r= 0.828, P <0.05) in rotenone group. In the rotenone plus erdosteine group, there was a negative correlation between XO activity and NO level in liver tissue (r= -0.833, P -0.05). In the light of these findings, erdosteine may be a protective agent for rotenone-induced liver oxidative injury in rats.
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Chen, Xiao-jun, Zhi-yuan Meng, Ya-jun Ren, Hao-tian Gu, and Chun-liang Lu. "Effects of ZnO Nanoparticle on Photo-Protection and Insecticidal Synergism of Rotenone." Journal of Agricultural Science 8, no. 2 (January 17, 2016): 38. http://dx.doi.org/10.5539/jas.v8n2p38.
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<p>Rotenone has an effective insecticidal activity. However, the photodegradation of rotenone under sunlight or UV (ultraviolet light) leads to negative effects on its insecticidal activity and persistence. This study examined the photo-protection of rotenone when exposed to UV combinated with various nanoparticles. The remaining concentration of rotenone was analyzed by LC-MS/MS (liquid chromatography-triple quadrupole tandem mass spectrometry) at particular intervals. It indicated that various nanoparticles had different effects and combination with ZnO nanoparticle provided remarkable degree of photo-protection of rotenone in UV radiation. In comparision with ZnO, SiO<sub>2 </sub>nanoparticle provided moderate degree of photo-protection of rotenone in UV radiation. In addition, TiO<sub>2</sub>, Fe<sub>2</sub>O<sub>3 </sub>and CuO nanoparticle exerted catalytic degradation effects on rotenone to a certain degree.The combination of rotenone and ZnO nanoparticle(4:1) increased the effciency of mortality to the highest compared with the same concentration of sole rotenone or ZnO nanoparticle treatment alone and their co-toxicity coefficient was 128.63. ZnO nanoparticle has good UV photo-protective properties and insecticidal synergism on rotenone. The application of this proposed method can provide significant and practical guidance for improving the photostability and insecticidal activity of rotenone as well as other biopesticides.</p>
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Zhang, Yu, Hui Guo, Xinyu Guo, Denfeng Ge, Yue Shi, Xiyu Lu, Jinli Lu, Juan Chen, Fei Ding, and Qi Zhang. "Involvement of Akt/mTOR in the Neurotoxicity of Rotenone-Induced Parkinson’s Disease Models." International Journal of Environmental Research and Public Health 16, no. 20 (October 10, 2019): 3811. http://dx.doi.org/10.3390/ijerph16203811.
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Rotenone has recently been widely used to establish Parkinson’s disease (PD) models to replicate the features of PD. However, the mechanisms involved in rotenone neurotoxicity have not been elucidated. The aim of the present study was to identify the neurotoxicity of rotenone through intraperitoneal injection in mice and to investigate the global changes of phosphorylation proteomic profiles in rotenone-injured SH-SY5Y cells through a label-free proteomic analysis using a PTMScan with LC–MS/MS. ICR (Institute of Cancer Research) mice were intraperitoneally injected with different dosages of rotenone (1 mg/kg/d or 3 mg/kg/d) daily for 21 consecutive days. Rotenone caused a dose-dependent decrease in locomotor activities and a decrease in the number of Nissl-positive and tyrosine hydroxylase (TH)-immunoreactive neurons in the substantia nigra pars compacta (SNpc). Here, 194 phosphopeptides on 174 proteins were detected in SH-SY5Y cells, and 37 phosphosites on 33 proteins displayed statistically significant changes in expression after rotenone injury. The downregulation of phosphorylated Akt and mTOR was further confirmed by western blot analysis. A specific Akt activator, SC79, could protect cell viability and induce autophagy in rotenone-injured SH-SY5Y cells. This study indicates the involvement of the Akt/mTOR (mammalian target of rapamycin) signaling pathway in rotenone-injured SH-SY5Y cells and provides molecular information for the neurotoxicity of rotenone.
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Toyoda, Hiroki, Ayano Katagiri, Takafumi Kato, and Hajime Sato. "Intranasal Administration of Rotenone Reduces GABAergic Inhibition in the Mouse Insular Cortex Leading to Impairment of LTD and Conditioned Taste Aversion Memory." International Journal of Molecular Sciences 22, no. 1 (December 29, 2020): 259. http://dx.doi.org/10.3390/ijms22010259.
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The pesticide rotenone inhibits mitochondrial complex I and is thought to cause neurological disorders such as Parkinson’s disease and cognitive disorders. However, little is known about the effects of rotenone on conditioned taste aversion memory. In the present study, we investigated whether intranasal administration of rotenone affects conditioned taste aversion memory in mice. We also examined how the intranasal administration of rotenone modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex that is critical for conditioned taste aversion memory. We found that the intranasal administration of rotenone impaired conditioned taste aversion memory to bitter taste. Regarding its cellular mechanisms, long-term depression (LTD) but not long-term potentiation (LTP) was impaired in rotenone-treated mice. Furthermore, spontaneous inhibitory synaptic currents and tonic GABA currents were decreased in layer V pyramidal neurons of rotenone-treated mice compared to the control mice. The impaired LTD observed in pyramidal neurons of rotenone-treated mice was restored by a GABAA receptor agonist muscimol. These results suggest that intranasal administration of rotenone decreases GABAergic synaptic transmission in layer V pyramidal neurons of the mouse insular cortex, the result of which leads to impairment of LTD and conditioned taste aversion memory.
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Miyazaki, Ikuko, Nami Isooka, Kouichi Wada, Ryo Kikuoka, Yoshihisa Kitamura, and Masato Asanuma. "Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice." Cells 8, no. 3 (March 7, 2019): 221. http://dx.doi.org/10.3390/cells8030221.
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Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian models, because the toxin induces PD-like pathology. Here, we examined the neuroprotective effects of CA and CGA against the rotenone-induced degeneration of central dopaminergic and peripheral enteric neurons. Male C57BL/6J mice were chronically administered rotenone (2.5 mg/kg/day), subcutaneously for four weeks. The animals were orally administered CA or CGA daily for 1 week before rotenone exposure and during the four weeks of rotenone treatment. Administrations of CA or CGA prevented rotenone-induced neurodegeneration of both nigral dopaminergic and intestinal enteric neurons. CA and CGA upregulated the antioxidative molecules, metallothionein (MT)-1,2, in striatal astrocytes of rotenone-injected mice. Primary cultured mesencephalic or enteric cells were pretreated with CA or CGA for 24 h, and then further co-treated with a low dose of rotenone (1–5 nM) for 48 h. The neuroprotective effects and MT upregulation induced by CA and CGA in vivo were reproduced in cultured cells. Our data indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus.
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Kline, David A., Garry R. Hanna, Carl B. Honaker, Gustav O. Kuhn, and C. William Jameson. "Preparation and Stability of Animal Feed Mixtures Dosed with Rotenone." Journal of AOAC INTERNATIONAL 69, no. 4 (July 1, 1986): 660–63. http://dx.doi.org/10.1093/jaoac/69.4.660.
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Abstract Studies at Midwest Research Institute for the National Toxicology Program show that rotenone/animal feed mixtures prepared by drymixing are more stable than mixtures produced by dosing the feed with alcoholic solutions of rotenone and then stripping the solvent. Also, recoveries of rotenone from the dry mix feeds are higher than those from feeds dosed by the solution method. A simplified analytical method from one previously reported for rotenone in feed is described.
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Ilesanmi, Omotayo B., Obade Efe, Temitope T. Odewale, Frances O. Atanu, Esther F. Adeogun, Afolabi C. Akinmoladun, and Tolulope M. Olaleye. "Reversal effect of Solanum dasyphyllum against rotenone-induced neurotoxicity." Current Issues in Pharmacy and Medical Sciences 33, no. 4 (December 1, 2020): 191–96. http://dx.doi.org/10.2478/cipms-2020-0034.
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Abstract We earlier reported the protective effect of Solanum dasyphyllum against cyanide neurotoxicity. In furtherance to this, we investigated the protective effect of S. dasyphyllum against rotenone, a chemical toxin that causes brain-related diseases. Mitochondria fraction obtained from the brain of male Wistar rats was incubated with various solvents (hexane, dichloromethane, ethylacetate, and methanol) extracts of S. dasyphyllum before rotenone exposure. Mitochondria respiratory enzymes (MRE) were evaluated along with markers of oxidative stress. The inhibition of MRE by rotenone was reversed by treatment with various fractions of S. dasyphyllum. The oxidative stress induced by rotenone was also reversed by fractions of S. dasyphyllum. In addition, the ethylacetate fraction of S. dasyphyllum was most potent against rotenone-induced neurotoxicity. In conclusion, S. dasyphyllum is rich in active phytochemicals that can prevent some neurotoxic effects of rotenone exposure. Further study can be done in an in vivo model to substantiate our results.
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Ameen, Angie M., Amany Y. Elkazaz, Hala M. F. Mohammad, and Bassant M. Barakat. "Anti-inflammatory and neuroprotective activity of boswellic acids in rotenone parkinsonian rats." Canadian Journal of Physiology and Pharmacology 95, no. 7 (July 2017): 819–29. http://dx.doi.org/10.1139/cjpp-2016-0158.
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There is evidence that inflammation and oxidative stress contribute to the neurodegenerative changes observed in Parkinson’s disease. Unfortunately, there is a lack of curative treatment for this debilitating movement disorder. Boswellic acids (BAs) are pentacyclic triterpene molecules of plant origin that have been utilized for treating many inflammatory conditions. The current study was conducted to explore the protective role of BAs against rotenone-induced experimental parkinsonism. Twenty-four rats were assigned to one of four treatment groups. The first two groups were a vehicle group (no rotenone) and a rotenone control group in which rats received rotenone (1 mg/kg) every 48 h. The next 2 groups received rotenone (1 mg/kg every 48 h) plus protective oral doses of BAs (125 or 250 mg/kg daily). Rats in the rotenone group showed motor dysfunction when tested in the open-field arena and cylinder and rotarod tests. Moreover, inflammatory markers increased, whereas the dopamine level was lower in the striata of rats in the rotenone group versus those in the vehicle group. BAs taken by rats with rotenone-induced parkinsonism showed enhanced general motor performance, reduced inflammatory markers, and increased striatal dopamine level and nigral tyrosine hydroxylase immunostaining. In conclusion, BAs are promising agents in slowing the progression of Parkinson’s disease if appropriate data become available about their safety and efficacy in humans.
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Chernivec, Ethan, Jacie Cooper, and Kari Naylor. "Exploring the Effect of Rotenone—A Known Inducer of Parkinson’s Disease—On Mitochondrial Dynamics in Dictyostelium discoideum." Cells 7, no. 11 (November 8, 2018): 201. http://dx.doi.org/10.3390/cells7110201.
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Current treatments for Parkinson’s disease (PD) only alleviate symptoms doing little to inhibit the onset and progression of the disease, thus we must research the mechanism of Parkinson’s. Rotenone is a known inducer of parkinsonian conditions in rats; we use rotenone to induce parkinsonian cellular conditions in Dictyostelium discoideum. In our model we primarily focus on mitochondrial dynamics. We found that rotenone disrupts the actin and microtubule cytoskeleton but mitochondrial morphology remains intact. Rotenone stimulates mitochondrial velocity while inhibiting mitochondrial fusion, increases reactive oxygen species (ROS) but has no effect on ATP levels. Antioxidants have been shown to decrease some PD symptoms thus we added ascorbic acid to our rotenone treated cells. Ascorbic acid administration suggests that rotenone effects may be specific to the disruption of the cytoskeleton rather than the increase in ROS. Our results imply that D. discoideum may be a valid cellular PD model and that the rotenone induced velocity increase and loss of fusion could prevent mitochondria from effectively providing energy and other mitochondrial products in high demand areas. The combination of these defects in mitochondrial dynamics and increased ROS could result in degeneration of neurons in PD.
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Ho, Dong Hwan, Daleum Nam, Mi Kyoung Seo, Sung Woo Park, Wongi Seol, and Ilhong Son. "LRRK2 Kinase Inhibitor Rejuvenates Oxidative Stress-Induced Cellular Senescence in Neuronal Cells." Oxidative Medicine and Cellular Longevity 2021 (July 8, 2021): 1–16. http://dx.doi.org/10.1155/2021/9969842.
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Background. Leucine-rich repeat kinase 2 (LRRK2) plays a critical role in the pathogenesis of Parkinson’s disease (PD). Aging is the most critical risk factor for the progression of PD. The correlation between aging and cellular senescence has been established. Cellular senescence is correlated with the dysregulation of the proteolytic pathway and mitochondrial dysfunction, which are also associated with the aggregation of α-synuclein (α-syn). Methods. Human dopaminergic neuron-like cells (differentiated SH-SY5Y cells) were treated with rotenone in the presence or absence of the LRRK2 kinase inhibitor GSK2578215A (GSK-KI) for 48 h. The markers of cellular senescence, including p53, p21Waf1/Cip1 (p21), β-galactosidase (β-gal), Rb phosphorylation, senescence-associated (SA) β-gal activity, and lysosomal activity, were examined. The dSH cells and rat primary cortical neurons were treated with α-syn fibrils 30 min before treatment with rotenone in the presence or absence of GSK-KI for 48 h. Mice were intraperitoneally injected with rotenone and MLi-2 (LRRK2 kinase inhibitor) once every two days for two weeks. Results. Rotenone upregulated LRRK2 phosphorylation and β-gal levels through the activation of the p53-p21 signaling axis and downregulated Rb phosphorylation. Additionally, rotenone upregulated SA β-gal activity, reactive oxygen species levels, and LRRK2 phosphorylation and inhibited lysosome activity. Rotenone-induced LRRK2 upregulation impaired the clearance of α-syn fibrils. Treatment with LRRK2 inhibitor mitigated rotenone-induced cellular senescence and α-syn accumulation. Conclusions. Rotenone-induced upregulation of LRRK2 kinase activity promoted cellular senescence, which enhanced α-syn accumulation. However, the administration of an LRRK2 kinase inhibitor rejuvenated rotenone-induced cellular senescence.
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Kweon, Gi-Ryang, Jeremy D. Marks, Robert Krencik, Eric H. Leung, Paul T. Schumacker, Keith Hyland, and Un Jung Kang. "Distinct Mechanisms of Neurodegeneration Induced by Chronic Complex I Inhibition in Dopaminergic and Non-dopaminergic Cells." Journal of Biological Chemistry 279, no. 50 (October 6, 2004): 51783–92. http://dx.doi.org/10.1074/jbc.m407336200.
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Chronic mitochondrial dysfunction, in particular of complex I, has been strongly implicated in the dopaminergic neurodegeneration in Parkinson's disease. To elucidate the mechanisms of chronic complex I disruption-induced neurodegeneration, we induced differentiation of immortalized midbrain dopaminergic (MN9D) and non-dopaminergic (MN9X) neuronal cells, to maintain them in culture without significant cell proliferation and compared their survivals following chronic exposure to nanomolar rotenone, an irreversible complex I inhibitor. Rotenone killed more dopaminergic MN9D cells than non-dopaminergic MN9X cells. Oxidative stress played an important role in rotenone-induced neurodegeneration of MN9X cells, but not MN9D cells: rotenone oxidatively modified proteins more in MN9X cells than in MN9D cells and antioxidants decreased rotenone toxicity only in MN9X cells. MN9X cells were also more sensitive to exogenous oxidants than MN9D cells. In contrast, disruption of bioenergetics played a more important role in MN9D cells: rotenone decreased mitochondrial membrane protential and ATP levels in MN9D cells more than in MN9X cells. Supplementation of cellular energy with a ketone body,d-β-hydroxybutyrate, decreased rotenone toxicity in MN9D cells, but not in MN9X cells. MN9D cells were also more susceptible to disruption of oxidative phosphorylation or glycolysis than MN9X cells. These findings indicate that, during chronic rotenone exposure, MN9D cells die primarily through mitochondrial energy disruption, whereas MN9X cells die primarily via oxidative stress. Thus, intrinsic properties of individual cell types play important roles in determining the predominant mechanism of complex I inhibition-induced neurodegeneration.
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Hou, Yi-Sheng, Jun-Jie Guan, Hai-Dong Xu, Feng Wu, Rui Sheng, and Zheng-Hong Qin. "Sestrin2 Protects Dopaminergic Cells against Rotenone Toxicity through AMPK-Dependent Autophagy Activation." Molecular and Cellular Biology 35, no. 16 (June 1, 2015): 2740–51. http://dx.doi.org/10.1128/mcb.00285-15.
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Dysfunction of the autophagy-lysosomal pathway (ALP) and the ubiquitin-proteasome system (UPS) was thought to be an important pathogenic mechanism in synuclein pathology and Parkinson's disease (PD). In the present study, we investigated the role of sestrin2 in autophagic degradation of α-synuclein and preservation of cell viability in a rotenone-induced cellular model of PD. We speculated that AMP-activated protein kinase (AMPK) was involved in regulation of autophagy and protection of dopaminergic cells against rotenone toxicity by sestrin2. The results showed that both the mRNA and protein levels of sestrin2 were increased in a TP53-dependent manner in Mes 23.5 cells after treatment with rotenone. Genetic knockdown of sestrin2 compromised the autophagy induction in response to rotenone, while overexpression of sestrin2 increased the basal autophagy activity. Sestrin2 presumably enhanced autophagy in an AMPK-dependent fashion, as sestrin2 overexpression activated AMPK, and genetic knockdown of AMPK abrogated autophagy induction by rotenone. Restoration of AMPK activity by metformin after sestrin2 knockdown recovered the autophagy activity. Sestrin2 overexpression ameliorated α-synuclein accumulation, inhibited caspase 3 activation, and reduced the cytotoxicity of rotenone. These results suggest that sestrin2 upregulation attempts to maintain autophagy activity and suppress rotenone cytotoxicity through activation of AMPK, and that sestrin2 exerts a protective effect on dopaminergic cells.
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Zhang, Qi, Jing Zhou, Mi Shen, Hui Xu, Shu Yu, Qiong Cheng, and Fei Ding. "Pyrroloquinoline Quinone Inhibits Rotenone-Induced Microglia Inflammation by Enhancing Autophagy." Molecules 25, no. 19 (September 23, 2020): 4359. http://dx.doi.org/10.3390/molecules25194359.
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Neuroinflammation is a feature common to neurodegenerative diseases, such as Parkinson’s disease (PD), which might be responsive to therapeutic intervention. Rotenone has been widely used to establish PD models by inducing mitochondrial dysfunction and inflammation. Our previous studies have reported that pyrroloquinoline quinone (PQQ), a naturally occurring redox cofactor, could prevent mitochondrial dysfunction in rotenone induced PD models by regulating mitochondrial functions. In the present study, we aimed to investigate the effect of PQQ on neuroinflammation and the mechanism involved. BV2 microglia cells were pre-treated with PQQ followed by rotenone incubation. The data showed that PQQ did not affect the cell viability of BV2 cells treated with rotenone, while the conditioned medium (CM) of BV2 cells pre-treated with PQQ significantly increased cell viability of SH-SY5Y cells. In rotenone-treated BV2 cells, PQQ dose-dependently decreased lactate dehydrogenase (LDH) release and suppressed the up-regulation of pro-inflammation factors, such as interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in the cultured media, as well as nitric oxide (NO) release induced by rotenone. PQQ pretreatment also increased the ratio of LC3-II/LC3-I and expression of Atg5 in BV2 cells stimulated with rotenone. Additionally, the autophagosome observed by transmission electron microscopy (TEM) and co-localization of mitochondria with lysosomes indicated that mitophagy was induced by PQQ in rotenone-injured BV2 cells, and the PINK1/parkin mediated mitophagy pathway was regulated by PQQ. Further, autophagy inhibitor, 3-methyladenine (3-MA), partially abolished the neuroprotective effect of PQQ and attenuated the inhibition of inflammation with PQQ pretreatment. Taken together, our data extend our understanding of the neuroprotective effect of PQQ against rotenone-induced injury and provide evidence that autophagy enhancement might be a novel therapeutic strategy for PD treatment.
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Chen, Peng, Youcui Wang, Leilei Chen, Ning Song, and Junxia Xie. "Apelin-13 Protects Dopaminergic Neurons against Rotenone—Induced Neurotoxicity through the AMPK/mTOR/ULK-1 Mediated Autophagy Activation." International Journal of Molecular Sciences 21, no. 21 (November 8, 2020): 8376. http://dx.doi.org/10.3390/ijms21218376.
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Parkinson’s disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Several brain–gut peptides are able to exert neuroprotective effects on the nigrostriatal dopaminergic system. Apelin-13 is a neuropeptide, conveying potential neuroprotective activities. However, whether, and how, apelin-13 could antagonize rotenone-induced neurotoxicity has not yet been elucidated. In the present study, rotenone-treated SH-SY5Y cells and rats were used to clarify whether apelin-13 has protective effects on dopaminergic neurons, both in vivo and in vitro. The results showed that apelin-13 could protect SH-SY5Y cells from rotenone-induced injury and apoptosis. Apelin-13 was able to activate autophagy, and restore rotenone induced autophagy impairment in SH-SY5Y cells, which could be blocked by the autophagy inhibitor 3-Methyladenine. Apelin-13 activated AMPK/mTOR/ULK-1 signaling, AMPKα inhibitor compound C, as well as apelin receptor blockage via siRNA, which could block apelin-13-induced signaling activation, autophagy activation, and protective effects, in rotenone-treated SH-SY5Y cells. These results indicated that apelin-13 exerted neuroprotective properties against rotenone by stimulating AMPK/mTOR/ULK-1 signaling-mediated autophagy via the apelin receptor. We also observed that intracerebroventricular injection of apelin-13 could alleviate nigrostriatal dopaminergic neuron degeneration in rotenone-treated rats. Our findings provide new insights into the mechanism by which apelin-13 might attenuate neurotoxicity in PD.
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Dosumu, O. O., E. N. Akang, O. K. Idowu, and G. J. Adeyemi. "Virgin Coconut (Cocos nucifera) Oil Attenuates Rotenone-Induced Toxicity in Fruit Flies (Drosophila melanogaster)." Journal of Basic and Social Pharmacy Research 2, no. 1 (2021): 26–37. http://dx.doi.org/10.52968/27458357.
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Background: Parkinson's disease (PD) is a multifactorial neurodegenerative disease with pathogenic mechanisms traceable to oxidative damage and mitochondrial dysfunction. Rotenone, a chemical compound commonly found in pesticides, has been found to inhibit mitochondrial complex-I and initiate PD-like symptoms in mammals and several invertebrates. Virgin Coconut Oil (VCNO) obtained from the coconut fruit has been found to possess anti-oxidative and anti-inflammatory properties. Objectives: The present study evaluated the effect of VCNO on rotenone-induced Parkinsonism in fruit flies- Drosophila melanogaster (D. melanogaster). Methods: Canton special (CS) strains of D. melanogaster, aged between 1 to 3 days were orally exposed for 7 days to 0, 250, 500 and 750 μM rotenone diet for toxicity assay, and 0, 2.5, 5 and 10 % w/w VCNO diet for longevity assay. Thereafter, 5 % VCNO diet was selected for evaluation against 500 μM rotenone. Subsequently, behavioural test (negative geotaxis), markers for redox status and enzyme activities were evaluated. Results: The results showed that rotenone induced toxicity in the flies, while VCNO increased the lifespan of D. melanogaster in a dose-dependent manner. In addition, VCNO ameliorated rotenone-induced locomotor deficits, elevated MDA, as well as the depleted GSH levels. It also mitigated the inhibited activities of SOD, CAT and ATPase in the flies. Conclusions: VCNO protected D. melanogaster against rotenone-induced toxicity by extending longevity, preventing locomotor deficits and reducing oxidative stress.
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Othman, Zetty Shafiqa, Nur Hasyareeda Hassan, and Saiful Irwan Zubairi. "Response Surface Optimization of Rotenone Using Natural Alcohol-Based Deep Eutectic Solvent as Additive in the Extraction Medium Cocktail." Journal of Chemistry 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/9434168.
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Rotenone is a biopesticide with an amazing effect on aquatic life and insect pests. In Asia, it can be isolated from Derris species roots (Derris elliptica and Derris malaccensis). The previous study revealed the comparable efficiency of alcohol-based deep eutectic solvent (DES) in extracting a high yield of rotenone (isoflavonoid) to binary ionic liquid solvent system ([BMIM]OTf) and organic solvent (acetone). Therefore, this study intends to analyze the optimum parameters (solvent ratio, extraction time, and agitation rate) in extracting the highest yield of rotenone extract at a much lower cost and in a more environmental friendly method by using response surface methodology (RSM) based on central composite rotatable design (CCRD). By using RSM, linear polynomial equations were obtained for predicting the concentration and yield of rotenone extracted. The verification experiment confirmed the validity of both of the predicted models. The results revealed that the optimum conditions for solvent ratio, extraction time, and agitation rate were 2 : 8 (DES : acetonitrile), 19.34 hours, and 199.32 rpm, respectively. At the optimum condition of the rotenone extraction process using DES binary solvent system, this resulted in a 3.5-fold increase in a rotenone concentration of 0.49 ± 0.07 mg/ml and yield of 0.35 ± 0.06 (%, w/w) as compared to the control extract (acetonitrile only). In fact, the rotenone concentration and yield were significantly influenced by binary solvent ratio and extraction time (P<0.05) but not by means of agitation rate. For that reason, the optimal extraction condition using alcohol-based deep eutectic solvent (DES) as a green additive in the extraction medium cocktail has increased the potential of enhancing the rotenone concentration and yield extracted.
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Choi, Ji Hee, Hye-Im Woo, Ye-Ji Jeong, Hyun Ho Noh, Kee Sung Kyung, Doo-Ho Kim, Min-Kyung Paik, and Ae Son Om. "Risk Assessment of the Exposure to Rotenone in Lettuce and Cucumber." Korean Journal of Pesticide Science 17, no. 4 (December 31, 2013): 302–6. http://dx.doi.org/10.7585/kjps.2013.17.4.302.
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Alegre-Cortés, Eva, Alicia Muriel-González, Saray Canales-Cortés, Elisabet Uribe-Carretero, Guadalupe Martínez-Chacón, Ana Aiastui, Adolfo López de Munain, et al. "Toxicity of Necrostatin-1 in Parkinson’s Disease Models." Antioxidants 9, no. 6 (June 15, 2020): 524. http://dx.doi.org/10.3390/antiox9060524.
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Parkinson’s disease (PD) is a neurodegenerative disorder that is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. This neuronal loss, inherent to age, is related to exposure to environmental toxins and/or a genetic predisposition. PD-induced cell death has been studied thoroughly, but its characterization remains elusive. To date, several types of cell death, including apoptosis, autophagy-induced cell death, and necrosis, have been implicated in PD progression. In this study, we evaluated necroptosis, which is a programmed type of necrosis, in primary fibroblasts from PD patients with and without the G2019S leucine-rich repeat kinase 2 (LRRK2) mutation and in rotenone-treated cells (SH-SY5Y and fibroblasts). The results showed that programmed necrosis was not activated in the cells of PD patients, but it was activated in cells exposed to rotenone. Necrostatin-1 (Nec-1), an inhibitor of the necroptosis pathway, prevented rotenone-induced necroptosis in PD models. However, Nec-1 affected mitochondrial morphology and failed to protect mitochondria against rotenone toxicity. Therefore, despite the inhibition of rotenone-mediated necroptosis, PD models were susceptible to the effects of both Nec-1 and rotenone.
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Dhanalakshmi, Chinnasamy, Thamilarasan Manivasagam, Jagatheesan Nataraj, Arokiasamy Justin Thenmozhi, and Musthafa Mohamed Essa. "Neurosupportive Role of Vanillin, a Natural Phenolic Compound, on Rotenone Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/626028.
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Vanillin, a phenolic compound, has been reported to offer neuroprotection against experimental Huntington’s disease and global ischemia by virtue of its antioxidant, anti-inflammatory, and antiapoptotic properties. The present study aims to elucidate the underlying neuroprotective mechanism of vanillin in rotenone induced neurotoxicity. Cell viability was assessed by exposing SH-SY5Y cells to various concentrations of rotenone (5–200 nM) for 24 h. The therapeutic effectiveness of vanillin against rotenone was measured by pretreatment of vanillin at various concentrations (5–200 nM) and then incubation with rotenone (100 nM). Using effective dose of vanillin (100 nM), mitochondrial membrane potential, levels of reactive oxygen species (ROS), and expression patterns of apoptotic markers were assessed. Toxicity of rotenone was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, release of cyt-c, and enhanced expressions of proapoptotic and downregulation of antiapoptotic indices via the upregulation of p38 and JNK-MAPK pathway proteins. Our results indicated that the pretreatment of vanillin attenuated rotenone induced mitochondrial dysfunction, oxidative stress, and apoptosis. Thus, vanillin may serve as a potent therapeutic agent in the future by virtue of its multiple pharmacological properties in the treatment of neurodegenerative diseases including PD.
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Bushway, Rodney J., Harold Johnson, and Donald W. Scott. "Simultaneous Liquid Chromatographic Determination of Rotenone and Pyrethrins in Formulations." Journal of AOAC INTERNATIONAL 68, no. 3 (May 1, 1985): 580–82. http://dx.doi.org/10.1093/jaoac/68.3.580.
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Abstract This paper describes a reverse phase liquid chromatographic (LC) method to simultaneously determine rotenone and pyrethrins in pesticide formulations. The mixed standards along with the formulations were accurately weighed to contain approximately 200 (μg rotenone and 150 (μg pyrethrins/mL. Stabilized tetrahydrofuran was used to dissolve all substances. An aliquot was injected into the LC system equipped with a Zorbax ODS column, and chromatographed with a mobile phase of acetonitrile-water (70 + 30). Rotenone and the pyrethrins were monitored at 240 nm and 0.4 AUFS. Retention times for rotenone, pyrethrin II, and pyrethrin I were approximately 7, 11.5, and 25.5 min, respectively. For 3 different formulations analyzed 6 times each, the percent coefficients of variation were all < 3. This method is also applicable to products containing either rotenone or pyrethrins. No significant interferences were observed from the inactive ingredients of the formulations at the concentrations added.
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Jayaraj, Richard L., Rami Beiram, Sheikh Azimullah, Nagoor Meeran MF, Shreesh K. Ojha, Abdu Adem, and Fakhreya Yousuf Jalal. "Valeric Acid Protects Dopaminergic Neurons by Suppressing Oxidative Stress, Neuroinflammation and Modulating Autophagy Pathways." International Journal of Molecular Sciences 21, no. 20 (October 16, 2020): 7670. http://dx.doi.org/10.3390/ijms21207670.
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Parkinson’s disease, the second common neurodegenerative disease is clinically characterized by degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) with upregulation of neuroinflammatory markers and oxidative stress. Autophagy lysosome pathway (ALP) plays a major role in degradation of damaged organelles and proteins for energy balance and intracellular homeostasis. However, dysfunction of ALP results in impairment of α-synuclein clearance which hastens dopaminergic neurons loss. In this study, we wanted to understand the neuroprotective efficacy of Val in rotenone induced PD rat model. Animals received intraperitoneal injections (2.5 mg/kg) of rotenone daily followed by Val (40 mg/kg, i.p) for four weeks. Valeric acid, a straight chain alkyl carboxylic acid found naturally in Valeriana officianilis have been used in the treatment of neurological disorders. However, their neuroprotective efficacy has not yet been studied. In our study, we found that Val prevented rotenone induced upregulation of pro-inflammatory cytokine oxidative stress, and α-synuclein expression with subsequent increase in vital antioxidant enzymes. Moreover, Val mitigated rotenone induced hyperactivation of microglia and astrocytes. These protective mechanisms prevented rotenone induced dopaminergic neuron loss in SNpc and neuronal fibers in the striatum. Additionally, Val treatment prevented rotenone blocked mTOR-mediated p70S6K pathway as well as apoptosis. Moreover, Val prevented rotenone mediated autophagic vacuole accumulation and increased lysosomal degradation. Hence, Val could be further developed as a potential therapeutic candidate for treatment of PD.
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K., Srimathi Priyanga, Vijayalakshmi K., and Selvaraj R. "BEHAVIORAL STUDIES OF WISTAR RATS IN ROTENONE INDUCED MODEL OF PARKINSON’S DISEASE." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 10 (November 1, 2017): 159. http://dx.doi.org/10.22159/ijpps.2017v9i11.21465.
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Objective: The objective of the study was to determine the behavioral activities of Wistar rats induced with rotenone. Methods: Thirty-six male Wistar rats were taken for the study and divided into six groups of six rats each. Group-I is the vehicle-treated, Group–II animals were induced with rotenone (3 mg/kg/bwt) by i. p. Group-III were co-treated with rotenone and L-DOPA (10 mg/kg/bwt) orally, Group-IV were co-treated with rotenone and quercetin (25 mg/kg/bwt) orally, Group-V were co-treated with rotenone and hesperidin (50 mg/kg/bwt) orally, Group-VI were treated with rotenone, quercetin and hesperidin in the same dosage regime for 60 d. The behavioural tests, such as open field test, ladder climbing test and hanging wire test were performed. The biochemical parameters such as urea, creatinine and activities of ALT and AST were also analysed.Results: All data are expressed as the mean±SD. Disability was noted in the behaviour of rats induced with Parkinson’s disease (PD). The deficits in behavioral activity were significantly changed when compared with an induced group (p<0.001) and biochemical parameters due to rotenone were significantly (p<0.001) restored by co-treatment with quercetin and hesperidin.Conclusion: In our in vivo study, we have demonstrated the combination of quercetin and hesperidin to serve as neuroprotective compounds by improving the behavioral abnormalities and restoring the biochemical parameters. Hence, these powerful antioxidants may protect brain cells.
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Shiga, Hideaki, Hiroshi Wakabayashi, Kohshin Washiyama, Tomohiro Noguchi, Tomo Hiromasa, Sadaharu Miyazono, Masami Kumai, et al. "Thallium-201 Imaging in Intact Olfactory Sensory Neurons with Reduced Pre-Synaptic Inhibition In Vivo." Molecular Neurobiology 57, no. 12 (August 20, 2020): 4989–99. http://dx.doi.org/10.1007/s12035-020-02078-y.
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Abstract In this study, we determined whether the 201Tl (thallium-201)-based olfactory imaging is affected if olfactory sensory neurons received reduced pre-synaptic inhibition signals from dopaminergic interneurons in the olfactory bulb in vivo. The thallium-201 migration rate to the olfactory bulb and the number of action potentials of olfactory sensory neurons were assessed 3 h following left side nasal administration of rotenone, a mitochondrial respiratory chain complex I inhibitor that decreases the number of dopaminergic interneurons without damaging the olfactory sensory neurons in the olfactory bulb, in mice (6–7 animals per group). The migration rate of thallium-201 to the olfactory bulb was significantly increased following intranasal administration of thallium-201 and rotenone (10 μg rotenone, p = 0.0012; 20 μg rotenone, p = 0.0012), compared with that in control mice. The number of action potentials was significantly reduced in the olfactory sensory neurons in the rotenone treated side of 20 μg rotenone-treated mice, compared with that in control mice (p = 0.0029). The migration rate of thallium-201 to the olfactory bulb assessed with SPECT-CT was significantly increased in rats 24 h after the left intranasal administration of thallium-201 and 100 μg rotenone, compared with that in control rats (p = 0.008, 5 rats per group). Our results suggest that thallium-201 migration to the olfactory bulb is increased in intact olfactory sensory neurons with reduced pre-synaptic inhibition from dopaminergic interneurons in olfactory bulb glomeruli.
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Radad, Khaled, Rudolf Moldzio, and Wolf-Dieter Rausch. "Minocycline Protects Dopaminergic Neurons Against Long-Term Rotenone Toxicity." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 37, no. 1 (January 2010): 81–85. http://dx.doi.org/10.1017/s0317167100009690.
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Background:In Parkinson's disease, most of current therapies only provide symptomatic treatment and so far there is no drug which directly affects the disease process.Objectives:To investigate the neuroprotective effects of minocycline against long-term rotenone toxicity in primary dopaminergic cell cultures.Methods:Embryonic mice of 14-days-old were used for preparation of primary dopaminergic cell cultures. On the 6th day in vitro, prepared cultures were treated both with minocycline alone (1, 5, 10 and 20 μM) and concomitantly with rotenone (5 and 20 nM) and minocycline. Cultures were incubated at 37°C for six consecutive days. On Day 12 in vitro culture medium was aspirated and used for measuring lactate dehydrogenase. Cultured cells were fixed in 4% paraformaldhyde and stained immunohistochemically against tyrosine hydroxylase.Results:Treatment of cultures with 5 and 20 nM of rotenone significantly decreased the survival of tyrosine hydroxylase immunoreactive neurons by 27 and 31% and increased the release of lactate dehydrogenase into the culture medium by 31 and 236%, respectively compared to untreated controls. Minocycline (1, 5, 10 μM) significantly protected tyrosine hydroxylase immunoreactive neurons by 17, 15 and 19% and 13, 22 and 23% against 5 and 20 nM of rotenone, respectively compared to rotenone-treated cultures. Minocycline (only at 10 μM) significantly decreased the release of lactate dehydrogenase by 79% and 133% against 5 and 20 nM of rotenone, respectively.Conclusion:Minocycline has neuroprotective potential against the progressive loss of tyrosine hydroxylase immunoreactive neurons induced by long-term rotenone toxicity in primary dopaminergic cultures.
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Ochi, Rikuo, Vidhi Dhagia, Anand Lakhkar, Dhara Patel, Michael S. Wolin, and Sachin A. Gupte. "Rotenone-stimulated superoxide release from mitochondrial complex I acutely augments L-type Ca2+ current in A7r5 aortic smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 9 (May 1, 2016): H1118—H1128. http://dx.doi.org/10.1152/ajpheart.00889.2015.
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Voltage-gated L-type Ca2+ current ( ICa,L) induces contraction of arterial smooth muscle cells (ASMCs), and ICa,L is increased by H2O2 in ASMCs. Superoxide released from the mitochondrial respiratory chain (MRC) is dismutated to H2O2. We studied whether superoxide per se acutely modulates ICa,L in ASMCs using cultured A7r5 cells derived from rat aorta. Rotenone is a toxin that inhibits complex I of the MRC and increases mitochondrial superoxide release. The superoxide content of mitochondria was estimated using mitochondrial-specific MitoSOX and HPLC methods, and was shown to be increased by a brief exposure to 10 μM rotenone. ICa,L was recorded with 5 mM BAPTA in the pipette solution. Rotenone administration (10 nM to 10 μM) resulted in a greater ICa,L increase in a dose-dependent manner to a maximum of 22.1% at 10 μM for 1 min, which gradually decreased to 9% after 5 min. The rotenone-induced ICa,L increase was associated with a shift in the current-voltage relationship ( I-V) to a hyperpolarizing direction. DTT administration resulted in a 17.9% increase in ICa,L without a negative shift in I–V, and rotenone produced an additional increase with a shift. H2O2 (0.3 mM) inhibited ICa,L by 13%, and additional rotenone induced an increase with a negative shift. Sustained treatment with Tempol (4-hydroxy tempo) led to a significant ICa,L increase but it inhibited the rotenone-induced increase. Staurosporine, a broad-spectrum protein kinase inhibitor, partially inhibited ICa,L and completely suppressed the rotenone-induced increase. Superoxide released from mitochondria affected protein kinases and resulted in stronger ICa,L preceding its dismutation to H2O2. The removal of nitric oxide is a likely mechanism for the increase in ICa,L.
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Kumar, Sachin, and Puneet Kumar. "The Beneficial Effect of Rice Bran Extract Against Rotenone-Induced Experimental Parkinson’s Disease in Rats." Current Molecular Pharmacology 14, no. 3 (August 16, 2021): 428–38. http://dx.doi.org/10.2174/1874467214666210126113324.
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Background: Neurodegenerative diseases have become an increasing cause of various disabilities worldwide, followed by aging, including Parkinson’s disease (PD). Parkinson’s disease is a degenerative brain disorder distinguished by growing motor & non-motor failure due to the degeneration of medium-sized spiked neurons in the striatum region. Rotenone is often employed to originate the animal model of PD. It is a powerful blocker of mitochondrial complex-I, mitochondrial electron transport chain that reliably produces Parkinsonism-like symptoms in rats. Rice bran (RB) is very rich in polyunsaturated fatty acids (PUFA) and nutritionally beneficial compounds, such as γ-oryzanol, tocopherols, and tocotrienols and sterols are believed to have favorable outcomes on oxidative stress & mitochondrial function. Objective: The present study has been designed to explore RB extract’s effect against rotenone-induced neurotoxicity in rats. Methods: In the present study, Rotenone (2 mg/kg, s.c) was administered systemically for 28 days. The hexane extract of RB was prepared using Soxhlation. Hexane extract (250 & 500 mg/kg) was administered per oral for 28 days in rotenone-treated groups. Behavioral parameters (grip strength, motor coordination, locomotion, and catalepsy) were conducted on the 7th, 14th, 21st, and 28th day. Animals were sacrificed on the 29th day for biochemical estimation in the striatum and cortex. Result: This study demonstrates significant alteration in behavioral parameters, oxidative burden (increased lipid peroxidation, nitrite concentration, and decreased glutathione, catalase, SOD) in rotenone-treated animals. Administration of hexane extract of RB prevented the behavioral, biochemical alterations induced by rotenone. The current research has been sketched to inspect RB extract’s effect against rotenone-developed neurotoxicity in rats. Conclusion: The findings support that PD is associated with impairments in motor activity. The results also suggest that the nutraceutical rice bran that contains γ-oryzanol, Vitamin-E, ferulic acid etc., may underlie the adjuvant susceptibility towards rotenone-induced PD in experimental rats.
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Yang, Shi-Ping, Xi-Bin Yu, Ji-Guang Huang, and Han-Hong Xu. "Rotenone α-oxime." Acta Crystallographica Section C Crystal Structure Communications 59, no. 7 (June 20, 2003): o392—o393. http://dx.doi.org/10.1107/s010827010301117x.
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