Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro

Little is known about the effects of As on the nervous system. To investigate whether As induces neurotoxicity and influences the oxidative stress in brain, different As exposure models where studied. Thus, active specie production, antioxidant consumption and oxidative stress ratios (known as damag...

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Autor principal: Bonetto, Julián Gerardo
Otros Autores: Villaamil Lepori, Edda
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: Facultad de Farmacia y Bioquímica 2019
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Acceso en línea:http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_5912
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_5912.dir/5912.PDF
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spelling I28-R145-HWA_59122022-04-06 Little is known about the effects of As on the nervous system. To investigate whether As induces neurotoxicity and influences the oxidative stress in brain, different As exposure models where studied. Thus, active specie production, antioxidant consumption and oxidative stress ratios (known as damage/protection in the hydrophilic and lipophilic cellular environment) where evaluated. The oxidation rate of the 2',7'-Dichlorodihydrofluorescein, a fluorescent probe used for detection of the generation of reactive oxygen species, was not affected by As exposure in any studied model. In the ex vivo model brain homogenates were exposure to As, and the lipophilic oxidative stress ratio was significantly increased in As-treated animals as compared to control homogenates, with a significant decrease in the content of glutathione (GSH). In the in vivo model of acute As treatment the same responses were observed in the lipophilic media and in the magnitude of the GSH consumption. Moreover, the acute exposure to As lead to a significant increase in NO production and protein nitration content. In the in vivo model of chronic As treatment the lipophilic oxidative stress ratio was increased, and GSH and ?-tocopherol consumption was observed. The data suggested the triggering of oxidative and nitrosative stress with damage to proteins, lipids and non-enzymatic antioxidants consumption in brain, even when different As models of exposure were employed. Fil: Bonetto, Julián Gerardo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Buenos Aires, Argentina Villaamil Lepori, Edda Facultad de Farmacia y Bioquímica Puntarulo, Susana Bonetto, Julián Gerardo 2019-10-25 Poco se sabe del efecto neurológico del As. Se planteó estudiar el efecto del As en cerebro de rata sobre el balance redox celular, explorando diferentes modelos de administración de As. Se evaluaron la producción de especies reactivas, el balance redox mediante la evaluación de índices daño/protección en medios hidrofílico, lipofílico y el consumo de antioxidantes no enzimáticos. Los índices de estrés oxidativo permitieron comparar los efectos tempranos de los tratamientos según el modelo de administración de As empleado. La velocidad de oxidación de la diclorofluoresceína diacetato, como índice general de la generación de especies activas, no mostró diferencias en cerebro por la exposición a As en ninguno de los modelos estudiados. Utilizando un modelo de exposición a As en cerebro ex vivo, se observó una condición de estrés oxidativo en el ambiente lipofílico celular, acompañado por un consumo del antioxidante glutatión (GSH). La administración aguda de As en un modelo in vivo desencadenó el mismo efecto a nivel lipofílico, con un aumento en la generación de NO y en la nitración de proteínas, sin consumo significativo de GSH. Por otro lado, empleando un modelo in vivo de administración crónica de As en el agua de bebida, se observó el mismo efecto sobre el índice de estrés oxidativo en el ambiente lipofílico celular, acompañado de un consumo de los antioxidantes GSH y ?-tocoferol. El efecto tóxico del As en cerebro se asocia parcialmente al daño oxidativo y nitrosativo en lípidos, proteínas y al consumo de antioxidantes en forma independiente del modelo de administración, con algunas características diferenciales probablemente vinculadas a las concentraciones de As alcanzadas en cada modelo. application/pdf Evelson, Pablo Perez Carrera, Alejo Castro, Gerardo Balance redox Arsénico Cerebro spa Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/2.5/ar/ Ciencias de la vida Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro info:eu-repo/semantics/doctoralThesis info:ar-repo/semantics/tesis doctoral info:eu-repo/semantics/acceptedVersion http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_5912 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_5912.dir/5912.PDF
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-145
collection Repositorio Digital de la Universidad de Buenos Aires (UBA)
language Español
orig_language_str_mv spa
topic Balance redox
Arsénico
Cerebro
Ciencias de la vida
spellingShingle Balance redox
Arsénico
Cerebro
Ciencias de la vida
Bonetto, Julián Gerardo
Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
topic_facet Balance redox
Arsénico
Cerebro
Ciencias de la vida
description Little is known about the effects of As on the nervous system. To investigate whether As induces neurotoxicity and influences the oxidative stress in brain, different As exposure models where studied. Thus, active specie production, antioxidant consumption and oxidative stress ratios (known as damage/protection in the hydrophilic and lipophilic cellular environment) where evaluated. The oxidation rate of the 2',7'-Dichlorodihydrofluorescein, a fluorescent probe used for detection of the generation of reactive oxygen species, was not affected by As exposure in any studied model. In the ex vivo model brain homogenates were exposure to As, and the lipophilic oxidative stress ratio was significantly increased in As-treated animals as compared to control homogenates, with a significant decrease in the content of glutathione (GSH). In the in vivo model of acute As treatment the same responses were observed in the lipophilic media and in the magnitude of the GSH consumption. Moreover, the acute exposure to As lead to a significant increase in NO production and protein nitration content. In the in vivo model of chronic As treatment the lipophilic oxidative stress ratio was increased, and GSH and ?-tocopherol consumption was observed. The data suggested the triggering of oxidative and nitrosative stress with damage to proteins, lipids and non-enzymatic antioxidants consumption in brain, even when different As models of exposure were employed.
author2 Villaamil Lepori, Edda
author_facet Villaamil Lepori, Edda
Bonetto, Julián Gerardo
format Tesis doctoral
Tesis doctoral
acceptedVersion
author Bonetto, Julián Gerardo
author_sort Bonetto, Julián Gerardo
title Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
title_short Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
title_full Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
title_fullStr Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
title_full_unstemmed Exposición a As : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
title_sort exposición a as : efectos sobre el metabolismo oxidativo y nitrosativo en el cerebro
publisher Facultad de Farmacia y Bioquímica
publishDate 2019
url http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_5912
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_5912.dir/5912.PDF
work_keys_str_mv AT bonettojuliangerardo exposicionaasefectossobreelmetabolismooxidativoynitrosativoenelcerebro
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