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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| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
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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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| Sumario: | 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. |
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