La contaminación ambiental y su efecto sobre la superficie ocular: evaluación del balance redox celular y los mecanismos inflamatorios involucrados
The ocular surface is exposed to the environment, which has made it a target for studying the effects of air pollutants. Several works have involved redox imbalance and inflammation as possible toxicity mechanisms triggered by particulate matter (PM) in other tissues. The aim of this work was to eva...
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| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
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Facultad de Farmacia y Bioquímica
2018
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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_5782 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_5782.dir/5782.PDF |
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| Sumario: | The ocular surface is exposed to the environment, which has made it a target for studying the effects of air pollutants. Several works have involved redox imbalance and inflammation as possible toxicity mechanisms triggered by particulate matter (PM) in other tissues. The aim of this work was to evaluate the oxidative stress markers and inflammatory mediators triggered by PM exposure on different ocular structures (conjunctiva, cornea and lens), using different experimental approaches. On human conjunctival culture, it was observed that oxidative stress followed by pro-inflammatory cytokine release could play an important role in the development of the toxic effects due to diesel exhaust particles exposure (50 y 100 µg/mL). On mice cornea exposed to urban air, an early adaptive response of the antioxidant system was observed, which after longer exposure times is insufficient to counteract the oxidative damage. The inflammatory response was mediated by an early increase in IL-10 levels. On the mice lens exposed to urban air, it was shown that exposure to air pollutants alters the redox balance and that this situation could affect surrounding structures. The toxic effects have in common that they are mediated by alterations on cellular redox homeostasis and by inflammatory cytokines. |
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