Efecto del cadmio en la progresión del daño hepático en esteatosis
Non alcoholic fatty liver disease is the most common chronic liver disease in the world and its progression may be due, in part, to the outcome of liver lipotoxicity produced by an excess of free fatty acids that promotes reactive oxygen species, and consequently, cell dysfunction and death by necro...
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| Tipo de recurso: | tesis de maestría |
| Estado: | Versión publicada |
| Fecha de publicación: | 2014 |
| País: | México |
| Institución: | Universidad Autónoma Metropolitana |
| Repositorio: | Repositorio Institucional de la UAM Iztapalapa |
| Idioma: | español |
| OAI Identifier: | oai:bindani.izt.uam.mx:hd76s024f |
| Acceso en línea: | https://doi.org/10.24275/uami.hd76s024f |
| Access Level: | acceso abierto |
| Palabra clave: | info:eu-repo/classification/LEM/Fatty liver info:eu-repo/classification/LEM/Hígado graso info:eu-repo/classification/LEM/Hígado info:eu-repo/classification/LEM/Liver -- Diseases info:eu-repo/classification/LEM/Biología experimental info:eu-repo/classification/LEM/Cadmium -- Toxicology info:eu-repo/classification/LEM/Cadmio info:eu-repo/classification/LEM/Biology, Experimental info:eu-repo/classification/cti/3 |
| Sumario: | Non alcoholic fatty liver disease is the most common chronic liver disease in the world and its progression may be due, in part, to the outcome of liver lipotoxicity produced by an excess of free fatty acids that promotes reactive oxygen species, and consequently, cell dysfunction and death by necrosis or apoptosis. However, research on this field indicates that progression of liver damage could be associated to a second liver aggression that produces inflammation, aggravates oxidative stress that could result in progression of liver damage to fibrosis. Cadmium is a pro-oxidant metal, that is considered an environmental pollutant, widely used in the industry. Cadmium could induce adverse effects on human health principally in liver and kidney. In this study we analyzed the effect of cadmium on the progression of liver damage in steatotic hepatocytes from mice feed with high cholesterol diet. Our results show that, although steatosis triggered survival mechanisms that compensates cadmium aggression, prolonged exposure with the metal causes cell death. The mechanism is an increase in reactive oxygen species and protein oxidation that induce oxidative stress, and a decrease in the antioxidant enzymes, producing an increase in the lipogenesis process. Thus, hepatocyte becomes unable to handle a second prooxidant aggression, which leads in hepatocyte death. |
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