- Carmen García-Ruiz;
María Miranda; María Miranda
Harvested from ORCID Public Data FileMaría Miranda in OpenAIRE María Muriach; María Muriach
Harvested from ORCID Public Data FileMaría Muriach in OpenAIRE Jorge M. Barcia; +4 AuthorsJorge M. Barcia
Harvested from ORCID Public Data FileJorge M. Barcia in OpenAIRECarmen García-Ruiz; María Miranda; María Miranda
Harvested from ORCID Public Data FileMaría Miranda in OpenAIRE María Muriach; María Muriach
Harvested from ORCID Public Data FileMaría Muriach in OpenAIRE Jorge M. Barcia; Jorge M. Barcia
Harvested from ORCID Public Data FileJorge M. Barcia in OpenAIRE Inmaculada Almansa; Francisco J. Romero; Anna Fernández;Inmaculada Almansa
Harvested from ORCID Public Data FileInmaculada Almansa in OpenAIRE José C. Fernández-Checa; José C. Fernández-Checa
Harvested from ORCID Public Data FileJosé C. Fernández-Checa in OpenAIREThe aim of this study was to demonstrate the existence of alterations in glutathione and cholesterol homeostasis in brain mitochondria from alcoholic rats. Glutathione concentration decreased, whereas oxidized glutathione and cholesterol contents increased in these organelles, suggesting the ethanol-induced generation of reactive oxygen species, and the impairment of mitochondrial uptake of glutathione, possibly due to the increase in cholesterol deposition. The release of apoptogenic proteins was increased after stimulating mitochondria from the brain of alcoholic rats with atractyloside. As a conclusion, chronic alcohol consumption might sensitize brain mitochondria to apoptotic stimuli, and promote the subsequent release of apoptotic proteins.
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