Instituto sobre Drogas y Conductas Adictivas, Universidad CEU Cardenal Herrera, 46113 Moncada, Valencia.
J Physiol Biochem. 2009 Sep;65(3):305-12. doi: 10.1007/BF03180583.
The 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.
本研究旨在证明酒精性大鼠脑线粒体中谷胱甘肽和胆固醇稳态的改变。谷胱甘肽浓度降低，而氧化型谷胱甘肽和胆固醇含量增加，提示乙醇诱导的活性氧生成，以及线粒体摄取谷胱甘肽的损伤，可能是由于胆固醇沉积增加所致。用远志糖苷刺激酒精性大鼠脑线粒体后，促凋亡蛋白的释放增加。总之，慢性酒精摄入可能使脑线粒体对凋亡刺激敏感，并促进随后促凋亡蛋白的释放。
