Khatoon Rehana, Fick Jordan, Elesinnla Abosede, Waddell Jaylyn, Kristian Tibor
Department of Anesthesiology and the Center for Shock, Trauma and Anesthesiology Research (S.T.A.R.), University of Maryland School of Medicine, 685 Baltimore St., Baltimore, MD 21201, USA.
Veterans Affairs Maryland Health Center System, 10 North Greene Street, Baltimore, MD 21201, USA.
Int J Mol Sci. 2024 Dec 22;25(24):13714. doi: 10.3390/ijms252413714.
The cerebellum, a key target of ethanol's toxic effects, is associated with ataxia following alcohol consumption. However, the impact of ethanol on Purkinje cell (PC) mitochondria remains unclear. To investigate how ethanol administration affects mitochondrial dynamics in cerebellar Purkinje cells, we employed a transgenic mouse model expressing mitochondria-targeted yellow fluorescent protein in Purkinje cells (PC-mito-eYFP). Both male and female PC-mito-eYFP mice received an intraperitoneal injection of ethanol or vehicle. One hour after ethanol administration, the animals were perfusion fixed or their cerebellum tissue or isolated mitochondria were collected. Cerebellum sections were analyzed using confocal microscopy to assess changes in mitochondrial length distribution. In vivo superoxide levels were measured using dihydroethidium (DHE), and mitochondrial NAD levels were determined by high-performance liquid chromatography (HPLC). Our findings revealed a sex-dependent response to ethanol administration in mitochondrial size distribution. While male Purkinje cell mitochondria exhibited no significant changes in size, female mitochondria became more fragmented after one hour of ethanol administration. This coincided with elevated phosphorylation of the fission protein Drp1 and increased superoxide production, as measured by DHE fluorescence intensity. Similarly, mitochondrial NAD levels were significantly reduced in female mice, but no changes were observed in males. Our results demonstrate that ethanol induced mitochondrial fragmentation through increased free radical levels, due to reduced NAD and increased p-Drp1, in PC cells of the female cerebellum.
小脑是乙醇毒性作用的关键靶点,与饮酒后的共济失调有关。然而,乙醇对浦肯野细胞(PC)线粒体的影响仍不清楚。为了研究乙醇给药如何影响小脑浦肯野细胞的线粒体动力学,我们采用了一种在浦肯野细胞中表达线粒体靶向黄色荧光蛋白的转基因小鼠模型(PC-mito-eYFP)。雄性和雌性PC-mito-eYFP小鼠均接受腹腔注射乙醇或赋形剂。乙醇给药1小时后,对动物进行灌注固定,或收集其小脑组织或分离的线粒体。使用共聚焦显微镜分析小脑切片,以评估线粒体长度分布的变化。使用二氢乙锭(DHE)测量体内超氧化物水平,并通过高效液相色谱(HPLC)测定线粒体NAD水平。我们的研究结果揭示了乙醇给药对线粒体大小分布的性别依赖性反应。虽然雄性浦肯野细胞线粒体大小没有显著变化,但乙醇给药1小时后,雌性线粒体变得更加碎片化。这与裂变蛋白Drp1的磷酸化增加以及通过DHE荧光强度测量的超氧化物产生增加相一致。同样,雌性小鼠的线粒体NAD水平显著降低,而雄性小鼠未观察到变化。我们的结果表明,乙醇通过降低NAD和增加p-Drp1导致自由基水平升高,从而诱导雌性小脑血管细胞中的线粒体碎片化。