Karadayian Analía G, Malanga Gabriela, Czerniczyniec Analía, Lombardi Paulina, Bustamante Juanita, Lores-Arnaiz Silvia
Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Cátedra de Fisicoquímica, Buenos Aires, Argentina; CONICET-Universidad de Buenos Aires, Instituto de Bioquímica y Medicina Molecular (IBIMOL), Buenos Aires, Argentina.
Universidad Abierta Interamericana, Centro de Altos Estudios en Ciencias de la Salud, Buenos Aires, Argentina.
Free Radic Biol Med. 2017 Jul;108:692-703. doi: 10.1016/j.freeradbiomed.2017.04.344. Epub 2017 Apr 24.
Alcohol hangover (AH) is the pathophysiological state after a binge-like drinking. We have previously demonstrated that AH induced bioenergetics impairments in a total fresh mitochondrial fraction in brain cortex and cerebellum. The aim of this work was to determine free radical production and antioxidant systems in non-synaptic mitochondria and synaptosomes in control and hangover animals. Superoxide production was not modified in non-synaptic mitochondria while a 17.5% increase was observed in synaptosomes. A similar response was observed for cardiolipin content as no changes were evidenced in non-synaptic mitochondria while a 55% decrease in cardiolipin content was found in synaptosomes. Hydrogen peroxide production was 3-fold increased in non-synaptic mitochondria and 4-fold increased in synaptosomes. In the presence of deprenyl, synaptosomal HO production was 67% decreased in the AH condition. Hydrogen peroxide generation was not affected by deprenyl addition in non-synaptic mitochondria from AH mice. MAO activity was 57% increased in non-synaptic mitochondria and 3-fold increased in synaptosomes. Catalase activity was 40% and 50% decreased in non-synaptic mitochondria and synaptosomes, respectively. Superoxide dismutase was 60% decreased in non-synaptic mitochondria and 80% increased in synaptosomal fractions. On the other hand, GSH (glutathione) content was 43% and 17% decreased in synaptosomes and cytosol. GSH-related enzymes were mostly affected in synaptosomes fractions by AH condition. Acetylcholinesterase activity in synaptosomes was 11% increased due to AH. The present work reveals that AH provokes an imbalance in the cellular redox homeostasis mainly affecting mitochondria present in synaptic terminals.
酒精性宿醉（AH）是一种类似暴饮后的病理生理状态。我们之前已经证明，AH会导致大脑皮层和小脑的新鲜线粒体总组分出现生物能量学损伤。这项工作的目的是确定对照动物和宿醉动物非突触线粒体和突触体中的自由基产生及抗氧化系统。非突触线粒体中的超氧化物产生没有改变，而突触体中观察到增加了17.5%。心磷脂含量也有类似反应，非突触线粒体中未发现变化，而突触体中心磷脂含量减少了55%。非突触线粒体中的过氧化氢产生增加了3倍，突触体中增加了4倍。在存在司来吉兰的情况下，AH状态下突触体中的HO产生减少了67%。AH小鼠非突触线粒体中添加司来吉兰对过氧化氢生成没有影响。非突触线粒体中的单胺氧化酶活性增加了57%，突触体中增加了3倍。过氧化氢酶活性在非突触线粒体和突触体中分别降低了40%和50%。超氧化物歧化酶在非突触线粒体中降低了60%，在突触体组分中增加了80%。另一方面，突触体和细胞质中的谷胱甘肽（GSH）含量分别降低了43%和17%。与GSH相关的酶在突触体组分中大多受AH状态影响。AH导致突触体中的乙酰胆碱酯酶活性增加了11%。目前的研究表明，AH会引发细胞氧化还原稳态失衡，主要影响突触终末中的线粒体。
