Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, Junín 956, C1113AAD Buenos Aires, Argentina.
Alcohol. 2012 Aug;46(5):473-9. doi: 10.1016/j.alcohol.2011.09.027. Epub 2012 May 16.
Ethanol has been known to affect various behavioral parameters in experimental animals, even several hours after ethanol (EtOH) is absent from blood circulation, in the period known as hangover. The aim of this study was to assess the effects of acute ethanol hangover on motor performance in association with the brain cortex energetic metabolism. Evaluation of motor performance and brain cortex mitochondrial function during alcohol hangover was performed in mice 6 hours after a high ethanol dose (hangover onset). Animals were injected i.p. either with saline (control group) or with ethanol (3.8 g/kg BW) (hangover group). Ethanol hangover group showed a bad motor performance compared with control animals (p < .05). Oxygen uptake in brain cortex mitochondria from hangover animals showed a 34% decrease in the respiratory control rate as compared with the control group. Mitochondrial complex activities were decreased being the complex I-III the less affected by the hangover condition; complex II-III was markedly decreased by ethanol hangover showing 50% less activity than controls. Complex IV was 42% decreased as compared with control animals. Hydrogen peroxide production was 51% increased in brain cortex mitochondria from the hangover group, as compared with the control animals. Quantification of the mitochondrial transmembrane potential indicated that ethanol injected animals presented 17% less ability to maintain the polarized condition as compared with controls. These results indicate that a clear decrease in proton motive force occurs in brain cortex mitochondria during hangover conditions. We can conclude that a decreased motor performance observed in the hangover group of animals could be associated with brain cortex mitochondrial dysfunction and the resulting impairment of its energetic metabolism.
乙醇已被证明会影响实验动物的各种行为参数，即使在血液中不再存在乙醇（EtOH）后的几个小时，也就是所谓的宿醉期间。本研究的目的是评估急性乙醇宿醉对运动表现的影响，并与大脑皮层能量代谢相关联。在高剂量乙醇（宿醉开始）后 6 小时，对小鼠进行了酒精宿醉期间运动表现和大脑皮层线粒体功能的评估。动物通过腹腔内注射盐水（对照组）或乙醇（3.8 g/kg BW）（宿醉组）。与对照组动物相比，乙醇宿醉组的运动表现较差（p<0.05）。与对照组相比，宿醉动物大脑皮层线粒体的耗氧量呼吸控制率降低了 34%。线粒体复合物活性降低，复合物 I-III 受宿醉状态影响较小；复合物 II-III 受乙醇宿醉的影响明显降低，活性比对照组低 50%。与对照组动物相比，复合物 IV 降低了 42%。与对照组相比，大脑皮层线粒体中过氧化氢的产生增加了 51%。跨膜电位的定量分析表明，与对照组相比，注射乙醇的动物维持极化状态的能力降低了 17%。这些结果表明，在宿醉状态下，大脑皮层线粒体中的质子动力明显下降。我们可以得出结论，在动物的宿醉组中观察到的运动性能下降可能与大脑皮层线粒体功能障碍以及由此产生的能量代谢受损有关。
