Samynathan Y M, Bondy S C
Department of Community and Environmental Medicine, University of California, Irvine 92717, USA.
Neurochem Res. 1995 Feb;20(2):171-6. doi: 10.1007/BF00970541.
The actions of ethanol and its primary oxidative metabolite, acetaldehyde, on plasma membrane and mitochondrial transmembrane potentials were examined in rat brain using fluorescence techniques. Subchronic treatment of adult rats with ethanol resulted in a significant depolarization of both the plasma and mitochondrial membranes when the mean blood ethanol level of the rats was 59 +/- 11 mM (mean +/- SEM, n = 6). Acute dosing of animals (4.5 g/kg, i.p.) failed to show any significant alterations. Various concentrations of ethanol, added in vitro to a crude synaptosomal preparation isolated from the rat cerebrocortex (P2) from untreated animals, depolarized both the plasma and mitochondrial transmembrane potentials in a dose-related manner. Addition of acetaldehyde in vitro did not reveal any significant effects on plasma or mitochondrial transmembrane potential.
利用荧光技术在大鼠脑中研究了乙醇及其主要氧化代谢产物乙醛对质膜和线粒体跨膜电位的作用。当成年大鼠的平均血液乙醇水平为59±11 mM(平均值±标准误,n = 6)时,用乙醇对成年大鼠进行亚慢性处理会导致质膜和线粒体膜均发生显著去极化。对动物进行急性给药(4.5 g/kg,腹腔注射)未显示出任何显著变化。将不同浓度的乙醇体外添加到从未经处理动物的大鼠大脑皮质(P2)分离得到的粗突触体制剂中,会以剂量相关的方式使质膜和线粒体跨膜电位去极化。体外添加乙醛未显示出对质膜或线粒体跨膜电位有任何显著影响。