Inhibition of plasma membrane and mitochondrial transmembrane potentials by ethanol.
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.
Samynathan
Y M
YM
Department of Community and Environmental Medicine, University of California, Irvine 92717, USA.
Bondy
S C
SC
D000437:Alcoholism / Q000503:physiopathology*; D000704:Analysis of Variance; D000818:Animals; D001921:Brain / Q000502:physiology*; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D007425:Intracellular Membranes / Q000187:drug effects / Q000502:physiology*; D016018:Least-Squares Analysis; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects*; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000502:physiology
D000431:Ethanol