Jm. Bertoni et Pm. Sprenkle, EFFECTS OF IN-VITRO ETHANOL ON THE BRAIN CATION PUMP IN ALCOHOLICS AND CONTROLS, Biochemical pharmacology, 48(2), 1994, pp. 435-437
In vivo ethanol exposure reduces in vitro Na+,K+-adenosine triphosphat
ase (Na+,K+- ATPase) sensitivity to ethanol in some animal models, but
very little is known about the effects of ethanol on human brain Na+,
K+-ATPase. Cerebral cortex homogenates from 13 male alcoholic and 9 co
ntrol subjects were assayed for K+-p-nitrophenylphosphatase (K+-pNPPas
e, a measure of Na+,K+-ATPase) and Mg2+-pNPPase activities at 37 degre
es for 20 min in 75 mM imidazole-HCl (pH 7.4), 5 mM p-nitrophenylphosp
hate, 5 mM MgCl2, and 20 mM KCI, with or without 1 mM ouabain. Native
K+-pNPPase activities were similar in control and alcoholic brains (61
.5 +/- 3.5 vs 55.3 +/- 3.1 nmol/mg/min). in vitro exposure to a near l
ethal ethanol level (0.5%, or 110 mM) was without effect, whereas 5% e
thanol inhibited K+-pNPPase activity by about 28% (P < 0.001) in both
groups. Both 0.5 and 5% ethanol in vitro significantly stimulated Mg2-pNPPase activity (1-2% and 19-20%, respectively). By comparison, mous
e brain K+-pNPPase was inhibited significantly by in vitro ethanol, an
d Mg+-pNPPase activity was unaffected. Ethanol levels attainable in hu
mans may not be sufficient to alter significantly brain Na+,K+-ATPase
activity.