Changes of acetylcholinesterase activity in brain areas and liver of sucrose- and ethanol-fed rats

The effects of chronic ethanol or sucrose administration to rats on acetylc holinesterase from brain and liver were investigated. Membrane-bound and so luble acetylcholinesterase activities were determined in fractions prepared by centrifugation, The thermal stability and the effects of temperature an d different types of alcohols on acetylcholinesterase activity were also st udied. Membrane-bound acetylcholinesterase activity increased (p < 0.01) in the liver after chronic ethanol administration, whereas no differences amo ng groups in the encephalic areas, except in the brain stem soluble form, w ere found. Membrane-bound acetylcholinesterase from the ethanol- and sucros e-treated groups was more stable at the different temperatures assayed betw een 10 and 50 degrees C than that corresponding to the control group. Non-l inear Arrhenius plots were obtained with preparations of membrane-bound ace tylcholinesterase from rat liver, with discontinuities at 30 degrees C (con trol or sucrose groups) or 34-35 degrees C (alcohol group). Assays made wit h membrane-bound or soluble enzyme from brain showed linear Arrhenius plots in all groups studied, The inhibitory effects of increasing concentrations of ethanol, n-propanol and n-butanol on acetylcholinesterase preparations from forebrain, cerebellum, brain stem and liver of the three experimental groups (control, sucrose-fed and ethanol-fed) were very similar. However, n -butanol displayed a biphasic action on particulate or soluble preparations of rat forebrain. n-butanol inhibited (competitive inhibition) at higher c oncentrations (250-500 mM), while at lower concentrations (10-25 mM), the a lcohol inhibited at low substrate concentrations but activated at high subs trate concentration. These results suggest that the liver is more affected by ethanol than the brain. Moreover, the lipid composition of membranes is probably modified by ethanol or sucrose ingestion and this would affect mem brane fluidity and consecuently the behaviour of acetylcholinesterase.