Summary - Derangements or inbalances in products of intermediary metabolism have been reported to cause brain malfunction. It is therefore, thought necessary to study the changes in blood and brain glucose, triacylglycerol (TAG) and cholesterol, as these analytes could be disturbed by ethanol consumption, and then, attempt to relate same to the pathological condition of the brain. Fourteen adult male albino rabbits in apparent good health with an initial mean body weight of 1.46kg were purchased and divided into control and test animals with seven animals in each group. The test group animals were given 1.5g (40%) ethanol/kg body weight as single daily dose, after about 45min, of feeding them in the morning for a regular period of 15 weeks. The control animals received the equivalent amount of normal saline in lieu. The results showed that ethanol treatment significantly (P<0.05) reduced plasma glucose from a basal value of 8.200 ± 0.120 mmol/L to 7.200 ± 1.177 mmol/L, but progressively increased triacylglycerol levels from 0.550 ± 0.010 mmol/L to 0.801 ± 0.020 mmol/L, P<0.05, at the end of the experimental exercise. Plasma cholesterol also increased but not to a significant proportion (P>0.05). Changes in brain glucose, triacylglycerol and cholesterol were observed to be similar in pattern. Brain morphology showed features of encephalitis. The metabolic alterations in both brain and blood glucose and lipids may play significant role(s) in the aetiology of brain damage observed during this experimental ethanol toxicity.
Key words: Blood, Brain, Cholesterol, Ethanol, Glucose.
After the oral administration of ethanol and before its distribution to all tissues and extracellular compartments, the concentrations of ethanol in brain and arterial blood are substantially higher than those in muscle and peripheral veins, and this condition may prevail for as long as 2 hours after ethanol consumption.1
Scientists who study the effects of alcohol on brain generally assume that individuals consume alcohol because alcohol is a psychoactive drug and the consumer is seeking to experience the CNS effects of alcohol. Evidence indicate that levels of alcohol expected to occur in brain of an individual consuming »moderate« quantities of alcohol do generate neurochemical and electrophysiological events.2 It has been demonstrated that the stimulatory, sedative, anxiolytic, and reinforcing effects of ethanol occur within different and relatively narrow dose ranges,3 and this constitutes the neurochemical basis of the dose-dependency of ethanol's behavioural effects. Thus, at a certain level, a specific receptor system may be more prominent than others in contributing to a particular behavioural effect of ethanol.
The capacity of brain to metabolize ethanol has been a subject of debate. Several groups have reported on the metabolism of ethanol in brain tissue under particular assay conditions.4 Earlier investigators observed that the rate of ethanol metabolism in the brain is in the range between 1/100* to 1/1000* of the liver's capacity.56 Catalase has been reported to oxidize alcohol resulting in the formation of acetaldehyde and hydrogen peroxide, and recent studies suggest that this mechanism may be important also in brain.7 Acetaldehyde is a toxic metabolite, which has potent vasoactive properties, and has been implicated in alcohol dependency via the formation of opioid-like insoquinolines. It could also damage tissues by direct toxicity via reactive oxygen species, and could form acetaldehyde adducts and immunological reactions. These effects could be compounded by the peroxidative activity of catalase, a cytosolic and peroxisomal enzyme.
The oxidation of alcohol in tissues affects central metabolic pathways that regulate the homeostasis of cellular glucose,8,9 lipids1011 and other components, and induces the alteration of lobular architecture of liver.12 Yet, information on changes in blood and brain glucose and lipids and their relation to brain morphology during ethanol toxicity in experimental rabbits has remained scarce. …