INTRODUCTION

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. This study therefore attempts to provide such link.

MATERIALS AND METHODS

Experimental animals: Fourteen adult male albino rabbits with an initial mean body weight of 1.46 kg were purchased from Yoha Farms, Warri, Nigeria. The rabbits were housed singly in clean metal hutches and acclimatized on growers' mash, a product of Bendel Feeds and Flour Mills (BFFM) Ltd; Ewu, Nigeria for 10 days before commencing the experiment. The rabbits were then divided into control (normal saline-treated) and test (ethanol-treated) groups, consisting of seven animals each.

Feeding: The animals were given about 80g wet weight of the growers' mash/kg body weight/day. The feeds were mixed with water in a ratio of 10:1 (w/v) in order to achieve a texture acceptable to the animals. Clean water was provided for the animals to drink ad libitum. Stale feed remnants were regularly disposed, and the feeding exercise was conducted at room temperature (about 29 °C).

Administration of the experimental solutions: The test-group animals were orally given 1.5g (40%) ethanol/kg body weight as single daily dose, while the control rabbits received the equivalent amount of normal saline (0.9% NaCl) solution in lieu. The administrations were carried out after about 45 min of breakfast. The animals were exposed to these treatments along with their usual feeding pattern for a routine period of 15 weeks. The dosing regimen and experimental design were based on previous reports13. …