Pathological Effects of Prolonged Voluntary Consumption of Alcohol by Mice

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Abstract
Under normal laboratory conditions and with normal food 20 C57BL/Crgl mice (150 days old) were given access ad libitum to 10% v/v ethanol instead of (10 mice) or in addition to (10 mice) normal water for a period of 75 weeks; 10 controls were maintained with access to water but not ethanol. Body weight, mortality and histological-ly assessed organ pathology were not markedly affected by the alcohol. Susceptibility to parasites (lice and mites) was apparently increased and coat condition was characteristically impaired in the alcohol-consuming animals which could be invariably distinguished from the water controls by gross appearance. The normal alcohol intake, consistently high throughout the study relative to estimated metabolic capacity, replaced approximately 20% of normal nutrition. When the protein-free, vitamin-free, mineral-free calorie content of the 10%-alcohol solution was increased by addition of sucrose (16 g added to 100 cc of 10% v/v ethanol) 10 C57BL/10J, 30 C3H/HeJ, 10 DBA/2J, 10 BALB/cJ and 8 R111/J mice (140-220 days old) all consumed increased amounts of alcohol, according to their expected strain differences in unsweetened-alcohol selection. The C57BL strain replaced approximately half of its normal diet with the sweetened alcohol solution. The other strains replaced proportionately less, to a low of 4% by the DBA/2. No significant weight changes occurred, indicating that the mice regulated their calorie intake. After 57 weeks of voluntary access to the sweetened alcohol, 1 of 5 C57BL males had died, and 3 had liver damage (vacuolar changes and inflammatory foci) similar to that seen in human alcoholics. In contrast, no mortality or morbidity was found in C57BL controls maintained with access to sucrose solution not containing alcohol, even though calorie intake from the sucrose solution approximated that from the alcohol solution. Other strains showed apparent differential vulnerability to the alcohol in proportion to their rate of consumption of the alcohol solution, with intermediate-selecting C3H and R111 strains showing somewhat greater vulnerability to the alcohol than to the sugar solution and the low-selecting DBA/2 and BALB/c strains showing somewhat greater vulnerability to the sugar than to the alcohol solution. The C3H water controls had less morbidity and mortality than either the alcohol or the sugar groups of that strain. Although several strains given access to the sugar solution had various pathological changes in tissues, the histological changes were not those characteristically associated with alcohol consumption in humans. The results suggest that specific strains of mice will develop liver pathology similar to that found in human alcoholism if given voluntary access to sweetened alcohol over a prolonged period of time.

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