Guinea-pigs were maintained for 5 weeks on a diet containing three different concentrations of vitamin C: a) traces (none added), b) medium (0.05 % w/w) and high (0.5 % w/w). Twenty-four hours before killing the animals received one i.p. dose of 3 g ethanol per kg body weight (a model of short-term acute intoxication). In a parallel experiment which lasted 5 weeks, the animals were treated every week with two i.p. doses of 1 g ethanol per kg body weight followed bv the final acute intoxication (3 g ethanol/kg) (a model of long-term chronic alcoholization). In both experiments, the guinea-pigs with the highest tissue concentration of vitamin C proved to have significantly decreased residual levels of ethanol and acetaldehyde in the liver and the brain, a decreased activity of alanine- and aspartate aminoacyl transferases in the serum and decreased contents of triacylglycerols and cholesterol in the serum and liver in comparison with the vitamin C-unsupplemented group. The regression curve expressing vitamin C levels versus residual ethanol and acetaldehyde concentrations in the liver confirmed the highly significant negative correlation between them. Administration of the guinea-pigs with large amounts of vitamin C appears to accelerate ethanol and acetaldehyde metabolism and reduce some of their adverse health effects.
The influence of regular moderate ethanol consumption on the status of vitamin C was followed in guinea-pigs and rats. In the guinea-pigs examined, 10-day consumption of ethanol (4.5 g per day and kg of body weight), administered in drinking water under a vitamin C-deficient diet, caused a greater decrease in the tissue concentrations and the body-pool of this vitamin than in the group without alcohol. In the rats, on the contrary, the daily consumption of ethanol (6 % vol) during 10 months resulted in an increase in the body stores of vitamin C, especially in the liver, adrenals, kidneys, and lungs. Moreover, the biosynthesis of ascorbate from D- glucuronolactone in vitro was more intensive (by 30 %) in the liver microsomes of alcoholized rats than in those of controls (without alcohol). These results indicate that the need of vitamin C during chronic consumption of moderate alcohol doses is enhanced. This is due to the participation of ascorbate in oxidoreducing processes connected with ethanol metabolism which leads to its irreversible destruction. In the rat, this loss is compensated by its enhanced biosynthesis, while in the guinea-pig it produces increased demands for its exogenous intake. If these are not satisfied, a partial vitamin C deficiency may occur, which potentiates the harmful effect of alcohol on the health status.