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A cloned mouse liver cell model (NCTC 1469) treated with either ethanol or one of its metabolites, acetaldehyde or acetate, was used to study proline uptake. Beginning with the stationary phase of cell growth, 14C-proline uptake was markedly accelerated by both ethanol and acetaldehyde (p less than 0.001). When ethanol treatment was combined with 4-methyl pyrazole so as to block ethanol oxidation, the ethanol-induced increase in proline uptake was significantly decreased to levels similar to that seen in controls. Acetaldehyde-induced stimulation of proline uptake was not significantly changed by the addition of 4-methyl pyrazole. While uptake of proline was markedly increased by ethanol and acetaldehyde, proline pool sizes were not significantly changed. An increase in uptake without an increase in pool size suggests an increased utilisation. These studies establish an increase in proline uptake associated with chronic alcoholism and indicate that acetaldehyde is the primary metabolite of ethanol responsible for this increase.

Altered proline uptake by mouse liver cells after chronic exposure to ethanol and its metabolites.