Effects of Aliphatic Alcohols on the Metabolism of Brain and Liver

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Abstract
The respira-tion of rat brain cortex slices, stimulated by changed cationic concentrations (increase of K+), is more sensitive to aliphatic alcohols than that of unstimulated respiration, the inhibitory effects increasing markedly as the length of the C chain increases. Brain mitochondrial respiration is relatively insensitive to concentrations of alcohol that greatly depress stimulated brain cortex respiration. It is suggested that alcohols exercise their major effects on the neuronal membranes. Ethanol at narcotic concentration inhibits incorporation of radioactive glycine into brain proteins in rat brain cortex. Studies of liver metabolism show that, with rat liver slices, propanol, butanol and pentanol have higher affinities for alcohol dehydrogenase than ethanol, as shown by their inhibitory effects on C14O2 formation from ethanol-1-C14. Propionate exerts a large inhibitory effect on C14O2 formation from ethanol-1-C14 probably due to competition for coenzyme A (CoA). Fructose, glucose and isopropanol stimulate the rate of C14O2 formation from ethanol-1-C14. Acetate oxidation of liver is inhibited by the lower aliphatic alcohols. Ethanol at small concentrations inhibits C14O2 from glucose-U-C14 in presence of rat liver slices. The results indicate that the lower aliphatic alcohols are rapidly converted in the liver to the corresponding acyl-CoA derivatives, or acetyl-CoA, which compete with the acetyl-CoA derived from fatty acids or sugars consumed in the liver. There is, in addition, however, an inhibitory effect of the alcohols at low concentrations on the metabolism of fatty acids and sugars not explained by conversion to acetyl-CoA. The presence of relatively large concentrations of ethanol in the liver leads to an accumulation of acetyl-CoA units which by condensation, and subsequent reduction due to the increased ratio of reduced diphosphopyridine nucleotide (DPNH) to DPN, leads to lipid synthesis.

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