Ethanol and acetaldehyde metabolism in rat strains genetically selected for their ethanol preference

Effect of ethanol administration on alcohol dehydrogenase activity in mouse hepatic cells: ultracytochemical study.

“…The same has been also reported for rats (16,35,36). Schlesinger et al (66) found that Antabuse, which inhibits aldehyde dehydrogenase activity, increases acetaldehyde accumulation in both C57BL and DBA mice following ethanol administration, but the effect was significantly greater in C57BL mice than in DBA mice.…”

“…On the basis of these reports and the present findings, it could be said that there is a distinct correlation between alcohol pre-EFFECT OF ETHANOL ON ALCOHOL DEHYDROGENASE 497 ference and liver ADH activity. Eriksson (16) reported that there was no significant difference in the elimination rate of ethanol between the ANA and AA rats. However, from study in the rates of ethanol metabolism in hamsters with high alcohol preference and rats with low alcohol preference, it has been recently indicated that a correlation does exist between alcohol preference and rate of metabolism (47,83).…”

Increase in hepatic NAD level ‐ its effect on the redox state and on ethanol and acetaldehyde metabolism

“…Both these techniques have been described previously [5]. For the calculation of the liver acetaldehyde an interpolation correction was made for the 'spontaneous' acetaldehyde formation from the ethanol present.…”

“…The freeze-clamped livers showed the same significant differences; 130 + 5 1 nmoles/g (n = 8) for the control rats and 71 + 19 nmoles/g of wet wt liver (n = 4) for the nicotinamide-treated rats. Previous studies with 'drinking' and 'non-drinking' rat strains have shown that at least enzyme activity may regulate the hepatic acetaldehyde oxidation during ethanol metabolism [5]. Other recent investigations also indicate the importance of the intra-mitochondrial redox state [ 191 and NADH re-oxidation [20].…”

Stimulation of Ethanol Metabolism Induced by Proline and Lysine Ingestion in Prolonged Ethanol-Administered Stroke-Prone Spontaneously Hypertensive Rats.

“…With respect to the role of acetaldehyde in the action of ethanol, Truitt and Walsh reported that the most important effect of acetaldehyde was its influence on the biogenic amine metabolism of the brain [21]. It was reported that a higher acetaldehyde output suggests a greater inhibitory influence on the metabolism of the brain, which could decisively affect behavior with respect to ethanol preference [22]. In the present study, the lower acetaldehyde levels encountered during the ethanol oxidation in the EtOH/Pro and EtOH/Lys groups as compared with that of the EtOH group could explain the nutritional and physiological meanings of the high preference for proline and lysine in prolonged ethanol-administered rats [1].…”