Abstract
Effect of hepatic redox-state on the rate of ethanol metabolism and citric acid cycle activity has been studied in rat and guinea pig liver. Cytoplasmic (NADH) (NAD) ratio in guinea pig liver is about 8-fold higher than in rat liver. Although, hepatic alcohol dehydrogenase (EC 1.1.1.1) activity is similar in the two species, ethanol metabolism by rat liver in vitro, is about 3 times greater than by guinea pig liver. Addition of ethanol results in a 3-fold increase in the hepatic redox-state in the rat but causes a small increase in the guinea pig. Ethanol-induced increase in hepatic (NADH) (NAD) ratio, results in a 40–60% inhibition of 14CO 2 formation from various radioactive substrates in the rat. However, in guinea pig liver where this ratio is high, 14CO 2 formation is already lower by 30–50% than in rat liver and ethanol addition does not result in a further decrease. The inhibitory effect of ethanol on 14CO 2 formation is also observed in rat kidney cortex slices. However, this effect can be abolished by the addition of methylene blue or pyrazole. This study shows that in normal liver cytoplasmic redox-state regulates the rate of ethanol metabolism and that the activity of hepatic alcohol dehydrogenase is not a rate-limiting factor. Furthermore, the inhibitory effect of ethanol on CO 2 production and therefore on citric acid cycle activity is a consequence of increased (NADH) (NAD) ratio in liver.
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