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A significant level of alcohol dehydrogenase activity has been demonstrated in the soluble fraction of rat brain. The pH optimum, kinetic properties and response to inhibitors are similar to those of liver alcohol dehydrogenase. The nutritional state of the animal, such as that associated with feeding or fasting, appeared to have no effect on the levels of the alcohol dehydrogenase activities in either liver or brain. A cerebral mechanism for the metabolism of ethanol may be involved in local biochemical adjustments in tissues during exposure to alcohol and may play a significant role in the pathogenesis of the neural disorders which can accompany chronic alcohol ingestion or acute withdrawal.
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Raskin et al. (1970) studied this question.
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