Abstract
The activities of liver and brain aldehyde dehydrogenase, an NAD(+) dependent enzyme, which controls acetaldehyde oxidation have been reported to play a role in voluntary ethanol consumption. It has been reported that nicotinamide administration to rats increases NAD(+) levels, that may increase acetaldehyde oxidation rates if basal NAD(+) levels are not saturating for the enzyme. In the present paper the effect of nicotinamide administration on voluntary ethanol consumption by genetically high ethanol consumer UChB rats and brain and liver mitochondrial acetaldehyde oxidation were studied. Administration of nicotinamide 250 or 500 mg/kg i.p. to UChB rats, produced a significant reduction in their voluntary ethanol consumption and increased brain acetaldehyde oxidation in brain but not liver homogenates.These results suggest that basal NAD(+) levels are not saturating for brain aldehyde dehydrogenase and that the reduction of ethanol consumption by UChB rats may be the consequence of a change in the brain redox state, rather than the local level of acetaldehyde.
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