The cerebral oxidative metabolic response to acute ethanol administration in rats and cats

Abstract

Ethanol effects on mitochondrial respiratory chain components in intact cerebral cortex of cats and rats are reported. Changes in redox levels were monitored by non-invasive optical techniques (microfluorometry for intramitochondrial NADH: dual wavelength reflection spectrophotometry for cytochrome a, a 3). Acute ethanol injections were accompanied by progressive increases in the level of reduced cytochrome a, a 3, a response consistent with the cytochrome response to other depressants such as phenobarbital and chlorpromazine. Low ethanol doses (below approx. 1 g/kg) were accompanied by increased levels of reduced NAD and it appeared that the ethanol effect in vivo is due to a decrease in tissue activity common to central depressants. Higher ethanol doses (1–3 g/kg) produced increased levels of oxidized NAD whereas phenobarbital and chlorpromazine each resulted in increased levels of reduced NAD. Since many of the effects of ethanol have been attributed to the activity of its primary metabolic product, acetaldehyde. the latter's effects on energy metabolism were also considered. Acetaldehyde at all effective doses produced similar changes in NAD (i.e. oxidation) and cytochrome a, a 3 (reduction) to those of the higher ethanol doses. The oxidation of NAD at higher ethanol doses and at all doses of acetaldehyde was interpreted as a unique effect of ethanol and due to acetaldehyde.