Ethanol and acetaldehyde alter brain mitochondrial redox responses to direct cortical stimulation in vivo.
To determine whether and how ethanol and acetaldehyde alter brain oxidative metabolic activity, reduction/oxidation shifts of components of the mitochondrial respiratory chain were optically measured, in situ, from cat cerebral cortex. Oxidative shifts of nicotinamide adenine dinucleotide (NADH) were recorded in response to increased energy demand provoked by stimulation of the cortical surface by electrical pulses. Ethanol or acetaldehyde did not alter the direction of the responses but each slowed the rates of oxidation with little effect upon the rates of subsequent re-reduction. There was no apparent change produced by either drug upon the kinetics of the negative shifts of the cortical steady potential in response to the stimulation. However, stimulus-evoked electrical and metabolic responses were decreased in amplitude with increasing drug doses. It is suggested that the slowed mitochondrial oxidation results from inhibition of Na+, K+-ATPase. This supports the concept that ethanol or acetaldehyde inhibit the processes that lead to increased oxygen consumption following cell depolarization in vivo, as has been demonstrated in vitro.
D000079:Acetaldehyde / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002415:Cats; D002540:Cerebral Cortex / Q000502:physiology; D000431:Ethanol / Q000494:pharmacology*; D005260:Female; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D010084:Oxidation-Reduction; D010101:Oxygen Consumption / Q000187:drug effects; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D009243:NAD; D000431:Ethanol; D000254:Sodium-Potassium-Exchanging ATPase; D000079:Acetaldehyde