Anesthesia. LVIII. Biochemical Effects of Acetaldehyde and Other Aldehydes on Oxidative Phosphorylation

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Abstract
A previous observation (Truitt, E.B., Jr. et al, Quart. J. Stud. Ale. 17: 594-600, 1956) that acetaldehyde (AcH) depressed the ratio of oxidative phosphorylation to O2 consumption (P/O ratio) by rat brain mitochondria in vitro has been quantitatively expanded and studied further. AcH depresses the P/O ratio of brain mitochondria only in the system utilizing pyruvate with catalytic amounts of fumarate as substrates. Formaldehyde, in contrast to AcH, causes a depression of P/O ratio which is non-specific among the substrates succinate, alpha-ketoglutarate, glutamate and beta-hydroxybutyrate. The depression by AcH is not reversible by excess amounts of Mg, Cu, Zn, cocarboxylase, reduced or oxidized di-phosphopyridlne nucleotlde, cytochrome c, coenzyme A, thioctic acid, insulin, dimercaprol (BAL) and pyruvate. Brain mitochondria are af-fected by AcH at much lower concentrations than are liver mito-chondria. However, addition of disulfiram (Antabuse) to the liver prep-aration in concentrations having no action acted synergistically with ineffective concentrations of AcH to produce marked P/O ratio depression. Though acetoin formation by liver is not reported in the literature brain mitochondria were found to be capable of forming acetoin from added AcH. Thus, the selective action of AcH on the brain is suggested to be attributable to the greater dependence of that organ on the condensation of AcH with an unknown 2-carbon fragment derived from pyruvate as its principal route of AcH metabolism.

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