Vitamin B1 and bacterial oxidation

Abstract

Acetate and propionate oxidation by vitamin B1-deficient propionic acid bacteria is accelerated, in the presence but not in the absence of vit. B1, by both Mg and K, and their effect is synergistic; Mn inhibits. A similar accelerating effect is noted with the Na salts of lactic and [alpha]-ketobutyric acids; it is scarcely perceptible with pyruvate and not with glycerol. In the absence of added vit. B1 Mg and K accelerate the oxidation of succinate, fumarate, lactate, ethyl and propyl alcohols, glucose; K augments the effect of Mg perhaps by increasing the permeability of the cells to Mg. Various other acids are feebly (or not) oxidized. The effects of Na hexosediphosphate are quantitatively the same as those of Mg, and K augments this action; sodium [alpha]-glycerophosphate has no effect. When vit. B1-deficient propionic acid bacteria are incubated aerobically for 1 hr. at 37[degree] in the presence of Mg and K, or of hexosediphosphate and are then thoroughly washed, they show greatly increased oxidation of acetate and pyruvate in the presence of vit. B1, and of succinate, fumarate, ethyl and propyl alcohols in its absence. Incubation is believed to enrich the cell with adenyltriphosphate thus producing the optimal rate of phosphorylation of vit. B1 to form cocarboxylase and hence optimal rate of acetate and pyruvate oxidation. Adenyltriphosphate is thus essential for the oxidation of fumarate and of ethyl and propyl alcohols in the intact cell. Propionic acid bacteria are able to deaminate adeno-sine and adenylic acid. Oxaloacetate has no accelerating effects comparable with those of vit. B1. Na iodoacetate but not NaF has an inhibitory action on the accelerating effects of hexosediphosphate.