Vitamin B1 and bacterial oxidations

Abstract

The presence of vitamin B1 at low conc. (e.g., ca. 10-7 [image]) greatly increases the rate of oxidation of acetic acid by vitamin B1-deficient propionic acid bacteria. The ratio of mol. oxygen consumed to mol. acetic acid utilized by these bacteria, in the presence and in the absence of vitamin B1, is approx. 2, showing complete oxidation of acetic acid. Formic, acetic, propionic and butyric acids are oxidized at about the same rate by vitamin Bi-deficient propionic acid bacteria. Pyruvic acid accumulates during the oxidation of glucose, lactic acid, glycerol and propionic acid by vitamin Bi-deficient propionic acid bacteria. Its amt. greatly diminishes in presence of the vitamin. No pyruvic acid accumulates when acetic acid is oxidized. In presence of semicarbazide a ketonic acid (probably pyruvic acid) accumulates during the oxidation of lactic, succinic and propionic acids. It does not accumulate during the oxidation of acetic acid. The presence of lactic acid, succinic acid, fumaric acid or glycerol greatly inhibits the utilization of pyruvic acid, when this is added together with any of these substrates, in presence of vitamin B1. Propionic acid also produces an inhibition of added pyruvic acid utilization, but acetic acid gives no inhibition within limits of exptl. error. The presence of vitamin B1 greatly stimulates the rates of respiration by vitamin Bi-deficient propionic acid bacteria with the following substrates: pyruvic acid, lactic acid, succinic acid, fumaric acid, glucose, glycerol. Definite but much less powerful effects of the vitamin are shown in the oxidations of l-malic acid, l-glutamic acid, dl-alanine, glycollic acid, glycine and fructose. The following substances are oxidized either feebly or not at all by the bacteria, with little or no stimulating action of vitamin B1: oxalic acid, citric acid, [beta]-hydroxybutyric acid. Oxidation of [alpha]-glycerophosphoric acid and hexose-diphosphoric acid takes place with little or no effect of added vitamin B1 on their rates of oxidation. Oxidation of fumaric acid takes place at a greater rate than that of 1-malic acid. The stimulant action of vitamin B1 may, in most cases, be attributed partially if not wholly to its effect on the oxidation of pyruvic acid formed as an intermediate. The effect of the vitamin on acetic acid oxidation cannot at present be ascribed to this cause. The evidence is in favor of the conclusion that cocarboxylase is the effective catalytic agent. The pyrimidine and thiazole components of vitamin B1 are, separately, unable to catalyse the oxidation of acetic acid by propionic acid bacteria; together they are as effective as vitamin B1 or cocarboxylase. Thus linkage of the 2 components will take place in presence of propionic acid bacteria.