Some Steps in the Tricarboxylic Acid Cycle

SOME STEPS IN THE TRICARBOXYLIC ACID CYCLE Oxidative Decarboxylation of Pyruvate The Intracellular Function of Vitamin Bj 

In 1936 Peters introduced the concept of a biochemical lesion as a basis of human disease, an illness attributable to an identifiable biochemical disorder. This idea was very influential in directing the 

The way in which thiamine participated in the oxidation of pyruvate became clearer when Lohmann and Schuster (1937) showed vitamin Bj to be present intracellularly as thiamine pyrophosphate. In yeast, decarboxylation of pyruvate yielded ethanal which was reduced by alcohol dehydrogenase to give ethanol. A cofactor was needed for this decarboxylation, co-carboxylase. Like the cofactor needed in animal cells for the decarboxylation of pyruvate, cocarboxylase was found to be identical to thiamine pyrophosphate. Vitamin Bj thus became the first vitamin whose intracellular function as a coenzyme had been established in vitro. Another aphorism therefore arose about vitamins—B vitamins are (parts of) coenzymes—an idea that was to be completely confirmed. 

Heavy Metal Poisoning The Involvement of Lipoic Acid 

By the late 1930s it was widely accepted that active acetate arose from pyruvate decarboxylation and fatty acid oxidation. Acetate itself 

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