Effect of nicotinic acid amide and sodium on glycolysis and oxygen uptake in brain homogenates.

The glycolytic activity of brain tissue is rapidly lost on destruction of its cell structure. Geiger (1) found that when brain cells are disrupted with distilled water an inhibitor of glycolysis is released. By simply diluting a water extract of rat brain, he reduced the effect of the inhibitor and obtained a rate of lactic acid production from glucose by far exceeding the vaiues obtained with brain slices or brain dispersions. These observations were confirmed by Ochoa (2). We attempted to obtain similar active extract’s from mouse brain but were unsuccessful. Extracts prepared by Geiger’s method were not only inactive, but markedly inhibitory when added to an actively glycolyzing rat brain extract,. It was decided to study the mechanism of this inhibition in the hope of finding means to eliminate the inhibitory factors and to obtain actively glycolyzing brain preparations. Evidence has been obtained that the inhibition in brain homogenates is caused by two components. One inhibitor affects the utilization of triose phosphate; the second inhibits the phosphorylation of glucose. >lany tissues contain an enzyme which inactivates diphosphopyridine nucleotidc (DPK). Mann and Quastel (3) have shown that the destruction of DPX can be prevented by the addition of nicotinic acid amide. When DPX and nicotinic acid amide were added to mouse brain homogenates in the presence of a phosphate acceptor, rapid utilization of hexose diphosphate took place. The breakdo;rn of glucose, however, was found to be markedly affected by the presence of Na+. Elimination of Naf from the added reagents and addition of adenosine triphosphate (ATP), DPX, and nicotinic acid amide resulted in a rapid product,ion of lactic acid from glucose.