Abstract
When solutions of streptolysin O were added to Warburg flasks containing, among other constituents, suspensions of mitochondria from the myocardium of rabbits and citrate, fumarate, or alpha-ketoglutarate as the substrate, there followed regularly a sharp reduction, and eventually complete cessation, of oxygen consumption. This phenomenon was not observed when succinate was the substrate in the flasks, the finding pointing to a selective interference with DPN as the underlying change. The agent in the solutions of streptolysin O responsible for this effect was shown to be a streptococcal product, and to be non-dialyzable and heat-labile. It differed from streptolysin O in that it did not appear to require prior activation with cysteine, and its effectiveness was not diminished by treatment with cholesterol or antistreptolysin globulins.
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