Abstract

SummaryIn animals fed diets containing sulfaguanidine, the response to Chloretone stimulation of ascorbic acid excretion was considerably suppressed. The enzymatic synthesis of the vitamin from glucuronolactone by liver homogenates of such animals was not decreased nor was the enzyme activity affected by addition of the sulfa drug to the system in vitro. A significant lowering was observed in the liver UDPG dehydrogenase activity in animals receiving sulfaguanidine but the incorporation of glucose-U-14C into either glucuronic or ascorbic acid was unaltered. These results indicate that the sulfa drug lowers the liver level and excretion of the vitamin by decreasing its biosynthesis via a pathway that may not directly involve glucose as the precursor.

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