Isolation and characterization of galactose from hydrolysates of glycogen.

\\hen the diet of chicks contains 15% n-galactose, physical manifestations occur, particularly in female chicks, which include epileptiform seizures and death (1, 2). Galactose and uridine diphosphate galactose accumulate in blood and liver whereas uridine diphosphate glucose levels are greatly reduced (3). Toxicity of dietary galactose in excess has been attributed to n-glucose starvation (4) or protein deficiency (5) which somehow result from accumulation of large quantities of galactose or n-galactose l-phosphate. Normal glucose utilization may be restricted as galactose l-phosphate in excess inhibits phosphoglucomutase (6), n-glucose B-phosphate dehydrogenase (7), and uridine triphosphate glucose l-phosphate pyrophosphorylase (8). Galactose ingestion reduces the ability of rats to store glycogen (4) but when chicks are fed galact.ose, liver glycogen levels are within normal limits under circumstances in which the chicks show physical evidence of galactose toxicity (2). Although quantitative changes in glycogen are not apparent, significant qualitative differences are observed. This communication reports the occurrence of galactose in polymeric form in highly purified glycogen from liver of chicks fed toxic levels of galactose. The galactose was identified and characterized from hydrolysates of glycogen by paper chromatography and by isolation ,as a crystalline derivative.