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Diagnosis of inherited disorders of galactose metabolism.

Current protocols in human genetics (2008-04-23)
Carla Cuthbert, Helene Klapper, Louis Elsas
ABSTRACT

Galactose metabolism occurs through an evolutionarily conserved pathway in which galactose and uridine diphosphoglucose are converted to glucose-1-phosphate and uridine diphosphogalactose through the action of three sequential enzymes: galactokinase (GALK, EC 2.7.1.6), galactose-1-phosphate uridyltransferase (GALT, EC 2.7.7.12), and uridine phosphogalactose 4'-epimerase (GALE, EC 5.1.3.2). Inborn errors of galactose metabolism occur with impaired activity for each of the enzymes. Classical galactosemia is the most common and the most severe of these diseases and is caused by deficiency of the GALT enzyme, affecting from approximately 1 in 10,000 to 1 in 30,000 live births. Deficiency of GALE is the rarest of the three diseases. Assays for galactitol and galactose-1-phosphate and methods for assaying enzyme activities of GALT, GALK, and GALE are provided here. Interpretation of diagnostic results for screen-positive newborns or symptomatic patients, as well as therapeutic interventions based on biochemical phenotype and molecular genotype, are also included as decision trees.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Urease from Canavalia ensiformis (Jack bean), Type III, powder, 15,000-50,000 units/g solid
Sigma-Aldrich
Phosphatase, Alkaline from bovine intestinal mucosa, buffered aqueous glycerol solution, ≥4,000 DEA units/mg protein