Biochemical and Molecular Medicine
Volume 59, Issue 1, October 1996, Pages 7-12
Regular ArticleA Mouse Model of Galactose-1-Phosphate Uridyl Transferase Deficiency
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Cited by (78)
Alterations of galactose metabolism caused by deficit of galactose-1-phosphate uridylyltransferase activity: An overview of galactosemia type I
2019, Molecular Nutrition CarbohydratesHereditary galactosemia
2018, Metabolism: Clinical and ExperimentalCitation Excerpt :The intracellular elevation of galactitol induces hyperosmotic and oxidative stress [7–9], which has been pointed out as the causative agent of cataracts in GALT- and GALK-deficiencies. Furthermore, the mouse exhibits low aldose reductase expression/activity in the lens, and indeed neither the GALK- nor the GALT-deficient mouse develops cataracts [10,11]. Pseudotumor cerebri is also hypothesized to be due to accumulation of galactitol.
Intracerebroventricular d-galactose administration impairs memory and alters activity and expression of acetylcholinesterase in the rat
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