Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activities of glycosidases neuromanidase, alpha-L-fucosidase, beta-galactosidase and beta-N-acetylglucosaminidase were studied in rat small intestine and liver tissue under conditions of hyper- and hypovitaminosis A. Both excessive and insufficient administrations of vitamin A were accompanied by distinct alterations in activity of the enzymes studied in small intestine and (although less distinct) in liver tissue. The most significant dependence on the presence of vitamin A exhibited beta-galactosidase and especially alpha-L-fucosidase, activity of which was decreased in hypervitaminosis and increased in hypovitaminosis A. Activity of neuraminidase was usually slightly altered but its marked activation was noted in liver tissue under conditions of hypervitaminosis A. Vitamin A appears to participate in allosteric control of the glycosidase activity in small intestine and in catabolism of glycoproteins. The alterations of the enzymatic activity found in hyper- and hypovitaminosis A might be responsible for changes in composition of membrane glycoproteins and, hence, for the typical for vitamin A disbalance impairments in cellular growth and differentiation.
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PMID:[Enzymatic activity of glycoprotein catabolism in the organs of rats with hyper- and hypovitaminosis A]. 677 13

Treatment with excessive amounts of Vitamin A during maternity induces fetal malformations. However, it is unclear whether these malformations are due to gene mutations or not. Using transgenic mice (containing lacZ gene showing beta-galactosidase enzymatic activity), we planned to observe whether gene mutations occur in the fetal tissues after treatment during maternity with Vitamin A (retinol palmitate). On the 11th day of pregnancy, mothers were given 30 mg (group 2), 150 mg (group 3) and 300 mg (group 4) of Vitamin A/kg body weight orally. Fetuses obtained on the 18th day of gestation showed malformations, such as cleft palate, origodactyly, brachydactyly and ectromeria. Most notably, cleft palate occurred dose dependently. The incidental rates were 100% in group 4, 58% in group 3 and 6% in group 2. The number of dead and absorbed fetuses also increased dose dependently with the treatments. DNA (integrated vectors containing lacZ genes) extracted from each fetus showed Vitamin A-induced lacZ mutations, especially in the malformed fetuses. The mutation frequencies were 4.99x10(-5) in group 4, 5.28x10(-5) in group 3 and 4.26x10(-5) in group 2. The frequencies of group 3 were significantly higher (p<0.05) than that of the controls (group 1), 2.79x10(-5). Maternal treatment with Vitamin A (150 mg/kg of body weight) was carried out on the 11th day of pregnancy. Fetuses obtained on the 14th day of gestation showed a much higher incidence of mutation, approximately 8.91x10(-5) (group 6) that was significantly higher (p<0.0001) than those from the controls (group 5), 2.94x10(-5). The present study indicates a possibility that hypervitaminosis A-induced fetal malformation and death might be caused by gene mutations.
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PMID:Hypervitaminosis A resulting in DNA aberration in fetal transgenic mice (Muta Mouse). 1605 64