Kon' I Ia, Valiakina T I, Temirkulova R S, Lavrova N V
Vopr Med Khim. 1980 Sep-Oct;26(5):704-11.
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.
在维生素A过多和过少的情况下,研究了大鼠小肠和肝脏组织中糖苷酶、神经氨酸酶、α-L-岩藻糖苷酶、β-半乳糖苷酶和β-N-乙酰氨基葡萄糖苷酶的活性。维生素A的过量和不足给药均伴随着小肠中所研究酶活性的明显改变,以及(尽管不太明显)肝脏组织中酶活性的改变。对维生素A的存在最为显著的依赖性表现为β-半乳糖苷酶,尤其是α-L-岩藻糖苷酶,其活性在维生素A过多时降低,在维生素A过少时增加。神经氨酸酶的活性通常略有改变,但在维生素A过多的情况下,在肝脏组织中观察到其明显激活。维生素A似乎参与小肠中糖苷酶活性的变构控制以及糖蛋白的分解代谢。在维生素A过多和过少时发现的酶活性改变可能是膜糖蛋白组成变化的原因,因此,也是维生素A失衡导致细胞生长和分化典型损伤的原因。