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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Pappu A S, Fatterpaker P, Sreenivasan A

Biochem J. 1978 Apr 15;172(1):115-21. doi: 10.1042/bj1720115.

The disturbance in 2-methylmalonate metabolism resulting in its increased urinary excretion observed in vitamin E deficiency is not caused by increased formation of methylmalonate from propionate as is evident from the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but can be traced to an impairment in the conversion of methylmalonate into succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA mutase (EC 5.4.99.2) in rat liver. 2. It is shown that the decrease in the activity of methylmalonyl-CoA mutase in vitamin E deficiency is not a consequence of a secondary vitamin B12 deficiency. Peroxidative destruction of the coenzyme in vitamin E deficiency was also ruled out. The results suggest a defect in the conversion of cyanocobalamin into its coenzyme form.

维生素E缺乏时观察到的2-甲基丙二酸代谢紊乱导致其尿排泄增加，这并非由丙酸盐生成甲基丙二酸增加所致，从丙酰辅酶A羧化酶（EC 6.4.1.3）的活性可明显看出，而是可追溯到大鼠肝脏中依赖维生素B12的酶甲基丙二酰辅酶A变位酶（EC 5.4.99.2）将甲基丙二酸转化为琥珀酸的过程受损。2. 研究表明，维生素E缺乏时甲基丙二酰辅酶A变位酶活性降低并非继发性维生素B12缺乏的结果。维生素E缺乏时辅酶的过氧化破坏也被排除。结果提示氰钴胺转化为其辅酶形式存在缺陷。

Pappu A S, Fatterpaker P, Sreenivasan A

Biochem J. 1978 Apr 15;172(1):115-21. doi: 10.1042/bj1720115.

The disturbance in 2-methylmalonate metabolism resulting in its increased urinary excretion observed in vitamin E deficiency is not caused by increased formation of methylmalonate from propionate as is evident from the activity of the enzyme propionyl-CoA carboxylase (EC 6.4.1.3), but can be traced to an impairment in the conversion of methylmalonate into succinate by the vitamin B12-requiring enzyme, methylmalonyl-CoA mutase (EC 5.4.99.2) in rat liver. 2. It is shown that the decrease in the activity of methylmalonyl-CoA mutase in vitamin E deficiency is not a consequence of a secondary vitamin B12 deficiency. Peroxidative destruction of the coenzyme in vitamin E deficiency was also ruled out. The results suggest a defect in the conversion of cyanocobalamin into its coenzyme form.

维生素E缺乏时观察到的2-甲基丙二酸代谢紊乱导致其尿排泄增加，这并非由丙酸盐生成甲基丙二酸增加所致，从丙酰辅酶A羧化酶（EC 6.4.1.3）的活性可明显看出，而是可追溯到大鼠肝脏中依赖维生素B12的酶甲基丙二酰辅酶A变位酶（EC 5.4.99.2）将甲基丙二酸转化为琥珀酸的过程受损。2. 研究表明，维生素E缺乏时甲基丙二酰辅酶A变位酶活性降低并非继发性维生素B12缺乏的结果。维生素E缺乏时辅酶的过氧化破坏也被排除。结果提示氰钴胺转化为其辅酶形式存在缺陷。