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维生素B12缺乏对大鼠肝脏胱硫醚β-合酶活性的影响。

Effect of vitamin B12-deficiency on the activity of hepatic cystathionine beta-synthase in rats.

作者信息

Doi T, Kawata T, Tadano N, Iijima T, Maekawa A

机构信息

Department of Agricultural Chemistry, Tokyo University of Agriculture, Japan.

出版信息

J Nutr Sci Vitaminol (Tokyo). 1989 Apr;35(2):101-10. doi: 10.3177/jnsv.35.101.

DOI:10.3177/jnsv.35.101
PMID:2732804
Abstract

The effect of vitamin B12(B12)-deficiency on the activities of hepatic methionine synthase, homocysteine methyltransferase, and cystathionine beta-synthase was investigated in rats. The rats bred from B12-deficient dams were fed the B12-deficient diets for 150 days after weaning. Growth retardation of the B12-deficient rats was already observed on day 30 and continued through 150 days. But dietary supplementation of 0.5% DL-methionine slightly improved the growth retardation. Urinary excretion of methylmalonic acid increased to about 15 mg/mg creatinine and hepatic B12 concentration declined to about 2 ng/g liver after a 150-day feeding of the B12-deficient diets. Hepatic methionine synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 5% of B12-supplemented controls. Hepatic betaine-homocysteine methyltransferase activity showed no significant change caused by B12-deficiency. Hepatic cystathionine beta-synthase activity in rats fed the B12-deficient diets supplemented with or without methionine decreased to about 61% and 27% of their B12-supplemented controls, respectively, but the decrease was partially improved by methionine supplementation. In conclusion, the rats bred from B12-deficient dams showed a severe B12-deficiency after a 150-day feeding of the B12-deficient diets. The decrease of hepatic cystathionine beta-synthase activity was supposed to be due to the adaptation by the defect of methionine resynthesis.

摘要

研究了维生素B12(B12)缺乏对大鼠肝脏蛋氨酸合酶、同型半胱氨酸甲基转移酶和胱硫醚β-合酶活性的影响。将由缺乏B12的母鼠所生的大鼠在断奶后喂食缺乏B12的饲料150天。在第30天时已观察到缺乏B12的大鼠生长迟缓,并持续至150天。但日粮中添加0.5%的DL-蛋氨酸可略微改善生长迟缓。在喂食缺乏B12的饲料150天后,甲基丙二酸的尿排泄量增加至约15mg/mg肌酐,肝脏B12浓度降至约2ng/g肝脏。喂食添加或未添加蛋氨酸的缺乏B12饲料的大鼠肝脏蛋氨酸合酶活性降至补充B12的对照组的约5%。肝脏甜菜碱-同型半胱氨酸甲基转移酶活性未因B12缺乏而发生显著变化。喂食添加或未添加蛋氨酸的缺乏B12饲料的大鼠肝脏胱硫醚β-合酶活性分别降至补充B12的对照组的约61%和27%,但蛋氨酸补充可部分改善这种下降。总之,由缺乏B12的母鼠所生的大鼠在喂食缺乏B12的饲料150天后表现出严重的B12缺乏。肝脏胱硫醚β-合酶活性的下降被认为是由于蛋氨酸再合成缺陷的适应性反应。

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