INTERRELATIONS OF VITAMIN B12 AND FOLIC ACID METABOLISM - FOLIC ACID CLEARANCE STUDIES

INTERRELATIONS OF VITAMIN B12 AND FOLIC ACID METABOLISM - FOLIC ACID CLEARANCE STUDIES
复制标题

DOI:
10.1172/jci104589
复制
发表时间:
1962-01-01
影响因子:
15.9
通讯作者:
ZALUSKY, R
ZALUSKY, R
中科院分区:
医学1区
文献类型:
--
作者:
HERBERT, V;ZALUSKY, R

文献摘要

被引文献

相似文献

在轻度至严重贫血的维生素B12缺乏受试者中,静脉注射每公斤体重15μg蝶酰谷氨酸(PGA)后,粪链球菌的叶酸活性迅速消失,但干酪乳杆菌的活性从血清中缓慢消失。在 100 名连续缺乏维生素 B12 的受试者中,有 17 名观察到干酪乳杆菌血清叶酸活性显着升高(25 毫克/毫升或更多)。在每日剂量5至1,000μg维生素B12的特定治疗期间,干酪乳杆菌的血清叶酸活性可能急剧下降,并且可能在再次上升到正常范围之前达到低于正常的水平。这种现象可能是由于缺乏维生素B12导致干酪乳杆菌叶酸活性利用受阻而释放,随后在造血过程中被快速利用,可能与治疗期间血清铁的下降类似。在每日剂量较小(1μg)的维生素B12的特定治疗期间,干酪乳杆菌的血清叶酸活性可能下降得更慢。这些发现表明,在维生素 B12 缺乏的受试者中,PGA 迅速转化为干酪乳杆菌活性且可能对代谢有用的形式(可能是 N5-甲基四氢叶酸),然后在血清中“堆积”,因为维生素 B12 是其正常利用所必需的。这种“堆积”的叶酸活性往往会减少可用于其他 1-碳单位转移的叶酸量。这些研究为正常叶酸代谢所需维生素 B12 的概念提供了证据,支持了这样一种可能性:许多维生素 B12 缺乏症患者明显的叶酸缺乏可能在很大程度上是由于继发性叶酸代谢紊乱所致。
In slightly to severely anemic vitamin Bl2-deficient subjects, after the intravenous injection of 15 [mu]g pteroylglutamic acid (PGA)per kg of body weight, folic acid activity for S. faecalis disappears rapidly but activity for L. casei disappears slowly from the serum. Markedly elevated serum folic acid activity for L. casei (25 or more m [mu]g per ml) was observed in 17 of 100 consecutive subjects with vitamin B12 deficiency. During specific therapy with daily doses of 5 to 1,000 [mu]g of vitamin B12, serum folic acid activity for L. casei may fall sharply and may reach levels below normal before rising again into the normal range. The phenomenon may be due to release of the block in utilization of L. casei folic acid activity caused by lack of vitamin B12, with subsequent rapid utilization in hematopoiesis, and may be similar to the fall in serum iron during therapy. Serum folic acid activity for L. casei may fall more slowly during specific therapy with smaller (1 [mu]g) daily doses of vitamin B12. These findings suggest that in the vitamin B12-deficient subject, PGA is rapidly converted to an L. casei-active and presumably metabolically useful form (probably N5- methyl-tetrahydro-folic acid) which then "piles up" in the serum because vitamin B12 is required for its normal utilization. This "piled up" folate activity would tend to reduce the amount of folic acid available for other 1-carbon unit transfers. These studies, by providing evidence for the concept that vitamin B12 is required for normal folic acid metabolism, support the possibility that the apparent folic acid deficiency in many patients with vitamin B12 deficiency may be in large measure due to secondarily deranged folic acid metabolism.