Brattström L E, Israelsson B, Jeppsson J O, Hultberg B L
Department of Internal Medicine, University of Lund, Malmö General Hospital, Sweden.
Scand J Clin Lab Invest. 1988 May;48(3):215-21. doi: 10.3109/00365518809167487.
With an improved highly reproducible method, we measured total plasma homocysteine (free plus protein-bound) and related amino acids in the fasting state in healthy subjects, before and after treatment with co-factors for homocysteine metabolism: 1 mg cyanocobalamin (n = 14), 5 mg folic acid (n = 13) or 40 mg pyridoxine hydrochloride (n = 15) daily for 14 days. Cyanocobalamin and pyridoxine hydrochloride had no effects on plasma levels of amino acids, but folic acid had a considerable homocysteine-lowering effect. Total plasma homocysteine was reduced in all but two subjects, from 19.9 +/- 4.4 (mean +/- SEM) to 9.5 +/- 1.0 mumol/l (-52%, p less than 0.01). We propose that folic acid in excess acts by enhancing the remethylation of homocysteine to methionine. The finding confirms a previous report by us. Since homocysteine is considered to be an atherogenic amino acid and recent reports suggest that mild to moderate homocysteinaemia is also associated with premature vascular disease, treatment with folic acid might be of use as prophylaxis.
采用一种改进的高重复性方法，我们在健康受试者空腹状态下，测定了同型半胱氨酸代谢辅助因子治疗前后血浆总同型半胱氨酸（游离型加蛋白结合型）及相关氨基酸水平：每日分别给予1毫克氰钴胺素（n = 14）、5毫克叶酸（n = 13）或40毫克盐酸吡哆醇（n = 15），持续14天。氰钴胺素和盐酸吡哆醇对血浆氨基酸水平无影响，但叶酸有显著降低同型半胱氨酸的作用。除两名受试者外，所有受试者的血浆总同型半胱氨酸均降低，从19.9±4.4（均值±标准误）降至9.5±1.0微摩尔/升（-52%，p<0.01）。我们认为过量叶酸通过增强同型半胱氨酸向蛋氨酸的再甲基化作用而起效。这一发现证实了我们之前的报告。由于同型半胱氨酸被认为是一种致动脉粥样硬化氨基酸，且近期报告表明轻度至中度高同型半胱氨酸血症也与血管疾病过早发生有关，因此叶酸治疗可能用作预防措施。
