She Q B, Hayakawa T, Tsuge H
United Graduate School of Agricultural Science, Gifu University, Japan.
Biosci Biotechnol Biochem. 1995 Feb;59(2):163-7. doi: 10.1271/bbb.59.163.
Rats fed with a vitamin B6-deficient 70% casein diet for 5 weeks were found to have decreased considerably in the content of phosphatidylcholine (PC) in liver microsomes, presumably because of the depressed PC biosynthesis from choline or phosphatidylethanolamine (PE). The activities of choline phosphokinase and choline phosphotransferase in liver decreased, apparently, as compared with the pair-fed control or control rats. The hepatic level of the PE methyltransferase co-substrate, S-adenosylmethionine (SAM), decreased about 1/3, but the level of the inhibitory metabolite, S-adenosylhomocysteine (SAH), was elevated due to the marked reduction in the activities of cystathionine beta-synthase and gamma-cystathionase. The resultant molar ratio of SAM/SAH decreased drastically such that the methylation of PE to PC was decreased in vivo, as confirmed by lowering the activity of PE methyltransferase in vitro in response to a decreased molar ratio of SAM/SAH. A similar effect on the PE methylation was also observed in the pair-fed control rats, but the PC biosynthesis from choline clearly compensated for the drop of PC biosynthesis from PE. Results of this study demonstrate that vitamin B6 deficiency modified methionine metabolism and decreased choline utilization, and thus indirectly affected the biosynthesis of PC in liver microsomes.
给大鼠喂食缺乏维生素B6的70%酪蛋白饮食5周后,发现其肝微粒体中磷脂酰胆碱(PC)的含量显著降低,这可能是由于胆碱或磷脂酰乙醇胺(PE)的PC生物合成受到抑制。与配对喂养的对照大鼠或正常对照大鼠相比,肝脏中胆碱磷酸激酶和胆碱磷酸转移酶的活性明显降低。PE甲基转移酶的共底物S-腺苷甲硫氨酸(SAM)的肝脏水平降低了约1/3,但由于胱硫醚β-合酶和γ-胱硫醚酶的活性显著降低,抑制性代谢物S-腺苷同型半胱氨酸(SAH)的水平升高。由此产生的SAM/SAH摩尔比急剧下降,使得体内PE向PC的甲基化减少,这一点通过体外实验得到证实,即随着SAM/SAH摩尔比的降低,PE甲基转移酶的活性也降低。在配对喂养的对照大鼠中也观察到了对PE甲基化的类似影响,但胆碱的PC生物合成明显补偿了PE的PC生物合成的下降。本研究结果表明,维生素B6缺乏会改变蛋氨酸代谢并降低胆碱利用,从而间接影响肝微粒体中PC的生物合成。