Morita E, Shirakami Y, Mizuno N
Faculty of Pharmaceutical Sciences, Mukogawa Women's University, Hyogo, Japan.
J Nutr Sci Vitaminol (Tokyo). 1988 Dec;34(6):553-65. doi: 10.3177/jnsv.34.553.
The intestinal absorption of pyridoxal 5'-phosphate (PLP) at physiological levels (10(-7) -10(-6) M) was studied in comparison with that of pyridoxal (PL) in rat, using in vitro everted sac and an intestinal preparation that permitted continuous in situ collection of mesenteric venous blood. After PLP administration (10(-6) -10(-3) M) in situ, larger amounts of PLP were found in the mesenteric venous plasma than after PL administration at the same dose. The amount of PLP found in the mesenteric venous plasma was dependent on its dose at lower concentrations up to 10(-4) M but became independent at higher concentrations. After PL administration at various doses, the amount of PL found in the mesenteric venous blood increased linearly with the dose. When various concentrations of PLP were added to the mucosal side, under the in vitro condition with protection from alkaline phosphate hydrolysis, PLP was detected in the serosal side and the extent of PLP transport was dependent on the initial concentration of PLP in the mucosal side. When various concentrations of PL were added to the mucosal side, the extent of PL transport was independent of the initial concentration of PL in the mucosal side. In rat pretreated with actinomycin D, PLP transport in vitro was inhibited but not that of PL. N2-induced anoxia and pyridoxamine 5'-phosphate and anion transport inhibitor (4,4'-diisothiocyanostilben-2,2'-disulfonic acid disodium salt) showed no effect on PLP transport. These results suggest that PLP can be absorbed in the phosphorylated form and imply the presence of a saturable process for direct absorption of PLP itself and a diffusive process for PL absorption. In addition, the result of the in vivo neonatal experiment suggests that the neonatal intestine also can transport PLP in phosphorylated form.
在大鼠体内，使用体外翻转肠囊和一种允许连续原位收集肠系膜静脉血的肠道制剂，研究了生理水平（10⁻⁷ - 10⁻⁶ M）的磷酸吡哆醛（PLP）与吡哆醛（PL）的肠道吸收情况。原位给予PLP（10⁻⁶ - 10⁻³ M）后，肠系膜静脉血浆中发现的PLP量比给予相同剂量PL后更多。在浓度低至10⁻⁴ M时，肠系膜静脉血浆中发现的PLP量取决于其剂量，但在较高浓度时则与之无关。给予不同剂量的PL后，肠系膜静脉血中发现的PL量随剂量呈线性增加。在体外条件下，当向黏膜侧添加不同浓度的PLP并防止碱性磷酸酶水解时，在浆膜侧检测到了PLP，并且PLP的转运程度取决于黏膜侧PLP的初始浓度。当向黏膜侧添加不同浓度的PL时，PL的转运程度与黏膜侧PL的初始浓度无关。在用放线菌素D预处理的大鼠中，体外PLP的转运受到抑制，但PL的转运不受影响。N₂诱导的缺氧以及磷酸吡哆胺和阴离子转运抑制剂（4,4'-二异硫氰基芪-2,2'-二磺酸钠盐）对PLP的转运没有影响。这些结果表明，PLP可以以磷酸化形式被吸收，这意味着存在PLP自身直接吸收的饱和过程以及PL吸收的扩散过程。此外，体内新生动物实验的结果表明，新生动物的肠道也能够转运磷酸化形式的PLP。
