Kimura T, Hasegawa K, Imamura H, Yoshida A
J Nutr Sci Vitaminol (Tokyo). 1983 Apr;29(2):153-9. doi: 10.3177/jnsv.29.153.
In order to clarify the mechanism of the adverse effects of dietary amaranth, trisodium 1-(4-sulfo-1-naphthylazo)-2-naphthyl-3,6 disulfonic acid, the effects of amaranth in vitro and in a jejunum perfusion in vivo on intestinal sucrase were investigated in rats. The inhibitory effect of amaranth in vitro on the sucrase activity was not detected even at the concentration of 1%, whereas the remarkable release of intestinal sucrase from intestine was observed with the jejunum perfusion of Ringer bicarbonate solution (RBS) containing amaranth at the 1% level. On the other hand, the perfusion of RBS containing tris(hydroxymethyl)-aminomethane, a strong inhibitor of intestinal disaccharidase activities, did not produce the release of intestinal alkaline phosphatase. These findings suggest that the toxicity of dietary amaranth is due to the exfoliating or solubilizing effects of amaranth on the brush border membrane of the small intestine.
为了阐明食用苋菜籽不良反应的机制，即1-(4-磺基-1-萘基偶氮)-2-萘基-3,6-二磺酸三钠，研究了苋菜籽在体外以及在大鼠空肠灌注实验中对肠道蔗糖酶的影响。即使在浓度为1%时，体外实验也未检测到苋菜籽对蔗糖酶活性有抑制作用，然而，当用含1%苋菜籽的林格氏碳酸氢盐溶液（RBS）进行空肠灌注时，可观察到肠道蔗糖酶从肠道中显著释放。另一方面，用含有三（羟甲基）氨基甲烷（一种肠道双糖酶活性的强抑制剂）的RBS进行灌注，并未导致肠道碱性磷酸酶的释放。这些发现表明，食用苋菜籽的毒性是由于苋菜籽对小肠刷状缘膜的剥落或增溶作用所致。
