Becking G C
Fed Proc. 1976 Nov;35(13):2480-5.
It is now apparent that the rate of microsomal drug metabolism in experimental animals is subject to alteration by such dietary deficiencies as protein, vatamins, fats and minerals. The evidence, both published and unpublished, showing the effects of iron, magnesium, and potassium dificiencies on the hepatic metabolism of foreign compounds in rats is discussed. Iron deficiency has been shown to lead to a marked stimulation in hepatic metabolism, in vitro and in vivo, of both Type I (aminopyrine) and Type II (aniline) substrates. Magnesium-deficient rats have been shown to have markedly lower in vivo and in vitro rates of hepatic drug metabolism, but the monovalent intracellular mineral potassium had no apparent effect on the in vitro enzymatic conversion of foreign compounds. Hypokalemia has been shown to alter the in vivo disposition of aminopyrine and pentobarbital as evidenced by an increased plasma half-life of aminopyrine and a longer pentobarbital sleeping time in potassium-deficient animals. Large segments of the world's population are in less than satisfactory nutritional status with respect to iron, magnesium, potassium, copper, and zinc and the relevancy to man of the data discussed must be ascertained. The role of dietary minerals in nonhepatic microsomal drug metabolism is also not yet known.
目前已清楚地表明，实验动物微粒体药物代谢速率会因蛋白质、维生素、脂肪和矿物质等饮食缺乏而发生改变。本文讨论了已发表和未发表的有关铁、镁和钾缺乏对大鼠体内外源性化合物肝脏代谢影响的证据。缺铁已被证明会在体外和体内显著刺激I型（氨基比林）和II型（苯胺）底物的肝脏代谢。缺镁大鼠已被证明其体内外肝脏药物代谢速率显著降低，但单价细胞内矿物质钾对体外外源性化合物的酶促转化没有明显影响。低钾血症已被证明会改变氨基比林和戊巴比妥的体内处置，这在缺钾动物中表现为氨基比林血浆半衰期延长和戊巴比妥睡眠时间延长。世界上很大一部分人口在铁、镁、钾、铜和锌的营养状况方面不尽人意，因此必须确定所讨论数据与人类的相关性。饮食矿物质在非肝脏微粒体药物代谢中的作用也尚不清楚。
