Hadley K, Sato P
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.
J Inherit Metab Dis. 1988;11(4):387-96. doi: 10.1007/BF01800427.
Gulonolactone oxidase, a key enzyme in the biosynthesis of ascorbic acid, is missing from guinea pigs and certain other scurvy-prone species. Weekly intraperitoneal injections of glutaraldehyde cross-linked immunoprecipitates of this enzyme have been shown to provide guinea pigs with the capability of synthesizing their own ascorbic acid and of surviving without an exogenous source of this vitamin. This protocol, however, was successful in only a small percentage of the animals tested. The reasons for the limited therapeutic success were investigated. Apparently, the gulonolactone oxidase-treated guinea pigs fed without ascorbic acid were receiving insufficient nutrition. By supplementing these enzyme-treated animals with vitamins A, B, D and E and selenium, we successfully maintained a high proportion of guinea pigs fed without vitamin C.
古洛糖酸内酯氧化酶是抗坏血酸生物合成中的关键酶，豚鼠和其他一些易患坏血病的物种体内缺乏该酶。每周腹腔注射这种酶的戊二醛交联免疫沉淀物已被证明能使豚鼠具备合成自身抗坏血酸的能力，并且在没有这种维生素外源供应的情况下存活。然而，该方案在仅一小部分受试动物中取得了成功。对治疗效果有限的原因进行了研究。显然，喂食不含抗坏血酸的经古洛糖酸内酯氧化酶处理的豚鼠营养摄入不足。通过给这些经酶处理的动物补充维生素A、B、D、E和硒，我们成功地使很大比例的豚鼠在不补充维生素C的情况下存活。
