Horio F, Ozaki K, Yoshida A, Makino S, Hayashi Y
J Nutr. 1985 Dec;115(12):1630-40. doi: 10.1093/jn/115.12.1630.
The activities of several enzymes involved in hepatic ascorbic acid synthesis and the requirement of dietary ascorbic acid were investigated in the OD (osteogenic disorder) rat, which has a hereditary defect in ascorbic acid-synthesizing ability. No activity of hepatic L-gulonolactone oxidase was detected in OD rats. However, OD rats maintained the normal activities of hepatic UDPglucose dehydrogenase, UDPglucuronyl transferase and beta-glucuronidase. Hemorrhage in muscle and leg joints, lower hepatic content of cytochrome P-450 and lower activities of hepatic drug-metabolizing enzymes, higher serum and adrenal levels of corticosterone and lower urinary excretion of hydroxyproline were observed in ascorbic acid-deficient OD rats than in OD rats fed 300 mg ascorbic acid/kilogram diet. Consequently, we conclude that OD rats cannot synthesize ascorbic acid because of the lack of activity of hepatic L-gulonolactone oxidase and that the dietary addition of about 300 mg ascorbic acid (per kilogram diet) is enough to prevent signs of vitamin C deficiency and to achieve maximum growth, and that more than 300 mg ascorbic acid per kilogram diet may be required for the maximum activity of hepatic drug-metabolizing enzymes.
在具有抗坏血酸合成能力遗传缺陷的OD（成骨障碍）大鼠中，研究了几种参与肝脏抗坏血酸合成的酶的活性以及膳食抗坏血酸的需求量。在OD大鼠中未检测到肝脏L-古洛糖酸内酯氧化酶的活性。然而，OD大鼠维持了肝脏UDP葡萄糖脱氢酶、UDP葡萄糖醛酸转移酶和β-葡萄糖醛酸酶的正常活性。与喂食300毫克抗坏血酸/千克饲料的OD大鼠相比，抗坏血酸缺乏的OD大鼠出现了肌肉和腿部关节出血、肝脏细胞色素P-450含量降低、肝脏药物代谢酶活性降低、血清和肾上腺皮质酮水平升高以及尿羟脯氨酸排泄量降低的情况。因此，我们得出结论，OD大鼠由于缺乏肝脏L-古洛糖酸内酯氧化酶的活性而无法合成抗坏血酸，并且膳食中添加约300毫克抗坏血酸（每千克饲料）足以预防维生素C缺乏的症状并实现最大生长，而每千克饲料超过300毫克抗坏血酸可能是肝脏药物代谢酶最大活性所必需的。
