Ho C Y, Clifford A J
J Nutr. 1977 May;107(5):758-66. doi: 10.1093/jn/107.5.758.
The effects of prolonged intravenous administration of bovine milk xanthine oxidase (EC 1.2.3.2.) on blood lipids and arterial integrity were measured to determine if the administration of this enzyme produces metabolic changes conducive to plaque formation. New Zealand White rabbits were injected intravenously with bovine milk xanthine oxidase at 4-day intervals during a 13-week test period. At the end of the test period, the rabbits were killed and blood, heart, aorta, liver, and kidneys were collected and evaluated. Rabbits injected with phosphate buffer or acid-denatured xanthine oxidase for the same length of time served as negative controls. Additional rabbits fed a diet containing 3% added cholesterol for the same time period served as positive controls. The administration of xanthine oxidase in large amounts over a prolonged period did not alter serum cholesterol or triglyceride levels and did not reduce plasmalogen levels in the aorta or heart. Xanthine oxidase administration did not induce arterial plaque formation. Cholesterol feeding over the same time period increased serum cholesterol levels, reduced liver xanthine oxidase activity levels and resulted in a marked development of arterial plaques. Althouth xanthine oxidase activity was found in liver from all rabbits, enzyme activity was not detectable in aorta, heart or kidneys from any rabbit. Free or complexed bovine milk xanthine oxidase could not be demonstrated in heart, aorta, liver or kidneys from any of the rabbits with immunodiffusion or with immunofluorescent techniques. The study showed that when large intravenous doses of bovine milk xanthine oxidase were given to rabbits, the enzyme was not deposited in heart, aorta, liver or kidneys. The study also showed that large intravenous doses of xanthine oxidase over prolonged periods did not deplete arterial or coronary tissue plasmalogens, and did not induce arterial plaque formation.
为了确定长时间静脉注射牛乳黄嘌呤氧化酶(EC 1.2.3.2.)是否会产生有利于斑块形成的代谢变化,对血脂和动脉完整性的影响进行了测量。在为期13周的试验期内,每隔4天给新西兰白兔静脉注射牛乳黄嘌呤氧化酶。在试验期结束时,处死兔子并收集血液、心脏、主动脉、肝脏和肾脏进行评估。注射相同时间的磷酸盐缓冲液或酸变性黄嘌呤氧化酶的兔子作为阴性对照。另外,在相同时间段内喂食含3%添加胆固醇饮食的兔子作为阳性对照。长时间大量给予黄嘌呤氧化酶不会改变血清胆固醇或甘油三酯水平,也不会降低主动脉或心脏中的缩醛磷脂水平。给予黄嘌呤氧化酶不会诱导动脉斑块形成。在相同时间段内喂食胆固醇会增加血清胆固醇水平,降低肝脏黄嘌呤氧化酶活性水平,并导致动脉斑块明显形成。尽管在所有兔子的肝脏中都发现了黄嘌呤氧化酶活性,但在任何兔子的主动脉、心脏或肾脏中均未检测到酶活性。用免疫扩散或免疫荧光技术在任何兔子的心脏、主动脉、肝脏或肾脏中均未证实存在游离或复合的牛乳黄嘌呤氧化酶。该研究表明,当给兔子静脉注射大剂量牛乳黄嘌呤氧化酶时,该酶不会沉积在心脏、主动脉、肝脏或肾脏中。该研究还表明,长时间静脉注射大剂量黄嘌呤氧化酶不会消耗动脉或冠状动脉组织中的缩醛磷脂,也不会诱导动脉斑块形成。