Harkness R A, McCreanor G M, Greenwood R
Division of Inherited Metabolic Diseases, MRC Clinical Research Centre, Middlesex, UK.
J Inherit Metab Dis. 1991;14(2):202-14. doi: 10.1007/BF01800592.
In order to explain features of severe hypoxanthine guanine phosphoribosyltransferase (HPRT) deficiency, the Lesch-Nyhan syndrome, a continuous supply of substrate, hypoxanthine, for the enzyme must be generated. This supply must be increased in association with increased ATP turnover. We have shown that ATP turnover continuously supplies hypoxanthine for recycling by the enzyme HPRT and that this supply increases curvilinearly with increasing ATP turnover. The effects of increasing exercise on ATP turnover were examined using a Latin square experimental design. The outputs of hypoxanthine, xanthine, urate and creatinine were measured. The data were then examined statistically.
为了解释严重的次黄嘌呤鸟嘌呤磷酸核糖转移酶(HPRT)缺乏症(莱施-奈恩综合征)的特征,必须为该酶持续提供底物次黄嘌呤。这种供应必须随着ATP周转率的增加而增加。我们已经表明,ATP周转率持续为HPRT酶提供次黄嘌呤以供循环利用,并且这种供应随着ATP周转率的增加呈曲线增加。使用拉丁方实验设计研究了增加运动对ATP周转率的影响。测量了次黄嘌呤、黄嘌呤、尿酸盐和肌酐的输出量。然后对数据进行统计学检验。