Sinatra F, Yoshida T, Applebaum M, Masion Hoogenraad N J, Sunshine P
Pediatr Res. 1975 Nov;9(11):829-33. doi: 10.1203/00006450-197511000-00005.
Urea cycle function was evaluated in liver obtained from six patients with Reye's syndrome and from five control subjects. Reye's syndrome patients demonstrated normal activities for the extramitochondrial portion of the urea cycle, but showed marked abnormalities of the mitochondrial enzymes, i.e., carbamyl phosphate synthetase (CPS) and ornithine transcarbamylase (OTC) (Tables 2,3). CPS activity was reduced to less than 15% of control values in all four patients from whom tissues was obtained during the first 72 hr after the onset of encephalopathy. Two patents from whom tissue was not obtained until after 9 days of symptoms showed no reduction in CPS activity. The OTC activity was also reduced (3-67% of control values) in the four patients from whom tissue was obtained early in the illness. In addition, greater than 60% reduction in Vmax and Km for carbamyl phosphate was noted in all four patients in whom sample size permitted kinetic analysis, including both patients in whom CPS and OTC activity were not markedly reduced. The same kinetic abnormality as well as decreased CPS activity were experimentally produced in normal rate liver incubated in the presence of 1.0 mM 4-pentenoic acid, a short chain fatty acid and known hepatic mitochondrial toxin (Table 4).
对6例瑞氏综合征患者和5例对照者的肝脏进行了尿素循环功能评估。瑞氏综合征患者尿素循环的线粒体外部分活性正常,但线粒体酶即氨甲酰磷酸合成酶(CPS)和鸟氨酸转氨甲酰酶(OTC)出现明显异常(表2、3)。在脑病发作后的最初72小时内获取组织的所有4例患者中,CPS活性降至对照值的15%以下。直到症状出现9天后才获取组织的2例患者,其CPS活性未降低。在疾病早期获取组织的4例患者中,OTC活性也降低了(为对照值的3% - 67%)。此外,在样本量允许进行动力学分析的所有4例患者中,包括CPS和OTC活性未明显降低的患者,均观察到氨甲酰磷酸的Vmax和Km降低超过60%。在含有1.0 mM 4 - 戊烯酸(一种短链脂肪酸和已知的肝线粒体毒素)的条件下孵育正常大鼠肝脏,实验中也产生了相同的动力学异常以及CPS活性降低(表4)。