Colombo J P, Berüter J, Bachmann C, Peheim E
Enzyme. 1977;22(6):391-8. doi: 10.1159/000458824.
At high systemic blood concentrations ammonia may be partially deviated into the pathway of pyrimidine synthesis, as has been observed in different genetic defects of the urea cycle. The portacaval shunt (PCS) rat presents an animal model to study ammonia detoxication without an underlying enzyme defect in the urea cycle. Since ammonia may induce a deviation into the pyrimidine pathway by influencing enzymatic reactions involved in this pathway, the activity of carbamylphosphate synthetase and aspartate transcarbamylase in liver as well as the excretion of orotic acid in the urine were measured in rats 10, 20 and 30 days after PCS. The results suggest that in this experimental model ammonia may be channeled into the pyrimidine pathway leading to a stimulation of the first enzymatic step and to an increased excretion of orotic acid.
在高全身血氨浓度时,氨可能会部分偏离进入嘧啶合成途径,正如在尿素循环的不同遗传缺陷中所观察到的那样。门腔分流(PCS)大鼠提供了一个动物模型,用于研究氨解毒,而不存在尿素循环潜在的酶缺陷。由于氨可能通过影响参与该途径的酶促反应而诱导进入嘧啶途径,因此在PCS后10、20和30天的大鼠中测量了肝脏中氨甲酰磷酸合成酶和天冬氨酸转氨甲酰酶的活性以及尿中乳清酸的排泄。结果表明,在这个实验模型中,氨可能被引导进入嘧啶途径,导致第一步酶促反应受到刺激,并增加乳清酸的排泄。