Löffler Monika, Fairbanks Lynette D, Zameitat Elke, Marinaki Anthony M, Simmonds H Anne
Institute for Physiological Chemistry, Philipps-University, Marburg, Germany.
Trends Mol Med. 2005 Sep;11(9):430-7. doi: 10.1016/j.molmed.2005.07.003.
Genetic defects involving enzymes essential for pyrimidine nucleotide metabolism have provided new insights into the vital physiological functions of these molecules in addition to nucleic acid synthesis. Such aberrations disrupt the haematological, nervous or mitochondrial systems and can cause adverse reactions to analogue therapy. Regulation of pyrimidine pathways is also known to be disrupted in malignancies. Nine genetic defects have now been identified but only one is currently treatable. Diagnosis is aided by the accumulation of specific metabolites. Recently, progress has been made in understanding the molecular mechanisms underlying inborn errors of pyrimidine metabolism, together with the key clinical issues and the implications for the future development of novel drugs and therapeutic strategies.
涉及嘧啶核苷酸代谢所必需酶的遗传缺陷,除了在核酸合成方面,还为这些分子的重要生理功能提供了新的见解。此类异常会扰乱血液、神经或线粒体系统,并可能导致对类似物疗法产生不良反应。已知嘧啶途径的调节在恶性肿瘤中也会受到破坏。现已确定九种遗传缺陷,但目前只有一种可治疗。特定代谢产物的积累有助于诊断。最近,在理解嘧啶代谢先天性缺陷的分子机制、关键临床问题以及对新型药物和治疗策略未来发展的影响方面取得了进展。