Fitzgerald D H, Tipton K F, Lyles G A
Department of Biochemistry, Trinity College, Dublin, Ireland.
J Neural Transm Suppl. 1998;52:259-64. doi: 10.1007/978-3-7091-6499-0_25.
The possibility that increased levels of the activity of the semicarbazide-sensitive amine oxidase (SSAO) might, to some extent, compensate for the loss of monoamine oxidase (MAO) activity in the atypical form of Norrie Disease, was examined using the rat as a model. Long-term treatment with the MAO inhibitor tranylcypromine (1 mg/kg/day) resulted in sustained inhibition of MAO-A and MAO-B activities in liver and brain. After one week, the SSAO activity in heart had increased by 79% above the control levels. This increase was maintained for 3 weeks. Since such alterations might result from enzyme induction, the turnover of the enzyme was studied in cultured cells from rat aortic smooth muscle. The time-course of recovery of enzyme activity following irreversible inhibition by MDL 72145 corresponded to a half-life of approximately 6 days for this process.
以大鼠为模型,研究了氨基脲敏感性胺氧化酶(SSAO)活性增加在一定程度上可能补偿诺里病非典型形式中单胺氧化酶(MAO)活性丧失的可能性。用单胺氧化酶抑制剂反苯环丙胺(1毫克/千克/天)进行长期治疗,导致肝脏和大脑中的MAO - A和MAO - B活性持续受到抑制。一周后,心脏中的SSAO活性比对照水平增加了79%。这种增加持续了3周。由于这种改变可能是由酶诱导引起的,因此在大鼠主动脉平滑肌的培养细胞中研究了该酶的周转情况。MDL 72145不可逆抑制后酶活性恢复的时间进程表明,这个过程的半衰期约为6天。