Schmidt C J, Taylor V L
Merrell Dow Research Institute, Cincinnati, OH 45215.
Eur J Pharmacol. 1990 May 31;181(1-2):133-6. doi: 10.1016/0014-2999(90)90254-4.
Recent evidence suggests that the acute 3,4-methylenedioxymethamphetamine (MDMA)-induced loss of tryptophan hydroxylase activity (TPH) may be due to the oxidation of critical sulf-hydryl groups on the molecule. To determine if TPH activity could be regenerated in vivo we administered a 5-HT uptake inhibitor at various times immediately after MDMA. Although enzyme activity began to decline immediately following MDMA administration, rats receiving the uptake inhibitor 1 h post MDMA showed a rapid recovery of TPH activity. Administration of an uptake inhibitor 3 h post MDMA was without effect on the time course of TPH inactivation. The results suggest that systems exist within the serotonergic neuron for the reductive regeneration of active TPH. Furthermore, these systems are acutely compromised following the administration of MDMA.
最近有证据表明，急性3,4-亚甲基二氧甲基苯丙胺（摇头丸）导致的色氨酸羟化酶活性（TPH）丧失可能是由于该分子上关键巯基的氧化。为了确定TPH活性是否能在体内再生，我们在给予摇头丸后立即在不同时间给予一种5-羟色胺摄取抑制剂。尽管在给予摇头丸后酶活性立即开始下降，但在给予摇头丸1小时后接受摄取抑制剂的大鼠显示TPH活性迅速恢复。在给予摇头丸3小时后给予摄取抑制剂对TPH失活的时间进程没有影响。结果表明，血清素能神经元内存在使活性TPH进行还原再生的系统。此外，在给予摇头丸后，这些系统会受到急性损害。
