Mannaioni G, Carpenedo R, Corradetti R, Carlà V, Venturini I, Baraldi M, Zeneroli M L, Moroni F
Department of Preclinical and Clinical Pharmacology, University of Florence, Italy.
Adv Exp Med Biol. 1999;467:155-67.
Oxindole administration (1-100 mg/kg i.p.) to mammals decreases locomotor activity, reduces muscular tone and blood pressure and at larger doses causes coma and death. Utilizing both HPLC and GC/MS, we showed that oxindole is present in the blood, brain and other organs of several animal species, including humans. We demonstrated that oxindole is a tryptophan metabolite able to significantly decrease neuronal excitability by modifying the function of voltage-operated sodium channels. Its synthesis requires the availability of indole, which is formed in the gut. When liver function is impaired, a sufficient amount of indole reaches systemic circulation and is oxidized into oxindole, which seems to be one of the responsible agents for the neurological symptoms found in the course of liver impairment.
给哺乳动物腹腔注射（1 - 100毫克/千克）羟吲哚会降低运动活性、减弱肌张力并降低血压，大剂量时会导致昏迷和死亡。利用高效液相色谱法（HPLC）和气相色谱 - 质谱联用仪（GC/MS），我们发现羟吲哚存在于包括人类在内的几种动物物种的血液、大脑和其他器官中。我们证明羟吲哚是一种色氨酸代谢产物，能够通过改变电压门控钠通道的功能来显著降低神经元兴奋性。其合成需要肠道中形成的吲哚。当肝功能受损时，足够量的吲哚进入体循环并被氧化为羟吲哚，这似乎是肝功能损害过程中出现神经症状的原因之一。
