Bender D A, Totoe L
J Neurochem. 1984 Sep;43(3):733-6. doi: 10.1111/j.1471-4159.1984.tb12793.x.
Acute administration of vitamin B6 to rats (10 mg/kg body weight) led to reduced urinary excretion of N1-methyl nicotinamide and methyl pyridone carboxamide, indicating inhibition of the oxidative metabolism of tryptophan. There was a considerable reduction in the production of 14CO2 from [ring-2-14C]tryptophan, and a significant inhibition of hepatic tryptophan oxygenase when measured in liver homogenates, together with an increase in the concentration of tryptophan in plasma. There was an increase in both the concentration of tryptophan in the brain and the uptake into the brain of peripherally administered [3H]tryptophan, accompanied by a small increase in the rate of synthesis of 5-hydroxytryptamine in the brain. It is suggested that this increase in the uptake of tryptophan into the brain following a relatively large dose of vitamin B6 may explain the beneficial action of the vitamin in some cases of depressive illness.
给大鼠急性注射维生素B6(10毫克/千克体重)会导致N1-甲基烟酰胺和甲基吡啶酮羧酰胺的尿排泄减少,这表明色氨酸的氧化代谢受到抑制。从[环-2-14C]色氨酸产生的14CO2显著减少,在肝匀浆中测定时,肝色氨酸加氧酶受到显著抑制,同时血浆中色氨酸浓度增加。脑内色氨酸浓度以及外周给予的[3H]色氨酸向脑内的摄取均增加,同时脑内5-羟色胺的合成速率略有增加。有人提出,在给予相对大剂量维生素B6后,色氨酸向脑内摄取的这种增加可能解释了该维生素在某些抑郁症病例中的有益作用。