David J C
Naunyn Schmiedebergs Arch Pharmacol. 1976;293(1):15-23. doi: 10.1007/BF00498866.
High doses of tyrosine were found to be lethal in mice. The lethality was potentiated by decarboxylase inhibitors which acted by elevating tissues tyrosine levels when given together with large amounts of tyrosine. The lethality of either tyrosine or tyrosine given in combination with decarboxylase inhibitors was found to be correlated with the elevation of tyrosine levels in liver. This toxicity does not appear to involve either tyramine or p-hydroxyphenylpyruvic acid formation. Ascorbic acid pretreatment afforded a marked protection against tyrosine toxicity. This compound was found to prevent the elevation of tissue tyrosine levels by stimulating p-hydroxyphenylpyruvic acid oxidase, increasing the urinary excretion and inhibiting the gastrointestinal absorption of tyrosine.
高剂量的酪氨酸对小鼠具有致死性。脱羧酶抑制剂可增强这种致死性，当与大量酪氨酸同时给药时，脱羧酶抑制剂通过提高组织中的酪氨酸水平发挥作用。单独的酪氨酸或与脱羧酶抑制剂联合使用的酪氨酸的致死性均与肝脏中酪氨酸水平的升高相关。这种毒性似乎不涉及酪胺或对羟基苯丙酮酸的形成。抗坏血酸预处理可显著保护机体免受酪氨酸毒性的影响。发现该化合物通过刺激对羟基苯丙酮酸氧化酶、增加酪氨酸的尿排泄并抑制酪氨酸的胃肠道吸收来防止组织酪氨酸水平升高。
