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正常615小棕鼠(615鼠)和小白鼠肝中的酪氨酸-α-酮戊二酸转氨酶(TAT)的活力可受氢化可的松、地塞米松、cAMP加茶碱、胰岛素和L-色氨酸的诱导,但两种鼠肝TAT的反应性有所差别。H615肝癌(H615)中的TAT活力仅为615鼠肝的1/2,虽能受上述五种诱导剂诱导,但比615鼠肝诱导后的水平低得多。其中cAMP加茶碱和胰岛素对H615中TAT诱导能力的降低较其他三种诱导剂更为明显,提示除DNA的转录、转录后或翻译等环节有异常外,尚有这两种化合物特殊诱导环节的缺损。Hep A小鼠腹水肝癌(Hep A)中的TAT活力极低,不受上述任何诱导剂的诱导;H 615和Hep A宿主肝中TAT的活力,后者低于前者,两者均低于正常肝,而分别高于H 615及Hep A,两者也可被五种诱导剂诱导,但诱导后的水平也低于正常肝而高于肝癌;由此推测,肝癌可能分泌一种化学物质对TAT的活力有抑制作用。
The activity of tyrosine-alpha-ketoglutarate aminotransferase (TAT) in normal 615 little brown rat (615 mice) and mouse white rat liver may be affected by hydrocortisone, dexamethasone, cAMP plus theophylline, insulin and L - Tryptophan induction, but two kinds of rat liver TAT reactivity difference. The TAT activity in H615 hepatocellular carcinoma (H615) was only 1/2 of the 615 rat liver, although it was induced by the above five inducers but much lower than the level induced by the 615 rat liver. Which cAMP plus theophylline and insulin on H615 TAT induced ability to reduce more than the other three inducers more obvious, suggesting that in addition to DNA transcription, transcription or translation and other links are abnormal, there are still two special compounds induced Of the defect. TAT activity in Hep A mice Hep A cells was extremely low and was not induced by any of the above inducing agents; T-cell viability in H-615 and Hep A-host liver was lower than the former, both lower than normal Liver, but higher than H 615 and Hep A respectively, both of which can be induced by five kinds of inducers, but the induced levels are also lower than those of normal liver and liver cancer. Therefore, it is speculated that liver cancer may secrete a chemical substance TAT vitality inhibition.