Feo F, Canuto R A, Garcea R, Brossa O, Caselli G C
Cancer Lett. 1978 Jul;5(1):25-30. doi: 10.1016/s0304-3835(78)80006-8.
Microsomes isolated from hyperplastic liver nodules and hepatomas, induced by DL-ethionine, exhibited a reduced cytochrome P-450 content and aminopyrine N-demethylase activity when compared to the organelles of control and surrounding non-nodular liver. Phenobarbital administration to rats caused an increase of microsomal protein, cytochrome P-450 and aminopyrine N-demethylase in all tissue tested. In the hepatoma the rise of cytochrome P-450 and aminopyrine N-demethylase/g of tissue was very low and it is compensated by a slight increase of microsomal protein. In hyperplastic nodules as well as in control and surrounding livers, cytochrome P-450 and aminopyrine N-demethylase increased more than microsomal protein. However, the phenobarbital-induced stimulation was significantly lower in hyperplastic nodules than in control and surrounding livers.
与对照和周围非结节性肝脏的细胞器相比,从由DL-乙硫氨酸诱导产生的增生性肝结节和肝癌中分离出的微粒体,其细胞色素P-450含量和氨基比林N-脱甲基酶活性降低。给大鼠施用苯巴比妥会导致所有测试组织中的微粒体蛋白、细胞色素P-450和氨基比林N-脱甲基酶增加。在肝癌中,每克组织的细胞色素P-450和氨基比林N-脱甲基酶的升高非常低,并且通过微粒体蛋白的轻微增加得到补偿。在增生性结节以及对照和周围肝脏中,细胞色素P-450和氨基比林N-脱甲基酶的增加幅度大于微粒体蛋白。然而,苯巴比妥诱导的刺激在增生性结节中明显低于对照和周围肝脏。