A relative deficiency of cytochrome P-450 and aryl hydrocarbon [benzo(a)pyrene] hydroxylase in hyperplastic nodules induced by 2-acetylaminofluorene in rat liver.
A relative deficiency of cytochrome P-450 and aryl hydrocarbon [benzo(a)pyrene] hydroxylase in hyperplastic nodules induced by 2-acetylaminofluorene in rat liver.
复制标题
大鼠肝脏 2-乙酰氨基芴诱导的增生结节中细胞色素 P-450 和芳基烃 [苯并（a）芘] 羟化酶相对缺乏。
作者：
R. Cameron;G. Sweeney;K. Jones;G. Lee;E. Farber
在用2-乙酰氨基芴诱导的大鼠肝脏中早期（灰白色）和重塑（棕色）增生结节中测定细胞色素P-450的浓度和芳烃[苯并（a）芘]羟化酶（AHH）和还原型烟酰胺腺嘌呤二核苷酸磷酸-细胞色素c还原酶的活性，并与对照肝脏和结节周围肝脏中的值进行比较。早期（14周）增生结节的细胞色素P-450含量是未经处理的对照肝脏活性的30%和周围肝脏活性的48%。早期结节的AHH活性是对照活性的10%，是周围非结节性肝脏活性的33%。早期结节微粒体中的烟酰胺腺嘌呤二核苷酸磷酸-细胞色素c还原酶活性是对照活性的76%，是周围肝脏中活性的78%。在晚期重塑结节中（22和25周），细胞色素P-450含量为对照的40%，AHH活性为对照活性的15%。在2-乙酰氨基芴诱发的原发性肝癌中，细胞色素P-450含量为对照的21%，AHH活性为对照的11%，还原酶活性为对照的50%。这些结果表明，在一些细胞成分的相对结节缺陷被认为是重要的肝致癌物和肝毒素的激活，提供了一个可能的解释相对抵抗致癌物的细胞毒性增生性肝结节。
The concentrations of cytochrome P-450 and the activities of aryl hydrocarbon [benzo(a)pyrene] hydroxylase (AHH) and reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase were measured in early (gray-white) and remodeled (brown) hyperplastic nodules induced in the livers of rats with 2-acetylaminofluorene and were compared to the values in control livers and in the liver surrounding the nodules. Cytochrome P-450 content of early (14 weeks) hyperplastic nodules is 30% of the activity of untreated control livers and 48% of the activity of the surrounding liver. AHH activity of the early nodules is 10% of the control activity and 33% of the activity in the surrounding nonnodular liver. Nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activity in the microsomes of early nodules is 76% of the control activity and 78% of the activity in the surrounding liver. In the late remodeled nodules, (22 and 25 weeks), the cytochrome P-450 content is 40% of that of controls and AHH activity is 15% of the control activity. In primary hepatomas induced by 2-acetylaminofluorene, cytochrome P-450 content is 21% of that of controls, AHH activity is 11% of the activity of controls, and reductase is 50% of the control activity. These results, indicating a relative nodule deficiency in some of the cellular components believed to be important in the activation of hepatocarcinogens and hepatotoxins, offer one possible explanation for the relative resistance to carcinogen cytotoxicity of hyperplastic liver nodules.