The quantitative analysis and stability of histochemical markers of altered hepatic foci in rat liver following initiation by diethylnitrosamine administration and promotion with phenobarbital.

The quantitative analysis and stability of histochemical markers of altered hepatic foci in rat liver following initiation by diethylnitrosamine administration and promotion with phenobarbital.
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在二乙基亚硝胺给药和苯巴比妥促进后,大鼠肝脏改变的肝病灶的组织化学标记物的定量分析和稳定性。

DOI:
10.1093/carcin/6.9.1261
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发表时间:
1985
期刊:
影响因子:
4.7
通讯作者:
Pitot,HC
Pitot,HC
中科院分区:
医学2区
文献类型:
--
作者:
Goldsworthy,TL;Pitot,HC

文献摘要

被引文献

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在部分肝切除术 (PH) 后 20-24 小时内给予单剂量二乙基亚硝胺 (DEN) 的大鼠,研究了在存在和停止 0.05% 苯巴比妥 (PB) 治疗的情况下,改变肝病灶 (AHF) 的组织化学表型的稳定性和反应。 AHF 通过三种生化标志物的表达进行评分:γ-谷氨酰转肽酶 (GGT)、三磷酸腺苷酶和葡萄糖 6-磷酸酶 (G6P)。 AHF 在标记物改变方面表现出显着的异质性。本研究中使用的三种标记物证实了我们早期研究的结果,该研究显示了 PH/DEN 启动后 GGT+AHF 对 PB 给药的最大反应,以及 PB 撤回后 PH/DEN/PB 方案诱导的 GGT+/AHF 的稳定性。在所采用的治疗方案中,仅 GGT 标记物就获得了所有三种标记物检测到的绝大多数 AHF。在连续 PB 给药期间的 AHF 中以及在 PB 促进的 AHF 和随后 6 个月喂养不含 PB 的饮食期间,组织化学表型的频率分布保持相对恒定。这些发现表明,个体 AHF 在整个 PB 促进阶段保持表型稳定,即不会从一种表型进展到另一种表型。在每个标记类别中,AHF 的平均体积在连续 PB 给药期间增加。这些数据说明了 PB 对 AHF 生长的增强作用。在 3 个月的 PB 治疗组中,AHF 的大小在停止 PB 后继续增加,但在治疗 4 个月的动物中则没有。讨论了可能解释这两个治疗组差异的机制。
The stability and response of histochemical phenotypes of altered hepatic foci (AHF) were studied both in the presence and following the withdrawal of 0.05% phenobarbital (PB) treatment in rats previously given a single dose of diethyl-nitrosamine (DEN) 20–24 h following partial hepatectomy (PH). AHF were scored by their expression of three biochemical markers: γ-glutamyl transpeptidase (GGT), adenosine triphosphatase and glucose-6-phosphatase (G6P). AHF demonstrated significant heterogeneity with respect to the marker alterations. The use of three markers in the present study confirmed the findings of our earlier study, which showed the maximal response of GGT+AHF to PB administration following PH/DEN initiation and the stability of GGT+/AHF induced by the PH/DEN/PB regimen after the withdrawal of PB. In the regimen employed, the GGT marker alone scored the great majority of the AHF detected by all three markers. The frequency distribution of histochemical phenotypes remained relatively constant in AHF during continuous PB administration and in AHF promoted by PB followed by a 6-month period of feeding a diet containing no PB. These findings suggest that individual AHF remain phenotypically stable throughout the PB promotion phase, i.e., do not progress from one phenotype to another. In every marker class, the mean volume of AHF increased during continuous PB administration. These data illustrate the enhancing effect of PB on the growth of the AHF. The size of AHF continued to increase following the withdrawal of PB in the 3-month PB treatment group, but not in the animals treated for 4 months. A mechanism that may account for the differences in these two treatment groups is discussed.