Lack of initiating activity of the peroxisome proliferator ciprofibrate in two-stage hepatocarcinogenesis.
Lack of initiating activity of the peroxisome proliferator ciprofibrate in two-stage hepatocarcinogenesis.
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过氧化物酶体增殖剂环丙贝特在两阶段肝癌发生中缺乏起始活性。
DOI：
10.1016/0304-3835(89)90003-7
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发表时间：
1989
期刊：
影响因子：
9.7
通讯作者：
Clark,TD
中科院分区：
文献类型：
--
作者：
Glauert,HP;Clark,TD
The peroxisome proliferator ciprofibrate was examined for its ability to initiate hepatocarcinogenesis in rats. Ciprofibrate was fed in the diet at levels of 0%, 0.01% and 0.025% for 2 weeks in order to induce steady-state peroxisome proliferation. Rats were then subjected to partial hepatectomy and then maintained for 6 months on a basal diet or one containing 0.05% phenobarbital. Ciprofibrate treatment did not increase the number or volume of altered hepatic foci (putative preneoplastic lesions). However, ciprofibrate treatment increased liver weights in a dose-dependent manner in rats which did not receive phenobarbital.结论是环丙贝特诱导的过氧化物酶体增殖不足以诱导启动，但会产生永久性变化，导致肝脏重量增加。
The peroxisome proliferator ciprofibrate was examined for its ability to initiate hepatocarcinogenesis in rats. Ciprofibrate was fed in the diet at levels of 0%, 0.01% and 0.025% for 2 weeks in order to induce steady-state peroxisome proliferation. Rats were then subjected to partial hepatectomy and then maintained for 6 months on a basal diet or one containing 0.05% phenobarbital. Ciprofibrate treatment did not increase the number or volume of altered hepatic foci (putative preneoplastic lesions). However, ciprofibrate treatment increased liver weights in a dose-dependent manner in rats which did not receive phenobarbital. It is concluded that ciprofibrate-induced peroxisome proliferation is not sufficient to induce initiation, but that a permanent change is produced which results in an increased liver weight.
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