Cunningham M L, Soliman M S, Badr M Z, Matthews H B
Chemistry Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Cancer Lett. 1995 Aug 16;95(1-2):93-7. doi: 10.1016/0304-3835(95)03869-x.
In previous National Toxicology Program (NTP) studies, rotenone reduced the background incidence of hepatocellular carcinoma in male B6C3F1 mice. In the present studies, rotenone reduced the basal hepatic labeling index of male B6C3F1 mice in a dose-dependent fashion and inhibited hepatocellular proliferation, but not peroxisome proliferation, induced by the peroxisome proliferator Wy-14,643. These results indicate that reduction of hepatic tumors by rotenone may have been due to decreased liver cell replication, that peroxisome proliferation can be induced in the absence of hepatocellular proliferation and suggest rotenone as a potential tool in studies of relationships of cell proliferation, peroxisomal proliferation and hepatocarcinogenesis.
在先前的国家毒理学计划（NTP）研究中，鱼藤酮降低了雄性B6C3F1小鼠肝细胞癌的背景发生率。在本研究中，鱼藤酮以剂量依赖性方式降低了雄性B6C3F1小鼠的基础肝脏标记指数，并抑制了过氧化物酶体增殖剂Wy-14,643诱导的肝细胞增殖，但未抑制过氧化物酶体增殖。这些结果表明，鱼藤酮导致肝脏肿瘤减少可能是由于肝细胞复制减少，过氧化物酶体增殖可在无肝细胞增殖的情况下被诱导，并提示鱼藤酮可作为研究细胞增殖、过氧化物酶体增殖与肝癌发生关系的潜在工具。
