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过氧化物酶体增殖物诱导的大鼠肝脏损伤对铁过载的抗性增强。

Increased resistance of peroxisome proliferator-induced hepatic lesions to iron overload in rats.

作者信息

Rao M S, Subbarao V, Reddy J K

出版信息

Cancer Lett. 1986 Jul;32(1):33-9. doi: 10.1016/0304-3835(86)90036-4.

Abstract

Altered areas (AA), neoplastic nodules (NN) and hepatocellular carcinomas (HCC) induced by chronic administration of ciprofibrate and Wy-14,643 were examined for iron accumulation after systemic iron overload. Eighty percent of AA, 90% NN and 100% HCC showed increased resistance to iron accumulation. However, marked heterogeneity was observed in the amount of iron from area to area within the same lesion with some cells containing no iron, while others showing blue reaction to iron. These findings indicate, that putative preneoplastic and neoplastic hepatic lesions induced by peroxisome proliferators exclude iron in a fashion similar to that of hepatic nodules and carcinomas induced by DNA damaging carcinogens.

摘要

对长期给予环丙贝特和Wy-14,643诱导产生的病变区域(AA)、肿瘤结节(NN)和肝细胞癌(HCC)在全身性铁过载后进行铁蓄积检测。80%的AA、90%的NN和100%的HCC对铁蓄积表现出增强的抗性。然而,在同一病变内不同区域的铁含量中观察到明显的异质性,一些细胞不含铁,而另一些细胞对铁呈蓝色反应。这些发现表明,过氧化物酶体增殖剂诱导产生的假定癌前和肿瘤性肝损伤以类似于DNA损伤致癌物诱导产生的肝结节和癌的方式排除铁。

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