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患有肝硬化和肝细胞癌的人类肝脏中的线粒体DNA缺失比正常人类肝脏少。

Human livers with cirrhosis and hepatocellular carcinoma have less mitochondrial DNA deletion than normal human livers.

作者信息

Kotake K, Nonami T, Kurokawa T, Nakao A, Murakami T, Shimomura Y

机构信息

Department of Surgery II, Nagoya University, School of Medicine, Japan.

出版信息

Life Sci. 1999;64(19):1785-91. doi: 10.1016/s0024-3205(99)00117-4.

Abstract

We measured the populations of mutated mitochondrial DNAs with the 7,436 bp or the 4,977 bp deletion from apparently normal human liver and human livers with chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The amount of the mutated mitochondrial DNA was at the same level between normal and chronically hepatitic livers but was significantly lower in human livers with cirrhosis and hepatocellular carcinoma, especially the latter, suggesting that the mutated mitochondrial DNAs may be decreased with the progress of liver disease from chronic hepatitis to cirrhosis and hepatocellular carcinoma. This phenomenon is opposite to that occuring in the ageing process.

摘要

我们测定了来自外观正常的人类肝脏以及患有慢性肝炎、肝硬化和肝细胞癌的人类肝脏中,带有7436bp或4977bp缺失的突变线粒体DNA的数量。突变线粒体DNA的量在正常肝脏和慢性肝炎肝脏之间处于同一水平,但在患有肝硬化和肝细胞癌的人类肝脏中显著更低,尤其是后者,这表明随着肝脏疾病从慢性肝炎发展到肝硬化和肝细胞癌,突变线粒体DNA可能会减少。这种现象与衰老过程中发生的现象相反。

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