Overexpression of mitochondrial manganese superoxide dismutase protects against radiation-induced cell death in the human hepatocellular carcinoma cell line HLE.
Overexpression of mitochondrial manganese superoxide dismutase protects against radiation-induced cell death in the human hepatocellular carcinoma cell line HLE.
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发表时间：
2001-07
期刊：
影响因子：
11.2
通讯作者：
Shigeatsu Motoori;H. Majima;M. Ebara;Hirotoshi Kato;Futoshi Hirai;S. Kakinuma;Chizuru Yamaguchi;T. Ozawa;T. Nagano;H. Tsujii;H. Saisho
中科院分区：
文献类型：
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作者：
Shigeatsu Motoori;H. Majima;M. Ebara;Hirotoshi Kato;Futoshi Hirai;S. Kakinuma;Chizuru Yamaguchi;T. Ozawa;T. Nagano;H. Tsujii;H. Saisho
我们研究了线粒体锰超氧化物歧化酶（Mn-SOD）的潜在作用，对辐射的保护活性，通过分析细胞活力的集落形成试验和通过检测细胞凋亡稳定的人Mn-SOD基因转染的肝细胞癌细胞系HLE。我们发现Mn-SOD的过度表达降低了线粒体中活性氧和细胞内磷脂过氧化产物（4-羟基-2-壬烯醛）的水平，并阻止了细胞死亡。Mn-SOD过表达不改变照射后细胞内一氧化氮的产生。结果提示，Mn-SOD可能通过调控线粒体活性氧的产生和细胞内脂质过氧化，对辐射诱导的细胞死亡起到保护作用。
We investigated the potential role of mitochondrial manganese superoxide dismutase (Mn-SOD) in protective activity against irradiation by analyzing cell viability by a colony formation assay and by detecting apoptosis in stably human Mn-SOD gene-transfected HLE, a hepatocellular carcinoma cell line. We found that overexpression of Mn-SOD reduced the levels of reactive oxygen species in the mitochondria and intracellular phospholipid peroxidation product (4-hydroxy-2-nonenal) and prevented cell death. The production of intracellular nitric oxide after irradiation was not changed by Mn-SOD overexpression. The results suggested that Mn-SOD might play an important role in protecting cells against radiation-induced cell death by controlling the generation of mitochondrial reactive oxygen species and intracellular lipid peroxidation.