Motoori S, Majima H J, Ebara M, Kato H, Hirai F, Kakinuma S, Yamaguchi C, Ozawa T, Nagano T, Tsujii H, Saisho H
Research Center of Charged Particle Therapy, National Institute of Radiological Sciences, Chiba 263-8555, Japan.
Cancer Res. 2001 Jul 15;61(14):5382-8.
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.
我们通过集落形成试验分析细胞活力，并检测稳定转染人锰超氧化物歧化酶（Mn-SOD）基因的肝癌细胞系HLE中的细胞凋亡，研究了线粒体锰超氧化物歧化酶（Mn-SOD）在抗辐射保护活性中的潜在作用。我们发现，Mn-SOD的过表达降低了线粒体中活性氧的水平和细胞内磷脂过氧化产物（4-羟基-2-壬烯醛），并防止了细胞死亡。Mn-SOD过表达并未改变辐射后细胞内一氧化氮的产生。结果表明，Mn-SOD可能通过控制线粒体活性氧的产生和细胞内脂质过氧化，在保护细胞免受辐射诱导的细胞死亡中发挥重要作用。
