Selenoprotein deficiency enhances radiation-induced micronuclei formation
Selenoprotein deficiency enhances radiation-induced micronuclei formation
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DOI：
10.1002/mnfr.200800020
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发表时间：
2008-11-01
影响因子：
5.2
通讯作者：
Diamond, Alan M.
中科院分区：
文献类型：
--
作者：
Baliga, Manjeshwar S.;Diwadkar-Navsariwala, Veda;Diamond, Alan M.
硒的可用性和特定硒蛋白的水平可能通过影响DNA损伤剂引起基因组不稳定性和突变的能力来影响癌症风险。表达硒蛋白水平降低的转基因小鼠和先前显示出更容易受到与癌症发展相关的病理学的影响，被用于研究这种可能性。将这些小鼠暴露于X射线，并在红细胞中评估DNA损伤，其中微核形成高于从辐照野生型对照中获得的相同细胞。为了确定硒蛋白谷胱甘肽过氧化物酶-1（GPx-1）是否可能参与这种保护，通过siRNA靶向LNCaP人前列腺细胞降低其水平。与对照转染细胞相比，这些细胞中UV诱导的微核频率更高。这些结果表明硒蛋白在保护DNA免受损伤中的作用，并支持人类数据暗示GPx-1作为硒的化学保护作用的可能靶点。
The availability of selenium and the levels of specific selenoproteins might affect cancer risk by influencing the ability of DNA damaging agents to cause genomic instability and mutations. Transgenic mice that express reduced levels of selenoproteins and previously shown to be more susceptible to pathology associated with cancer development were used to study this possibility. These mice were exposed to X-rays and DNA damage assessed in the erythrocytes, where micronuclei formation was higher compared to the same cells obtained from irradiated wild-type controls. To determine whether the selenoprotein glutathione peroxidase-1 (GPx-1) might be involved in this protection, its levels were reduced by siRNA targeting in LNCaP human prostate cells. UV-induced micronuclei frequency was higher in these cells compared to control-transfected cells. These results indicate a role for selenoproteins in protecting DNA from damage and support human data implicating GPx-1 as a possible target of the chemoprotective effect of selenium.