Lai Ruiping, Wang Yipei, Li Xiaonuan, Yu Ri-an
Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, MOE Key Lab of Environment and Health, Wuhan 430030, China.
Wei Sheng Yan Jiu. 2008 Nov;37(6):645-8.
To study alone and combined effect of selenium and arsenic on oxidative stress, DNA oxidative damage and repair.
HepG2 cells were treated with selenium (2.5, 5.0 and 10.0 micromol/L sodium selenite) alone, arsenic (1.56, 3.13, 6.25, 12.5 and 25.0 micromol/L arsenious acid) alone and combined selenium plus arsenic. The quantitative analysis of malondialdehyde (MDA), 8-OHdG and hOGG1 was carried out by fluorometric method, HPLC-EC and Western Blot to represent oxidative stress, DNA oxidative damage and repair, respectively.
Under the condition of alone treatment, sodium selenite (5.0 and 10.0 micromol/L) as well as arsenious acid (6.25, 12.5 and 25.0 micromol/L) resulted in significant increased levels of MDA and 8-OHdG, and inhibition of hOGG1 expression in HepG2 cells compared with solvent control (P < 0.05, P < 0.01). Sodium selenite at the relative low dose (2.5 micromol/L) displayed certain anti-oxidative ability (P > 0.05). Combined treatment of sodium selenite (2.5 micromol/L) and arsenious acid (6.25 micromol/L) caused significant lower levels of MDA and 8-OHdG than those of correspondent arsenic alone treatment (P < 0.05). hOGG1 expression showed no difference between combined treatment (2.5 micromol/L of selenium selenite plus 6.25, 12.5 and 25.0 micromol/L of arsenious acid, respectively) and correspondent arsenic alone treatment (P > 0.05).
Sodium selenite at the concentrations of 5.0, 10.0 micromol/L and arsenious acid at the concentrations of 6.25, 12.5, 25.0 micromol/L induced enhanced oxidative stress and 8-OHdG production, and inhibition of hOGG1 expression, respectively. Selenium at certain concentration (2.5 micromol/L of selenium selenite) has ameliorative effects on oxidative stress and DNA oxidative damage induced by arsenic, but no effect on repair of DNA oxidative damage.
研究硒和砷单独及联合作用对氧化应激、DNA氧化损伤及修复的影响。
用硒（2.5、5.0和10.0微摩尔/升亚硒酸钠）、砷（1.56、3.13、6.25、12.5和25.0微摩尔/升亚砷酸）单独处理及硒与砷联合处理HepG2细胞。采用荧光法、高效液相色谱-电化学法和蛋白质免疫印迹法分别对丙二醛（MDA）、8-羟基脱氧鸟苷（8-OHdG）和人8-氧代鸟嘌呤糖苷酶1（hOGG1）进行定量分析，以分别代表氧化应激、DNA氧化损伤及修复情况。
单独处理条件下，与溶剂对照组相比，亚硒酸钠（5.0和10.0微摩尔/升）以及亚砷酸（6.25、12.5和25.0微摩尔/升）均导致HepG2细胞中MDA和8-OHdG水平显著升高，hOGG1表达受到抑制（P<0.05，P<0.01）。相对低剂量（2.5微摩尔/升）的亚硒酸钠表现出一定的抗氧化能力（P>0.05）。亚硒酸钠（2.5微摩尔/升）与亚砷酸（6.25微摩尔/升）联合处理导致MDA和8-OHdG水平显著低于相应的单独砷处理组（P<0.05）。联合处理组（分别为2.5微摩尔/升亚硒酸钠加6.25、12.5和25.0微摩尔/升亚砷酸）与相应的单独砷处理组相比，hOGG1表达无差异（P>0.05）。
5.0、10.0微摩尔/升的亚硒酸钠和6.25、12.5、25.0微摩尔/升的亚砷酸分别诱导氧化应激增强、8-OHdG生成增加及hOGG1表达受到抑制。一定浓度的硒（2.5微摩尔/升亚硒酸钠）对砷诱导的氧化应激和DNA氧化损伤具有改善作用，但对DNA氧化损伤的修复无影响。
