title: [Effect of selenium and arsenic on oxidative stress, DNA oxidative damage and repair in HepG2 cells].
abstract: OBJECTIVE
  To study alone and combined effect of selenium and arsenic on oxidative stress, DNA oxidative damage and repair.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: 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.
authors.forename: Ruiping
authors.initials: R
authors.lastname: Lai
authors.forename: Yipei
authors.initials: Y
authors.lastname: Wang
authors.forename: Xiaonuan
authors.initials: X
authors.lastname: Li
authors.forename: Ri-an
authors.initials: RA
authors.lastname: Yu
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D001151:Arsenic / Q000633:toxicity*; D006528:Carcinoma, Hepatocellular / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage; D004260:DNA Repair / Q000187:drug effects*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000032:analysis; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D056945:Hep G2 Cells; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics / Q000378:metabolism*; D008315:Malondialdehyde / Q000032:analysis; D018384:Oxidative Stress / Q000187:drug effects*; D012643:Selenium / Q000494:pharmacology* / Q000633:toxicity
chemical_list: D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D012643:Selenium; D001151:Arsenic