Article

Cardiovascular Toxicology

, Volume 10, Issue 3, pp 153-160

First online:

Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways

  • Yanfen ShiAffiliated withKey Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University
  • , Yudan WeiAffiliated withDepartment of Community Medicine, Mercer University School of Medicine Email author 
  • , Shanshan QuAffiliated withKey Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University
  • , Yang WangAffiliated withKey Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University
  • , Yulin LiAffiliated withKey Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University
  • , Ronggui LiAffiliated withKey Laboratory of Pathobiology, Ministry of Education, Norman Bethune College of Medicine, Jilin University Email author 

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Abstract

To clarify the molecular mechanisms through which arsenic causes injuries to blood vessels, we analyzed the effects of sodium arsenite (NaAsO2) on the apoptosis of human umbilical vein endothelial cells (HUVECs), mitochondrial membrane potential (ΔΨm), intracellular reactive oxygen species (ROS), and the expression of the related genes. HUVECs apoptosis increased and ΔΨm decreased in a dose-dependent manner following arsenic treatment. Intracellular ROS showed 2 phase alterations: a slight decrease with low levels of arsenic (5 and 10 μM) treatment; but a sharp increase at higher concentrations (≧20 μM). The arsenic-induced cell apoptosis and intracellular ROS were blocked by the addition of the antioxidant N-acetyl-l-cysteine (NAC). The mRNAs of superoxide dismutase 2 (SOD2) and NAD(P)H:quinone oxidoreductase 1 (NQO1) increased strikingly when cells were treated with a low concentration of NaAsO2 (5 μM) and the level of induction was decreased with higher concentrations of arsenic treatment. Based on the results, we suggest that the decrease of ΔΨm caused by arsenic and the resulting cell apoptosis may contribute to the injuries of blood vessel in arsenism. The decrease in intracellular ROS and the increase in SOD2 and NQO1 expressions observed when HUVECs were treated with low concentration of NaAsO2, suggest the role of the two enzymes in protecting HUVECs from injuries of arsenic exposure.

Keywords

Arsenic Apoptosis Reactive oxygen species Human umbilical vein endothelial cells Mitochondria