Arsenic Induces Apoptosis of Human Umbilical Vein Endothelial Cells Through Mitochondrial Pathways
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- Shi, Y., Wei, Y., Qu, S. et al. Cardiovasc Toxicol (2010) 10: 153. doi:10.1007/s12012-010-9073-z
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.