The differential effects of arsenic compounds and the effect of selenium on arsenic-induced changes in cytotoxicity, viability, and cell cycle of porcine aorta endothelial cells (PAECs) were investigated. MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay indicated that arsenic trioxide (As2O3) and sodium arsenite (NaAsO2) showed similar cytotoxicity, whereas sodium arsenate ( Na2HAsO4) did not show cytotoxicity in PAECs. As2O3 and NaAsO2 at 20 muM decreased PAEC viability, decreased G0/G1 phase, and increased apoptosis. An increased G2/M phase was observed in NaAsO2-treated PAECs, whereas an increase in secondary necrosis ( late apoptosis) was observed in As2O3-treated PAECs. As2O3-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO2-induced apoptosis was associated with p53 upregulation. Sodium selenite (Na2SeO3) at 1 nM reduced 20 muM As2O3-induced cytotoxicity, but not apoptosis, at 24 h. Increased glutathione peroxidase (GPX) activity by Na2SeO3 pretreatment in 20 muM As2O3-treated PAECs suggests that Na2SeO3 modulates As2O3-induced cytoxicity by GPX modulation.
