Monomethylarsonous Acid Induced Cytotoxicity and Endothelial Nitric Oxide Synthase Phosphorylation in Endothelial Cells

Abstract Chronic arsenic poisoning is reported to be associated with peripheral and cardiovascular disease, arteriosclerosis, Raynaud’s syndrome, hypertension, and Blackfoot disease. Monomethylarsonous acid (MMAIII) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS). Ar-senic is also reported to phosphorylate eNOS in cultured keratinocyte and Human T cell leukemia Jurkat cells, respectively. In the present study, we examined the cyto-toxicity and eNOS phosphorylation by MMAIII exposure in cultured bovine aortic endothelial cells (BAEC). Results showed that MMAIII is more toxic than arsenite in BAEC cells. The IC50 values for MMA III and arsenite were determined to be approximately 1.7 and 24.1 lmol/L