Abstract

Environmental exposure to arsenic is known to induce immunotoxicity . Macrophages are the professional phagocytes that are important in the immune system. In this study, we utilized the macrophages derived from the THP-1 human monocyte cell line as the experimental model to study the functional suppression induced by arsenite (As +3 ), one of the most prevalent forms of inorganic arsenic, at environmentally-relevant concentrations. Apoptosis was observed in the THP-1 derived macrophages treated with 500 nM As +3 for 18 h. Suppression of phagocytosis was induced by 18 h As +3 treatment starting from 100 nM. Suppressive effects on the production of two pro-inflammatory cytokines, IL-1β and TNF-α, were also found with the treatment of low to moderate doses of As +3 in lipopolysaccharides-stimulated THP-1 derived macrophages. The nitric oxide production was also inhibited by As +3 treatments, which was negatively correlated with the production of superoxide. Collectively, the results from the study demonstrated that environmentally-relevant concentrations of As +3 induced cytotoxicity and suppressed the major cellular functions in THP-1 derived macrophages. The macrophages were showed to be relatively sensitive to As +3 , and could be the essential target of the toxicity induced by environmental arsenic exposures.