Abstract

Environmental context Antimony is found at high concentrations in airborne particulate matter in urban cities. Contaminants that enter humans through the breathing of fine particulate matter are released directly into the blood after overcoming the first barrier of the immune system including macrophages. We investigated the effects of antimony on the inflammatory response in macrophages and its potentially harmful effects. Antimony (Sb) is a metalloid whose increased presence in atmospheric particulate matter is of concern since its effects on living beings are unknown. The present study aims to characterise the redox chemical changes of Sb-V in vitro using a murine macrophage cell line, RAW 264.7. Analysis of the redox chemical changes revealed that Sb-V is partially reduced to Sb-III when in culture. Sb-V induces the formation of reactive oxygen species, which may be causally related to the reduction of this chemical species. The expression of pro-inflammatory genes, which includes TNF-alpha and COX-2, was upregulated in response to Sb-V. The secretion of TNF-alpha protein was significantly higher from cells treated with Sb-V than the untreated controls. The pro-inflammatory response to Sb-V was determined to be dose-dependent. The signalling pathway underlying the cellular response to Sb-V is likely to be independent from the TLR4-mediated mechanism of lipopolysaccharide activation. This is the first study to describe the potentially pro-inflammatory effects of Sb-V on mammalian cells.