Oxidative metabolism of lung macrophages exposed to sodium arsenite

Abstract

Arsenic pollution has become increasingly severe. It occurs as the result of geological processes and different human activities. Arsenic toxicity at the respiratory level occurs mainly by inhalation of products of coal combustion. The aim of this study was to evaluate sodium arsenite (As 3+) toxicity in murine alveolar macrophages (AMs) in vitro and its association with the alterations in cell metabolism. No changes in viability, apoptosis or cell area were detected in AMs treated with As 3+ concentrations up to 2 μM for 24–96 h. A marked decrease in these end-points was observed for As 3+ concentrations ranging from 2.5 μM to 10 μM. Regarding the dynamics of the endo-exocytic process triggered by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell incorporation, no variations were detected for As 3+ concentrations lower than 2 μM while higher concentrations markedly modified this response. MTT specific activity, as a measure of cell metabolic activity, was not modified irrespective of the As 3+ concentration assayed. However, nitroblue tetrazolium (NBT) specific activity, as a measure of superoxide anion generation, is responsive but only to low As 3+ doses. Although this study focuses on lung macrophages, the effects of As 3+ described herein may also apply to the response of macrophages residing in other organs. Arsenite modifies the metabolic and the oxidative status of AMs in vitro. When macrophages are in an As 3+ rich medium, they exhibit a reduction in respiratory burst levels and lose their intrinsic capacity to respond to toxicants.