Glycine and Selenium (Separately and in Combination) Reduced Bromate-Mediated Oxidative Stress and Inflammatory Response in U937 Cells

Abstract

The toxicity of bromate is ascribed to DNA damage and alteration in carbohydrate mechanism that could result to lipid peroxidation and oxidative stress. The effects of glycine and selenium on bromate-induced alterations on U937 cells and U937-derived macrophages were investigated. In the first experiment, U937 cells were incubated with or without glycine or selenium or both before subjecting cells to bromate exposure. Cell viability and production of ROS were assessed via MTT and DCHF-DA assays. In the other experiment, U937 cells were transformed to the macrophage form using phorbol 12-myristate 13-acetate before incubating with or without glycine and selenium before exposure to bromate. Secretion of nitric oxide and cytokines (tumour necrosis factor-alpha, interleukin 1 and interleukin 6) were later measured. The production of superoxide dismutase and catalase was also evaluated. The results revealed that bromate caused significant cytotoxicity and ROS production that was reduced when cells were pre-incubated by glycine and selenium (both separately and in combination). Bromate also increased macrophage secretion of nitric oxide and cytokines which was reduced by glycine and selenium. Bromate also suppressed the production of superoxide dismutase and catalase which was reversed by glycine and selenium (both separately and in combination) close to control values. The effects of glycine and selenium are ascribed to their antioxidant nature. Implications of the findings are discussed.