Aqueous particulate matter (PM2.5) from Brazil alters antioxidant profile responses and causes oxidative stress

Abstract In vitro assays were used to determine the effects of aqueous fine particulate matter (PM2.5) extracts on different homogenates of rat organs. The PM2.5 collected from two regions (Seropedica and Duque de Caxias) in Rio de Janeiro, Brazil, were used to evaluate different oxidative damages and redox state. Two PM2.5 extract concentrations (concentrate and 10x dilution) were evaluated using tissue homogenates (heart, lung, liver, and kidney). Measurements of total antioxidant capacity (ACAP), lipid peroxidation levels (LPO), reduced glutathione concentrations (GSH), activity of glutamate cysteine ligase (GCL), activity of glutathione S-transferase (GST) and catalase (CAT) were performed. Most PM2.5 aqueous extract concentrations contain numerous metals (e.g. Li, Ti, Fe, Cu, Cd, Sr, among others), which reduced ACAP and generated LPO in most tissue homogenates. Besides this, GST activity decreased in liver and lung, increasing in kidney and heart homogenates. GCL activity increased in lung, liver and kidney and undergo decrease in the heart homogenate. All concentrations of PM2.5 evaluated decreased GSH levels. PM2.5 concentrations for both sites (regions) raised catalase activity in most tissue homogenates except in the liver. In vitro toxicity of the PM2.5 in different tissues, presented an ability to interact with cellular antioxidant defense system, causing depletion of the sulfhydryl stocks, resulting in the damage of biological molecules and inducing oxidative imbalance.