Effects of airborne fine particulate matter on antioxidant capacity and lipid peroxidation in multiple organs of rats.

The purpose of this research was to determine whether airborne fine particulate matter (PM(2.5)) could increase levels of lipid peroxidation and alter intracellular redox status in multiple organs of rats. Thirty-two male Wistar rats were randomly divided into the treated groups using PM(2.5) at different dosages (1.5, 7.5, 37.5 mg/kg) and with a control group using saline. Rats were sacrificed 24 h after one-time intratracheal instillation. Then we investigated the activities of Cu, Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the levels of glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) in hearts, livers, spleens, lungs, kidneys, brains, and testicles. It was found that PM(2.5) at dosages of 7.5 and 37.5 mg/kg significantly increased lipid peroxidation levels in the hearts, livers, lungs, and testicles, decreased SOD, CAT, and GPx activities in the lungs, livers, kidneys, and brains, and depleted GSH levels in all the measured organs compared to the control. There were also differences in the changes of antioxidative enzymes activities and lipid peroxidation levels in seven organs. These results led to a conclusion that airborne PM(2.5) was a systemic toxic agent, not only to respiratory and cardiovascular systems. Its toxic effects might be attributed to oxidative damage mediated by prooxidant/antioxidant imbalance or excess free radicals. Further work is required to explain the toxicity role of PM(2.5) on multiple organs of mammals.