52 Cerebral oxidative stress response to acute diesel exhaust and world trade center dust exposures

Abstract Background In acute settings, particulate matter related oxidative stress presents a significant risk factor for cerebrovascular disease and stroke. In this study, we aim to investigate the effect of particulate matter from two sources with heterogeneous chemical compositions: diesel exhaust particles (DEP) and World Trade Center dust (WTC). Methods 2-month-old C57BL/6 mice (n = 6/sex/group) were exposed via inhalation for 5 h to DEP or WTC dust at 100ug/m3 concentration or filtered air as a control. After humane euthanasia and PBS perfusion, brains were prepared either in −80 freezing or fixated in PFA. Oxidative stress was measured using whole cell lysate assays (GPx enzyme, PCOOH assay, and 4-HNE) and immunofluorescence for 4-HNE and 8-OHdG. Results In the whole cell lysate cortex assays, antioxidant GPx and PCOOH activity were reduced in DEP and WTC compared to Filter group. 4-HNE increased in the cortex of DEP and WTC animals compared to Filter. On the immunofluorescent analysis in the cortex 8-OHdG was elevated in the DEP group compared to Filter, while in the corpus callosum, both 4-HNE and 8-OHdG increased in DEP group but not in WTC group. Discussion Our data suggests that an acute exposure to chemically different pollutants results in cerebral oxidative stress damage. Both DEP and WTC exposures blunt oxidized lipid detoxification and promotes oxidative stress response, although with variability across brain areas. Further research is needed to characterize biochemical elements contributing to cerebral oxidative stress in exogenous environmental exposure.