Hippocampal inflammation and oxidative stress following exposure to diesel exhaust nanoparticles in male and female mice.

Air pollution exposure is among the most prevalent reasons for environmentally-induced oxidative stress and inflammation, both of which are involved in the development and progression of central nervous system (CNS) diseases. Ultrafine particles (UFPs) plays an important role in global air pollution and the diesel exhaust particles (DEPs) are the most important component in this regard. There are more than 40 toxic air pollutants in diesel exhaust (DE), which is one of the main constituents of an environmental pollutant and including particulate matter (PM) especially UFPs. Thus, in this study, adult female and male NMRI mice were exposed to DEPs (350-400 μg/m) for 14 weeks (6 h per day and 5 days per week). After 14 weeks of exposure, expression of pro-inflammatory cytokines (IL-1α, IL-1β, IL-6, TNF-α), nNOS, HO1, NR2A, and NR2B and malondialdehyde (MDA) level were analyzed in various brain regions such as the hippocampus (HI) and olfactory bulb (OB). Exposure to DEPs caused neuroinflammation and oxidative stress in female and male mice. That these effects observed in females were less pronounced than in male mice. The male mice emerged to be more susceptible significantly than the female mice to induced neuroinflammation following DEPs exposure. Also, our findings indicate that long term exposure to DEPs results in altered expression of hippocampal NMDA receptor subunits, and suggests that gender can play important role in the modulating susceptibility to neurotoxicity induced by DEPs exposure.