PM(2.5)-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats

Exposure to PM(2.5) (particulate matter ≤2.5 μm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM(2.5) exposure on the inflammatory response, oxidative stress, the enzyme activities of Na(+)K(+)-ATPase and Ca(2+)-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM(2.5) occurred through inhalation of a PM(2.5) solution aerosol. The results show that the PM(2.5) exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na(+)K(+)-ATPase, and Ca(2+)-ATPase in rat nasal mucosa. PM(2.5) significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM(2.5). Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM(2.5).