PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats.
Exposure to PM2.5(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 PM2.5exposure on the inflammatory response, oxidative stress, the enzyme activities of Na⁺K⁺-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5occurred through inhalation of a PM2.5solution aerosol. The results show that the PM2.5exposure 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 Ca2+-ATPase in rat nasal mucosa. PM2.5significantly 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 PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China. gzqhblove@126.com.
Zhiqiang
Z
Guo
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China. hongzhc@163.com.
Zhicong
Z
Hong
Center for Atmospheric Chemistry Study, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China. weiyangdongfudan@hotmail.com.
Weiyang
W
Dong
Center for Atmospheric Chemistry Study, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China. congruidengfudan@hotmail.com.
Congrui
C
Deng
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China. zhaorw007@163.com.
Renwu
R
Zhao
Center for Atmospheric Chemistry Study, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China. jianxufudan@hotmail.com.
Jian
J
Xu
Center for Atmospheric Chemistry Study, Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China. guoshunzhuangfudan@hotmail.com.
Guoshun
G
Zhuang
Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai 200040, China. zhangruxinent2015@163.com.
Ruxin
R
Zhang
D000393:Air Pollutants / Q000494:pharmacology* / Q000633:toxicity; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D007249:Inflammation / Q000473:pathology*; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects; D024101:Mitochondrial Proteins / Q000378:metabolism*; D009297:Nasal Mucosa / Q000473:pathology*; D018384:Oxidative Stress / Q000187:drug effects*; D010316:Particle Size; D052638:Particulate Matter / Q000633:toxicity; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000393:Air Pollutants; D015850:Interleukin-6; D016209:Interleukin-8; D024101:Mitochondrial Proteins; D052638:Particulate Matter; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde
fine particulate matter (PM2.5); inflammatory response; mitochondria; nasal mucosa; oxidative stress