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Mitochondrial damage: an important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats.

Authors: Li, Ruijin  Kou, Xiaojing  Geng, Hong  Xie, Jingfang  Tian, Jingjing  Cai, Zongwei  Dong, Chuan 
Citation: Li R, etal., J Hazard Mater. 2015 Apr 28;287:392-401. doi: 10.1016/j.jhazmat.2015.02.006. Epub 2015 Feb 4.
Pubmed: (View Article at PubMed) PMID:25677476
DOI: Full-text: DOI:10.1016/j.jhazmat.2015.02.006

Epidemiological studies suggested that ambient fine particulate matter (PM2.5) exposure was associated with cardiovascular disease. However, the underlying mechanism, especially the mitochondrial damage mechanism, of PM2.5-induced heart acute injury is still unclear. In this study, the alterations of mitochondrial morphology and mitochondrial fission/fusion gene expression, oxidative stress, calcium homeostasis and inflammation in hearts of rats exposed to PM2.5 with different dosages (0.375, 1.5, 6.0 and 24.0mg/kg body weight) were investigated. The results indicated that the PM2.5 exposure induced pathological changes and ultra-structural damage in hearts such as mitochondrial swell and cristae disorder. Furthermore, PM2.5 exposure significantly increased specific mitochondrial fission/fusion gene (Fis1, Mfn1, Mfn2, Drp1 and OPA1) expression in rat hearts. These changes were accompanied by decreases of activities of superoxide dismutase (SOD), Na(+)K(+)-ATPase and Ca(2+)-ATPase and increases of levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS) and nitric oxide (NO) as well as levels of pro-inflammatory mediators including TNF-α, IL-6 and IL-1ß in rat hearts. The results implicate that mitochondrial damage, oxidative stress, cellular homeostasis imbalance and inflammation are potentially important mechanisms for the PM2.5-induced heart injury, and may have relations with cardiovascular disease.


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RGD ID: 12437078
Created: 2017-01-27
Species: All species
Last Modified: 2017-01-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.