title: Mitochondrial damage: an important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats.
abstract: 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-1β 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.
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China.
authors: Ruijin
authors: R
authors: Li
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China.
authors: Xiaojing
authors: X
authors: Kou
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China.
authors: Hong
authors: H
authors: Geng
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China.
authors: Jingfang
authors: J
authors: Xie
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China.
authors: Jingjing
authors: J
authors: Tian
authors: State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong SAR, China. Electronic address: zwcai@hkbu.edu.hk.
authors: Zongwei
authors: Z
authors: Cai
authors: Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China. Electronic address: dc@sxu.edu.cn.
authors: Chuan
authors: C
authors: Dong
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D006321:Heart / Q000187:drug effects*; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects; D052638:Particulate Matter / Q000633:toxicity*; D017207:Rats, Sprague-Dawley
chemical_list: D000393:Air Pollutants; D016207:Cytokines; D024101:Mitochondrial Proteins; D052638:Particulate Matter
keywords: Fusion/fission; Inflammation; Oxidative stress; PM(2.5); Rat heart mitochondrial damage