TY - JOUR
T1 - Mitochondrial damage
T2 - An important mechanism of ambient PM2.5 exposure-induced acute heart injury in rats
AU - Li, Ruijin
AU - Kou, Xiaojing
AU - Geng, Hong
AU - Xie, Jingfang
AU - Tian, Jingjing
AU - CAI, Zongwei
AU - Dong, Chuan
N1 - Funding Information:
This research was supported by the National Natural Science Foundation of China (Nos. 21177078 , 21175086 and 21175025 ), the Research Project Supported by Shanxi Scholarship Council of China ( 2013-16 ), the Nature Science Foundation of Shanxi Province in China ( 2014011036-2 ) and the 100 Talents Program of Shanxi Province.
PY - 2015/4/8
Y1 - 2015/4/8
N2 - 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 Ca2+-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.
AB - 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 Ca2+-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.
KW - Fusion/fission
KW - Inflammation
KW - Oxidative stress
KW - PM
KW - Rat heart mitochondrial damage
UR - http://www.scopus.com/inward/record.url?scp=84922449721&partnerID=8YFLogxK
U2 - 10.1016/j.jhazmat.2015.02.006
DO - 10.1016/j.jhazmat.2015.02.006
M3 - Journal article
C2 - 25677476
AN - SCOPUS:84922449721
SN - 0304-3894
VL - 287
SP - 392
EP - 401
JO - Journal of Hazardous Materials
JF - Journal of Hazardous Materials
ER -
