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

Ruijin Li, Xiaojing Kou, Hong Geng, Jingfang Xie, Jingjing Tian, Zongwei CAI, Chuan Dong*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

73 Citations (Scopus)

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 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.

Original languageEnglish
Pages (from-to)392-401
Number of pages10
JournalJournal of Hazardous Materials
Volume287
DOIs
Publication statusPublished - 8 Apr 2015

Scopus Subject Areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution
  • Health, Toxicology and Mutagenesis

User-Defined Keywords

  • Fusion/fission
  • Inflammation
  • Oxidative stress
  • PM
  • Rat heart mitochondrial damage

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