http://dx.doi.org/10.1016/j.jhazmat.2015.02.006">
 

Document Type

Journal Article

Department/Unit

Department of Chemistry

Title

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

Language

English

Abstract

© 2015 Elsevier B.V. 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.

Keywords

Fusion/fission, Inflammation, Oxidative stress, PM2.5, Rat heart mitochondrial damage

Publication Date

2015

Source Publication Title

Journal of Hazardous Materials

Volume

287

Start Page

392

End Page

401

Publisher

Elsevier

ISSN (print)

03043894

ISSN (electronic)

18733336

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