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FEBS Lett. 2008 Oct 29;582(25-26):3601-6. doi: 10.1016/j.febslet.2008.09.030. Epub 2008 Sep 24.

Air pollution induces enhanced mitochondrial oxidative stress in cystic fibrosis airway epithelium.

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  • 1Stanford University School of Medicine, Stanford, CA 94305, USA.

Abstract

We studied the effects of airborne particulate matters (PM) on cystic fibrosis (CF) epithelium. We noted that PM enhanced human CF bronchial epithelial apoptosis, activated caspase-9 and PARP-1; and reduced mitochondrial membrane potential. Mitochondrial inhibitors (4,4-diisothiocyanatostilbene-2,2'disulfonic acid, rotenone and thenoyltrifluoroacetone) blocked PM-induced generation of reactive oxygen species and apoptosis. PM upregulated pro-apoptotic Bad, Bax, p53 and p21; and enhanced mitochondrial localization of Bax. The anti-apoptotic Bcl-2, Bcl-xl, Mcl-1 and Xiap remained unchanged; however, overexpression of Bcl-xl blocked PM-induced apoptosis. Accordingly, we provide the evidence that PM enhances oxidative stress and mitochondrial signaling mediated apoptosis via the modulation of Bcl family proteins in CF.

PMID:
18817777
[PubMed - indexed for MEDLINE]
PMCID:
PMC2603298
Free PMC Article
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