Journal
APOPTOSIS
Volume 15, Issue 12, Pages 1507-1516Publisher
SPRINGER
DOI: 10.1007/s10495-010-0532-6
Keywords
Apoptosis; Cytochrome c; NF-kappa B; AP-1; p53; DNA damage
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Funding
- NASA [NNX08BA47A: NCC-1-02038: NIH 1P20MD001822-1]
- Division Of Human Resource Development
- Direct For Education and Human Resources [1036494] Funding Source: National Science Foundation
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Our previous report on multiwall carbon nanotubes (MWCNT) has demonstrated the generation of reactive radicals and depletion of intracellular antioxidants which in turn cause cell death through activation of caspases. The molecular mechanism of cellular death due to MWCNT is not clear yet. In this study, we investigated the signaling pathways implicated in MWCNT-induced apoptosis in rat lung epithelial cells. First, we assessed the DNA damage in response to MWCNT treatment and showed the significant DNA damage as compared to control. The collapse of the mitochondrial membrane integrity, release of cytochrome c into the cytosol, reduction in cellular ATP content, increased levels of mitochondrial apoptogenic factor and activation and nuclear translocation of NF-kappa B were observed in MWCNT treated cells. In addition, a time-dependent induction of phosphorylated I kappa B alpha and its degradation were detected in cells exposed to MWCNT. Furthermore, MWCNT activated several death related proteins including apoptosis inducing factor, p53, p21 and bax. Together, our results suggest that signaling pathways such as NF-kappa B and AP-1 are activated upon MWCNT treatment for cellular cytotoxicity.
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