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  • Artcle KNL

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    Kunal Ranjan
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    Multiwall carbon nanotubes cause cell death in rat lung epithelial cells through apoptosis by activating several signaling pathways. DNA damage was observed along with collapse of the mitochondrial membrane, release of cytochrome c, and reduction of ATP. Treatment with multiwall carbon nanotubes also led to activation of NF-κB and induction of phosphorylated IκBα and degradation, as well as increased levels of mitochondrial apoptogenic factors and activation of death-related proteins including apoptosis inducing factor, p53, p21 and bax. These results suggest that NF-κB and AP-1 signaling pathways are activated by multiwall carbon nanotubes and contribute to cellular cytotoxicity.

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    Multiwall carbon nanotubes cause cell death in rat lung epithelial cells through apoptosis by activating several signaling pathways. DNA damage was observed along with collapse of the mitochondrial membrane, release of cytochrome c, and reduction of ATP. Treatment with multiwall carbon nanotubes also led to activation of NF-κB and induction of phosphorylated IκBα and degradation, as well as increased levels of mitochondrial apoptogenic factors and activation of death-related proteins including apoptosis inducing factor, p53, p21 and bax. These results suggest that NF-κB and AP-1 signaling pathways are activated by multiwall carbon nanotubes and contribute to cellular cytotoxicity.

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    4 views1 page

    Artcle KNL

    Uploaded by

    Kunal Ranjan
    Multiwall carbon nanotubes cause cell death in rat lung epithelial cells through apoptosis by activating several signaling pathways. DNA damage was observed along with collapse of the mitochondrial membrane, release of cytochrome c, and reduction of ATP. Treatment with multiwall carbon nanotubes also led to activation of NF-κB and induction of phosphorylated IκBα and degradation, as well as increased levels of mitochondrial apoptogenic factors and activation of death-related proteins including apoptosis inducing factor, p53, p21 and bax. These results suggest that NF-κB and AP-1 signaling pathways are activated by multiwall carbon nanotubes and contribute to cellular cytotoxicity.

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    Sudhakar sir Apoptosis Abstract

    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 MWCNTinduced 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-B were observed in MWCNT treated cells. In addition, a time-dependent induction of phosphorylated IB 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-B and AP-1 are activated upon MWCNT treatment for cellular cytotoxicity

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