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Apoptosis intracellular induction

Induction of apoptosis has been reported in various mammalian cell lines. In previous studies, it has been reported that TBT induces apoptosis in isolated thymocytes at concentrations which are relevant to those causing thymus atrophy in vivo. TBT can also induce apoptosis in PC12 cells, and in human T-lymphoblastoid CEM cells. While the mechanism of TBT-induced apoptosis is still unknown, it has been reported that TBT stimulates thymocyte apoptosis by a mechanism independent of protein synthesis and under conditions where intracellular ATP levels are severely depleted. ... [Pg.419]

Singh, J., Pritchard, D. E., Carlisle, D. L., McClean, J. A., Montaser, A., Orenstein, J. M. and Patierno, S. R. (1999). Internalization of carcinogenic lead chromate particles by cultured normal human lung epithelial cells formation of intracellular lead-inclusion bodies and induction of apoptosis, Toxicol. Appl. Pharmacol., 161, 240-248. [Pg.400]

After the binding of TNF-a to its receptors, there is induction of two major intracellular signaling pathways. One pathway leads to the transcription of other genes, and the other pathway leads to cell death or apoptosis. The two main transcription factors activated by TNF-a are AP-1 and NF-kB. [Pg.51]

Figure 15.4 Mechanisms of apoptosis induction by resveratrol. Resveratrol selectively induces apoptosis in various cancer cells in culture by several mechanisms including activation of death receptor-mediated signaling, mitochondria-dependent cytochrome c release and caspase activation, induction of p53 and p53-regulated proapototic genes, activation of MAP kinase-mediated p53 phosphorylation, blockade of Akt-mediated cell survival pathways, and accumulation of intracellular ceramide level. Figure 15.4 Mechanisms of apoptosis induction by resveratrol. Resveratrol selectively induces apoptosis in various cancer cells in culture by several mechanisms including activation of death receptor-mediated signaling, mitochondria-dependent cytochrome c release and caspase activation, induction of p53 and p53-regulated proapototic genes, activation of MAP kinase-mediated p53 phosphorylation, blockade of Akt-mediated cell survival pathways, and accumulation of intracellular ceramide level.

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Apoptosis, induction

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