cytochrome-c-t and 1-(carboxymethylthio)tetradecane

cytochrome-c-t has been researched along with 1-(carboxymethylthio)tetradecane* in 1 studies

Other Studies

1 other study(ies) available for cytochrome-c-t and 1-(carboxymethylthio)tetradecane

Article	Year
Mitochondrial-targeted fatty acid analog induces apoptosis with selective loss of mitochondrial glutathione in promyelocytic leukemia cells. Chemistry & biology, 2003, Volume: 10, Issue:7 Some fatty acids and derivatives are known to induce cell death in cancer cells. Mitochondria may have important roles in the death process. Therefore, we investigated the mitochondrial contribution in cell death induced by a modified fatty acid, tetradecylthioacetic acid (TTA), which cannot be beta-oxidized. TTA treatment induced apoptosis in IPC-81 leukemia cells via depolarization of the mitochondrial membrane potential (deltapsi) and early release of cytochrome c, accompanied by depletion of mitochondrial glutathione. Caspase-3 activation and cleavage of poly (ADP-ribose) polymerase (PARP) occurred at a late stage, but the broad-spectra caspase inhibitor zVAD-fmk did not block TTA-induced apoptosis. Overexpression of Bcl-2 partially prevented TTA-induced apoptosis, whereas cAMP-induced cell death was completely blocked. In conclusion, TTA seems to trigger apoptosis through mitochondrial-mediated mechanisms and selective modulation of the mitochondrial redox equilibrium. Topics: Animals; Antineoplastic Agents; Apoptosis; Blotting, Western; Caspases; Cell Line, Tumor; Cell Nucleus; Cyclic AMP; Cytochromes c; Cytosol; Fluorescent Dyes; Gene Expression Regulation, Neoplastic; Genes, bcl-2; Glutathione; Image Processing, Computer-Assisted; Immunoassay; Leukemia, Promyelocytic, Acute; Mice; Mitochondria; Subcellular Fractions; Sulfides; Thionucleotides	2003

Article

Year

Mitochondrial-targeted fatty acid analog induces apoptosis with selective loss of mitochondrial glutathione in promyelocytic leukemia cells.

Chemistry & biology, 2003, Volume: 10, Issue:7

Some fatty acids and derivatives are known to induce cell death in cancer cells. Mitochondria may have important roles in the death process. Therefore, we investigated the mitochondrial contribution in cell death induced by a modified fatty acid, tetradecylthioacetic acid (TTA), which cannot be beta-oxidized. TTA treatment induced apoptosis in IPC-81 leukemia cells via depolarization of the mitochondrial membrane potential (deltapsi) and early release of cytochrome c, accompanied by depletion of mitochondrial glutathione. Caspase-3 activation and cleavage of poly (ADP-ribose) polymerase (PARP) occurred at a late stage, but the broad-spectra caspase inhibitor zVAD-fmk did not block TTA-induced apoptosis. Overexpression of Bcl-2 partially prevented TTA-induced apoptosis, whereas cAMP-induced cell death was completely blocked. In conclusion, TTA seems to trigger apoptosis through mitochondrial-mediated mechanisms and selective modulation of the mitochondrial redox equilibrium.

Topics: Animals; Antineoplastic Agents; Apoptosis; Blotting, Western; Caspases; Cell Line, Tumor; Cell Nucleus; Cyclic AMP; Cytochromes c; Cytosol; Fluorescent Dyes; Gene Expression Regulation, Neoplastic; Genes, bcl-2; Glutathione; Image Processing, Computer-Assisted; Immunoassay; Leukemia, Promyelocytic, Acute; Mice; Mitochondria; Subcellular Fractions; Sulfides; Thionucleotides

2003