These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Mechanism of ziram-induced apoptosis in human natural killer cells. Author: Li Q, Kobayashi M, Kawada T. Journal: Int J Immunopathol Pharmacol; 2012; 25(4):883-91. PubMed ID: 23298479. Abstract: We previously found that ziram, a dithiocarbamate fungicide, significantly inhibited natural killer (NK) activity in a dose-dependent manner. To explore the mechanism of this inhibition, we investigated ziram-induced apoptosis in human NK cells. Human NK-92MI cells were treated with ziram at 0.0625-4 µM for 2-64 h. Apoptosis was determined by FITC-Annexin-V/PI staining. To explore the mechanism of apoptosis, intracellular levels of active caspases 3, 3/7, 8, and 9 and pan-caspase and mitochondrial cytochrome-c release were determined by flow cytometry. Disruption to mitochondrial transmembrane potential was determined with a MitoLight? Apoptosis Detection Kit. It was found that ziram induced apoptosis in a dose- and time-dependent manner in human NK cells. Ziram increased the intracellular levels of active caspases 3, 3/7, 8, and 9 and pan-caspase in a dose-dependent manner, and a caspase-3 inhibitor, Z-DEVD-FMK, and a general caspase inhibitor, Z-VAD-FMK, partially but significantly inhibited the apoptosis. Ziram also disrupted mitochondrial transmembrane potential and caused mitochondrial cytochrome-c release in a dose-dependent manner. These findings indicate that ziram can induce apoptosis in human NK cells, and the apoptosis is at least mediated by both the caspase-cascade and the mitochondria/cytochrome-c pathways.[Abstract] [Full Text] [Related] [New Search]