2001
DOI: 10.1016/s0891-5849(01)00629-3
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Effect of glutathione depletion on caspase-3 independent apoptosis pathway induced by curcumin in Jurkat cells

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Cited by 77 publications
(35 citation statements)
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“…This might explain the decrease in the fragmentation percentage in the curcumin positive control group. This scavenging activity of curcumin lead to attenuated DNA fragmentation due to the elevation of glutathione (Piwocka et al, 2001).…”
Section: Dna Fragmentation Assaymentioning
confidence: 96%
“…This might explain the decrease in the fragmentation percentage in the curcumin positive control group. This scavenging activity of curcumin lead to attenuated DNA fragmentation due to the elevation of glutathione (Piwocka et al, 2001).…”
Section: Dna Fragmentation Assaymentioning
confidence: 96%
“…Curcumin is also a potent inhibitor of protein kinase C, EGF-receptor tyrosine kinase and I kappa B kinase . In addition, curcumin inhibits the expression of c-fos, c-myc and c-jun (Kakar & Roy 1994;Limtrakul et al 2001) and induces apoptosis (Piwocka et al 2001). Despite the fact that 1) curcumin and its derivatives have shown a significant protection against tumourigenesis in several animal tumour bioassay systems (Sharma 1976;Satoskar et al 1986;Huang et al 1992;Goel et al 2001;Mori et al 2001Surh et al 2001 2) depletion in the activities of antioxidant and phase II enzymes occur during tumourigenesis (Perchellet & Perchellet 1989;Sun 1990) 3) cancer chemopreventive agents enhances the activity of these enzymes in target tissues (Wattenberg & Loccia 1990).…”
mentioning
confidence: 99%
“…The MAPK signaling pathways modulate gene expression, mitosis, proliferation, motility, metabolism, and programmed cell death [24]. Furthermore, curcumin is reported to inhibit proliferation and induce apoptosis in T lymphocytes and Jurkat cells [25,26]. Since in the present study, T 3 administration had shown a 37% augmentation in mitochondrial LPX level indicating ROS predominance over antioxidants (Table 1), it is hypothesized that the increased ROS level as a consequence of T 3 -induced hyper-thyroidism may be responsible for the increased cell proliferation probably via MAPK and/or redox active kinases signaling pathways.…”
Section: Resultsmentioning
confidence: 99%