ROS mediate selenite-induced apoptosis in colon cancer cells |
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Authors: | Věra Králová Miroslav ?ervinka Emil Rudolf |
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Institution: | (1) Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA;(2) Pathology and Laboratory Medicine Service, William S. Middleton Memorial Veterans Hospital, Madison, WI 53705, USA; |
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Abstract: | Selenite-induced oxidative stress and its relationship to mitochondrial apoptosis was studied in human adenocarcinoma HT-29
cells. It is shown that selenite induces caspase-dependent apoptosis, which is mediated by mitochondria via released cytochrome c, apoptosis-inducing factor (AIF) and Smac/Diablo. Selenite activates stress kinases p38 and JNK while
suppressing reduced glutathione (GSH) and thioredoxin reductase (TrxR) levels, transiently inducing heme oxygenase (HO-1)
system as well as reducing Akt expression. Pre-treatment of cells with selected antioxidants and stress kinase inhibitors
significantly prevented selenite-induced cell death, thereby implicating oxidative stress as a direct (Bax) as well as indirect
(via kinases) cause of HT-29 cells demise. These results thus demonstrate for the first time active proapoptotic and anti-survival
effects of selenite in colon cancer cells. |
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