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Molecular ordering of ROS production, mitochondrial changes, and caspase activation during sodium salicylate-induced apoptosis

Title
Molecular ordering of ROS production, mitochondrial changes, and caspase activation during sodium salicylate-induced apoptosis
Authors
Chung Y.M.Bae Y.S.Lee S.Y.
Ewha Authors
배윤수이수영
SCOPUS Author ID
배윤수scopus; 이수영scopus
Issue Date
2003
Journal Title
Free Radical Biology and Medicine
ISSN
0891-5849JCR Link
Citation
vol. 34, no. 4, pp. 434 - 442
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Salicylates and nonsteroidal anti-inflammatory drugs (NSAIDs) induce apoptosis in a variety of cancer cells, including those of colon, prostate, breast, and leukemia. We examined the effects of sodium salicylate (NaSal) on reactive oxygen species (ROS) production and the association of these effects with apoptotic tumor cell death. We demonstrate that NaSal mediates ROS production followed by a decrease in mitochondrial membrane potential (Δψm), release of cytochrome c, and activation of caspase-9 and caspase-3. However, expression of Bcl-2 or Bcl-xL prevents ROS production and subsequent loss of Δψm, thereby inhibiting apoptotic cell death. The presence of ROS scavengers and an inhibitor of NADPH oxidase or expression of a dominant negative form of Rac1 blocks ROS production, Δψm collapse, and the subsequent activation of caspases. These observations indicate that NaSal mediates ROS production critical in the triggering of apoptotic tumor cell death through a Rac1-NADPH oxidase-dependent pathway. Our data collectively imply that NaSal-induced ROS are key mediators of Δψm collapse, which leads to the release of cytochrome c followed by caspase activation, culminating in tumor apoptosis. © 2003 Elsevier Science Inc.
DOI
10.1016/S0891-5849(02)01301-1
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자연과학대학 > 생명과학전공 > Journal papers
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