2004
DOI: 10.1016/j.aquatox.2004.05.011
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Cadmium-induced apoptosis through the mitochondrial pathway in rainbow trout hepatocytes: involvement of oxidative stress

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Cited by 102 publications
(54 citation statements)
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“…So, it is possible that Á OH triggers death receptors activation that stimulates caspase-8 with subsequent mitochondrial generation of ROS and release of cytochrome c that activates caspase-3, which results in DNA fragmentation and PS exposure in the young erythrocytes of fish. This is in agreement with the report that cadmium induces apoptosis through caspase-8 and 3 activation and the mitochondrial generation of ROS and release of cytochrome c in rainbow trout hepatocytes (de Faverney et al 2004). Lang et al (2005a) levels.…”
Section: Discussionsupporting
confidence: 82%
See 1 more Smart Citation
“…So, it is possible that Á OH triggers death receptors activation that stimulates caspase-8 with subsequent mitochondrial generation of ROS and release of cytochrome c that activates caspase-3, which results in DNA fragmentation and PS exposure in the young erythrocytes of fish. This is in agreement with the report that cadmium induces apoptosis through caspase-8 and 3 activation and the mitochondrial generation of ROS and release of cytochrome c in rainbow trout hepatocytes (de Faverney et al 2004). Lang et al (2005a) levels.…”
Section: Discussionsupporting
confidence: 82%
“…Although no reports have been published on the connection between the caspase-8 and death receptors (CD95) in fish erythrocytes, it is speculated that Á OH may activate caspase-8 by enhancing CD95 expression. This is not only because caspase-8 is a key component in the CD95-triggered apoptosis pathway (Krammer 2000;Schulze-Osthoff et al 1998), but also because many other apoptotic pathways initiated by distinct stimuli require CD95 involvement (de Faverney et al 2004). Moreover, oxidative stress triggers CD95 ligand expression in mouse microglial cells (Markus et al 1998).…”
Section: Discussionmentioning
confidence: 99%
“…Or, a cell-free assays were performed as described by Berg et al [43] with slight modifications. Briefly, after washing with PCS, 5 Â 10 7 erythrocytes in positive control were lysed in 100 μl of lysis buffer (Beyotime, Nantong, China) and lysis buffer containing 100 μM of Z-LEHD-fmk, 2.0 μg/ml of Anti-Cyt C [44] or 2.0 μg/ml of Anti-Cyt C and 1.40 mM of Ala, Cit or Pro, respectively.…”
Section: Erythrocyte Treatmentsmentioning
confidence: 99%
“…Although no reports have been published on that caspase-8 activation is death receptors (CD95) dependent in fish erythrocytes, it is speculated that • OH may activate caspase-8 by triggering CD95. This is not only because caspase-8 is a key component of the CD95-triggered apoptosis pathway [87,88], but also because many other apoptotic pathways initiated by distinct stimuli require CD95 involvement [44]. Moreover, studies indicated that oxidative stress causes CD95 ligand expression in mouse microglial cells [89].…”
Section: • Oh-induced Apoptosis In Fish Erythrocytesmentioning
confidence: 99%
“…Cd toxicity has been shown to be caused by oxidative stress (22,23); Cd can indirectly generate free radicals by replacing iron or copper ions in cytoplasmic and membrane proteins, leading to an increase of free or chelated metals (23), which in turn can lead to oxidative stress via Fenton reactions (24,25). ROS production was associated with Cd-induced cell death in rainbow trout (26), murine splenocytes (27), and human hepatoma cells (28). ROS triggered by Cd can react with several biomolecules within cells and may lead to DNA mutation, alterations in protein structure and function, lipid peroxidation, shifts in gene expression, and apoptosis (23,29).…”
mentioning
confidence: 99%