Apoptotic vs. Nonapoptotic Cytotoxicity Induced by Hydrogen Peroxide

Gardner, Agnes; Xu, Fei; Fady, Catherine; Jacoby, F; Duffey, Dianne C.; Tu, Yiping; Lichtenstein, Alan

doi:10.1016/s0891-5849(96)00235-3

Cited by 326 publications

(195 citation statements)

References 32 publications

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“…Bcl-2 has been demonstrated to prevent apoptosis only at low concentration of hydrogen peroxide (0.1 mM). The cellular damage to strong oxidant stimuli like hydrogen peroxide appears to be dose dependent: the process is a continuum from apoptosis at low concentration to necrosis at high concentration (Gardner et al, 1997). In our study, 0.5 mM hydrogen peroxide induced the decrease of bcl-2 protein as well as bcl-2 mRNA.…”

Section: Discussionsupporting

confidence: 45%

“…The reasons for this are that UV irradiation or many chemotherapeutic agents increase intracellular hydrogen peroxide levels at the same time while they induce apoptosis, and that cells tend to resist to the apoptosis-inducing agents when cells are pre-treated with antioxidants. (Gardner et al, 1997;Gorman et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…(Ueda et al, 1992). High concentration of hydrogen peroxide induces necrosis and low concentration induces apoptosis (Gardner et al, 1997;Lennon et al, 1991;Ueda et al, 1992). Although apoptosis and necrosis have different impacts on cellular physiology, the cellular response to hydrogen peroxide is continuum from apoptosis to necrosis (Gardner et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of bcl-2 family in hydrogen peroxide-induced apoptosis in human leukemia HL-60 cells

Lee

Sohn²,

Lee³

et al. 2000

Exp Mol Med

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Numerous types of cells have been shown to undergo apoptosis when exposed to oxidant agent such as hydrogen peroxide. In order to understand the functional relationship between the anti-and pro-apoptotic regulatory proteins in the cells under oxidant stress, we have studied the level of expression of apoptosis regulatory proteins, bcl-2 and bax, in human leukemia HL-60 cells. The exposure of HL-60 cells to different concentrations of H 2 O 2 for 6 h resulted in a typical apoptosis of the cells as characterized by flow cytometry, cell cycle analysis, and DNA fragmentation. There was a block in G1 to S transition and apoptotic cells were mainly derived from S and G2 cells. Kinetic study demonstrated that the levels of both bcl-2-mRNA and -protein expression were decreased with the progression of cellular apoptosis whereas the level of bax-mRNA was unchanged but the expressed bax-protein was not detectable. Cycloheximide, a nonspecific translation inhibitor, did not prevent the hydrogen peroxide-mediated apoptosis in HL-60 cells. These results suggest that the regulation of bcl-2, but not of bax are important factor in the oxidative stress-induced apoptosis in HL-60 cells.

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Section: Discussionsupporting

confidence: 45%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of bcl-2 family in hydrogen peroxide-induced apoptosis in human leukemia HL-60 cells

Lee

Sohn²,

Lee³

et al. 2000

Exp Mol Med

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“…Also, H 2 O 2 induces DNA damage and cell damage by lipid peroxidation [3] . Although apoptosis and necrosis have different impacts on cellular physiology, the cellular response to H 2 O 2 is continuing from apoptosis to necrosis [4] i.e. high concentration induces necrosis converse is applicable for apoptosis [3][4][5] .…”

Section: Introductionmentioning

confidence: 99%

Evaluation of anti–apoptotic activity of different dietary antioxidants in renal cell carcinoma against hydrogen peroxide

Rai

Mangal

Sahu

et al. 2011

Asian Pacific Journal of Tropical Biomedicine

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“…[1][2][3] Accumulation of ROS (i.e., oxidative stress) on exposure to xenobiotic agents or environmental toxins can cause cellular damage and death via apoptotic or nonapoptotic pathways. [4][5][6] Oxidative stress-induced cellular damage and death have been implicated in aging, ischemia-reperfusion injury, inflammation, and the pathogenesis of diseases (e.g., neurodegeneration and cancer). 7 Oxidative stress also contributes to the antitumor effects of many chemotherapeutic drugs, including camptothecin 8,9 and selenite.…”

mentioning

confidence: 99%

Nuclear ULK1 promotes cell death in response to oxidative stress through PARP1

et al. 2015

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Reactive oxygen species (ROS) may cause cellular damage and oxidative stress-induced cell death. Autophagy, an evolutionarily conserved intracellular catabolic process, is executed by autophagy (ATG) proteins, including the autophagy initiation kinase Unc-51-like kinase (ULK1)/ATG1. Although autophagy has been implicated to have both cytoprotective and cytotoxic roles in the response to ROS, the role of individual ATG proteins, including ULK1, remains poorly characterized. In this study, we demonstrate that ULK1 sensitizes cells to necrotic cell death induced by hydrogen peroxide (H 2 O 2 ). Moreover, we demonstrate that ULK1 localizes to the nucleus and regulates the activity of the DNA damage repair protein poly (ADP-ribose) polymerase 1 (PARP1) in a kinase-dependent manner. By enhancing PARP1 activity, ULK1 contributes to ATP depletion and death of H 2 O 2 -treated cells. Our study provides the first evidence of an autophagy-independent prodeath role for nuclear ULK1 in response to ROS-induced damage. On the basis of our data, we propose that the subcellular distribution of ULK1 has an important role in deciding whether a cell lives or dies on exposure to adverse environmental or intracellular conditions. Cell Death and Differentiation (2016) 23, 216-230; doi:10.1038/cdd.2015; published online 3 July 2015Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide (H 2 O 2 ), are formed by the incomplete reduction of oxygen during oxidative phosphorylation and other enzymatic processes. ROS are signaling molecules that regulate cell proliferation, differentiation, and survival. 1-3 Accumulation of ROS (i.e., oxidative stress) on exposure to xenobiotic agents or environmental toxins can cause cellular damage and death via apoptotic or nonapoptotic pathways. [4][5][6] Oxidative stress-induced cellular damage and death have been implicated in aging, ischemia-reperfusion injury, inflammation, and the pathogenesis of diseases (e.g., neurodegeneration and cancer). 7 Oxidative stress also contributes to the antitumor effects of many chemotherapeutic drugs, including camptothecin 8,9 and selenite. 10,11 Autophagy, an evolutionarily conserved intracellular catabolic process, involves lysosome-dependent degradation of superfluous and damaged cytosolic organelles and proteins. 12 It is typically upregulated under conditions of perceived stress and in response to cellular damage. The consequence of autophagy activation -whether cytoprotective or cytotoxicappears to depend on the cell type and the nature and extent of stress. Although most studies indicate a cytoprotective role for autophagy, some evidence suggests that it contributes to cell death in response to oxidative stress. [13][14][15][16][17] Studies have also indicated that autophagy may be suppressed in response to oxidative stress, thereby sensitizing certain cells to apoptosis. 18,19 Unc-51-like kinase/autophagy 1 (ULK1/ATG1) is a mammalian serine-threonine kinase that regulates flux through the autophagy pathway by activating the VPS34 PI(3) kinas...

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Apoptotic vs. Nonapoptotic Cytotoxicity Induced by Hydrogen Peroxide

Cited by 326 publications

References 32 publications

Regulation of bcl-2 family in hydrogen peroxide-induced apoptosis in human leukemia HL-60 cells

Regulation of bcl-2 family in hydrogen peroxide-induced apoptosis in human leukemia HL-60 cells

Evaluation of anti–apoptotic activity of different dietary antioxidants in renal cell carcinoma against hydrogen peroxide

Nuclear ULK1 promotes cell death in response to oxidative stress through PARP1

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