scholarly journals The Regulation of Reactive Oxygen Species Production during Programmed Cell Death

1998 ◽  
Vol 141 (6) ◽  
pp. 1423-1432 ◽  
Author(s):  
Shirlee Tan ◽  
Yutaka Sagara ◽  
Yuanbin Liu ◽  
Pamela Maher ◽  
David Schubert
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Glutamate Toxicity ◽  
Ros Production ◽  
Oxygen Species ◽  
Ht22 Cells

Reactive oxygen species (ROS) are thought to be involved in many forms of programmed cell death. The role of ROS in cell death caused by oxidative glutamate toxicity was studied in an immortalized mouse hippocampal cell line (HT22). The causal relationship between ROS production and glutathione (GSH) levels, gene expression, caspase activity, and cytosolic Ca2+ concentration was examined. An initial 5–10-fold increase in ROS after glutamate addition is temporally correlated with GSH depletion. This early increase is followed by an explosive burst of ROS production to 200–400-fold above control values. The source of this burst is the mitochondrial electron transport chain, while only 5–10% of the maximum ROS production is caused by GSH depletion. Macromolecular synthesis inhibitors as well as Ac-YVAD-cmk, an interleukin 1β–converting enzyme protease inhibitor, block the late burst of ROS production and protect HT22 cells from glutamate toxicity when added early in the death program. Inhibition of intracellular Ca2+ cycling and the influx of extracellular Ca2+ also blocks maximum ROS production and protects the cells. The conclusion is that GSH depletion is not sufficient to cause the maximal mitochondrial ROS production, and that there is an early requirement for protease activation, changes in gene expression, and a late requirement for Ca2+ mobilization.

scholarly journals Expression of death-related genes and reactive oxygen species production in Skeletonema tropicum upon exposure to the polyunsaturated aldehyde octadienal

2015 ◽  
Vol 6 (1/2) ◽  
Author(s):  
Alessandra A. Gallina ◽  
Chih-Ching Chung ◽  
Raffaella Casotti
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Marine Diatom ◽  
Ros Production ◽  
Oxygen Species ◽  
Diatom Population ◽  
Polyunsaturated Aldehydes ◽  
Species Production

<p>The effects of 4<em>E</em>/<em>Z</em>-octadienal (OCTA) on <em>ScDSP-1 </em>and <em>ScDSP-2 </em>gene expression and reactive oxygen species (ROS) production were investigated in the marine diatom <em>Skeletonema tropicum</em> (formerly <em>costatum</em>) using qRTPCR and flow cytometry. <em>ScDSP-1 </em>and <em>ScDSP-2 </em>genes have been previously shown to be involved in cell death in ageing cells and in response to photosynthetic stress. OCTA induced a differential, concentration-dependent <em>DSP</em> gene expression associated to ROS production, 821.6 and 97.7 folds higher for <em>ScDSP-1</em> and <em>ScDSP-2</em>, respectively. Among the concentrations tested, only 8 μM OCTA, which caused a reduction of 50% in cell concentrations at 24 h, was able to elicit an expression pattern consistent with a signalling role. Interestingly, only intermediate levels of reactive oxygen species (ROS) (<em>i.e</em>., 1.5±0.1 increase) were observed to be elicited by such concentration. These results suggest that ROS are key components of the molecular cascade triggered by polyunsaturated aldehydes (PUA) and leading to cell death. This could have implications for bloom final stages at sea, where PUA may act as effectors of diatom population dynamics through ROS acting as modulators.</p>

scholarly journals The role of reactive oxygen species and nitric oxide in programmed cell death associated with self-incompatibility

2015 ◽  
Vol 66 (10) ◽  
pp. 2869-2876 ◽  
Author(s):  
Irene Serrano ◽  
María C. Romero-Puertas ◽  
Luisa M. Sandalio ◽  
Adela Olmedilla
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Self Incompatibility

scholarly journals Intradialytic granulocyte reactive oxygen species production: a prospective, crossover trial.

1993 ◽  
Vol 4 (2) ◽  
pp. 178-186 ◽  
Author(s):  
J Himmelfarb ◽  
K A Ault ◽  
D Holbrook ◽  
D A Leeber ◽  
R M Hakim
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Ros Production ◽  
Oxygen Species ◽  
Susceptibility To Infection ◽  
Flow Cytometric ◽  
Ros Formation ◽  
Dialysis Membranes ◽  
Species Production

By the use of flow cytometric techniques, this prospective, randomized crossover study was designed to analyze intradialytic granulocyte reactive oxygen species (ROS) formation in whole blood with complement-activating and noncomplement-activating hollow fiber membranes. Dialysis with a complement-activating membrane resulted in a 6.5-fold increase in granulocyte hydrogen peroxide production 15 min after dialysis initiation and remained significantly elevated (P < 0.01) through the first 30 min with this membrane in comparison to both predialysis values and simultaneous values with a noncomplement-activating membrane. Further studies demonstrated that blood obtained at 15 min with a complement-activating membrane generated significantly less granulocyte ROS production in response to Staphylococcus aureus incubation than blood obtained either predialysis or at the same time in dialysis with a noncomplement-activating membrane. Both complement-activating and noncomplement-activating dialysis membranes caused slightly decreased granulocyte responsiveness to phorbol myristate acetate. It was concluded that hemodialysis with complement-activating membranes results in increased granulocyte ROS production and decreased responsiveness to S. aureus challenge during the dialysis procedure. These results document the potential role of ROS in hemodialysis-associated pathology and susceptibility to infection.

scholarly journals Initiation and Execution of Programmed Cell Death and Regulation of Reactive Oxygen Species in Plants

2021 ◽  
Vol 22 (23) ◽  
pp. 12942
Author(s):  
Chanjuan Ye ◽  
Shaoyan Zheng ◽  
Dagang Jiang ◽  
Jingqin Lu ◽  
Zongna Huang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Stress ◽  
Reactive Oxygen ◽  
Signalling Pathways ◽  
Oxygen Species ◽  
Signalling Molecules ◽  
Plant Stress Tolerance ◽  
The Relationship

Programmed cell death (PCD) plays crucial roles in plant development and defence response. Reactive oxygen species (ROS) are produced during normal plant growth, and high ROS concentrations can change the antioxidant status of cells, leading to spontaneous cell death. In addition, ROS function as signalling molecules to improve plant stress tolerance, and they induce PCD under different conditions. This review describes the mechanisms underlying plant PCD, the key functions of mitochondria and chloroplasts in PCD, and the relationship between mitochondria and chloroplasts during PCD. Additionally, the review discusses the factors that regulate PCD. Most importantly, in this review, we summarise the sites of production of ROS and discuss the roles of ROS that not only trigger multiple signalling pathways leading to PCD but also participate in the execution of PCD, highlighting the importance of ROS in PCD.

scholarly journals Rosmarinic acid induces programmed cell death in Arabidopsis seedlings through reactive oxygen species and mitochondrial dysfunction

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208802 ◽  
Author(s):  
Fabrizio Araniti ◽  
Aitana Costas-Gil ◽  
Luz Cabeiras-Freijanes ◽  
Antonio Lupini ◽  
Francesco Sunseri ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Dysfunction ◽  
Rosmarinic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species

Histone Deacetylase Inhibitor (HDACi) PCI-24781 and Bortezomib Result in Synergistic Apoptosis in Hodgkin Lymphoma (HL) and Non-Hodgkin’s Lymphoma (NHL) Cell Lines: Investigation of Cell Death and NFKB-Mediated Pathways.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3589-3589 ◽  
Author(s):  
Savita Bhalla ◽  
Kevin David ◽  
Lauren Mauro ◽  
Sheila Prachand ◽  
Mint Sirisawad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Lines ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Oxygen Species ◽  
Minimal Cell ◽  
Histone 3 ◽  
Dichlorofluorescein Diacetate ◽  
20 Nm

Abstract HDACi block cancer cell proliferation by mechanisms that involve epigenetic gene regulation leading to cell growth arrest, differentiation, and apoptosis. Bortezomib inhibits NFKB signaling and induces apoptosis. Furthermore, anti-tumor activity of HDACi and bortezomib both depend in part on reactive oxygen species (ROS)-mediated pathways. Both have activity in NHL. We reasoned that these agents may be synergistic in part due to their dependence on overlapping pathways. We investigated the biology of PCI-24781, a pan-HDACi currently in clinical trials, and bortezomib both alone, and in combination, in HL (L428) and NHL cell lines (HF1, Ramos, & SUDHL4). Cells were incubated with increasing concentrations of PCI-24781 and bortezomib (0.25–2.0μM and 2.5–20nM, respectively) for 24–72 hour (hr). Apoptosis was determined by fluorescence-activated cell sorting (FACS) using AnnexinV-FITC/propidium iodide (AnnexinV+/PI+) staining. Reactive oxygen species (ROS) were measured by oxidation of 2′7′dichlorofluorescein diacetate (H2DCFDA) to DCF and detected by FACS. Downstream targets of NFKB such as NFKB1, Myc and IL-8 were measured in Ramos using quantitative real time polymerase chain reaction (RT-PCR) following 24 hr incubation of cells with PCI-24781 and bortezomib alone, and in combination. Dose-dependent apoptosis was seen with PCI-24781 and bortezomib alone in all HL and NHL cell lines. IC70 (dose to achieve 70% AnnexinV+/PI+) was 1μM for PCI-24781 and 2μM for L428. With bortezomib, the IC50 was 10nM in Ramos, HF1, and SUDHL4 and 20 nM in L428. The combination of PCI-24781 and bortezomib resulted in synergistic apoptosis (combination index &lt;0.2) in all 3 NHL cell lines (IC80=0.25μM PCI-24781/5nM bortezomib) and L428 (IC80=0.5μM PCI-24781/10nM bortezomib) compared with minimal cell death using each agent alone at those concentrations. Furthermore, immunoblots of L428 and Ramos showed enhanced caspase 3 and caspase 8 cleavage with the combination of PCI-24781 and bortezomib compared to either agent alone, suggesting that the synergy seen was in part caspase-dependent. HL and NHL cell lines showed a 3- to 4-fold increase in ROS with PCI-24781 or bortezomib alone and in combination at 24hr. Moreover, we found that hyperacetylation of histone-3 and histone-4 on immunoblots of cells treated with combination PCI-2478/bortezomib was significantly increased compared to PCI-24781 alone. Finally, we found that in Ramos cells PC-24781/bortezomib together resulted in downregulation of NFKB targets NFKB1 and Myc, but not IL-8. We conclude that PCI-24781 and bortezomib are active in lymphoma cell lines and that the combination results in synergistic apoptosis. Apoptosis was accompanied by caspase activation and synergistic downregulation of the NFkB pathway. These data have important clinical implications for NHL and HL.

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