scholarly journals Cytochrome c Is Released in a Reactive Oxygen Species-Dependent Manner and Is Degraded via Caspase-Like Proteases in Tobacco Bright-Yellow 2 Cells en Route to Heat Shock-Induced Cell Death

2006 ◽  
Vol 141 (1) ◽  
pp. 208-219 ◽  
Author(s):  
Rosa Anna Vacca ◽  
Daniela Valenti ◽  
Antonella Bobba ◽  
Riccardo Sandro Merafina ◽  
Salvatore Passarella ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Heat Shock ◽  
Cytochrome C ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Bright Yellow

Involvement of Caspases in Neutrophil Apoptosis: Regulation by Reactive Oxygen Species

Blood ◽  
1998 ◽  
Vol 92 (12) ◽  
pp. 4808-4818 ◽  
Author(s):  
Bengt Fadeel ◽  
Anders Åhlin ◽  
Jan-Inge Henter ◽  
Sten Orrenius ◽  
Mark B. Hampton
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Human Neutrophils ◽  
Neutrophil Apoptosis ◽  
Dependent Manner ◽  
Caspase Activity ◽  
Oxygen Species ◽  
Spontaneous Apoptosis

Abstract Human neutrophils have a short half-life and are believed to die by apoptosis or programmed cell death both in vivo and in vitro. We found that caspases are activated in a time-dependent manner in neutrophils undergoing spontaneous apoptosis, concomitant with other characteristic features of apoptotic cell death such as morphologic changes, phosphatidylserine (PS) exposure, and DNA fragmentation. The treatment of neutrophils with agonistic anti-Fas monoclonal antibodies (MoAbs) significantly accelerated this process. However, in cells treated with the potent neutrophil activator phorbol 12-myristate 13-acetate (PMA), caspase activity was only evident after pharmacologic inhibition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Similarily, inhibition of the NADPH oxidase in constitutive and Fas/APO-1–triggered apoptosis resulted in increased rather than suppressed levels of caspase activity, suggesting that reactive oxygen species may prevent caspases from functioning optimally in these cells. Moreover, oxidants generated via the NADPH oxidase were essential for PS exposure during PMA-induced cell death, but not for neutrophils undergoing spontaneous apoptosis. We conclude that caspases are an important component of constitutive and Fas/APO-1–triggered neutrophil apoptosis. However, these redox sensitive enzymes are suppressed in activated neutrophils, and an alternate oxidant-dependent pathway is used to mediate PS exposure and neutrophil clearance under these conditions.

scholarly journals P2X7 Receptor Activation Induces Reactive Oxygen Species Formation and Cell Death in Murine EOC13 Microglia

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Rachael Bartlett ◽  
Justin J. Yerbury ◽  
Ronald Sluyter
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Line ◽  
Purinergic Receptor ◽  
Reactive Oxygen ◽  
Receptor Activation ◽  
Organic Cations ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Ros Formation

The P2X7 purinergic receptor is a ligand-gated cation channel expressed on leukocytes including microglia. This study aimed to determine if P2X7 activation induces the uptake of organic cations, reactive oxygen species (ROS) formation, and death in the murine microglial EOC13 cell line. Using the murine macrophage J774 cell line as a positive control, RT-PCR, immunoblotting, and immunolabelling established the presence of P2X7 in EOC13 cells. A cytofluorometric assay demonstrated that the P2X7 agonists adenosine-5′-triphosphate (ATP) and 2′(3′)-O-(4-benzoylbenzoyl) ATP induced ethidium+or YO-PRO-12+uptake into both cell lines. ATP induced ethidium+uptake into EOC13 cells in a concentration-dependent manner, with an EC50of~130 μM. The P2X7 antagonists Brilliant Blue G, A438079, AZ10606120, and AZ11645373 inhibited ATP-induced cation uptake into EOC13 cells by 75–100%. A cytofluorometric assay demonstrated that P2X7 activation induced ROS formation in EOC13 cells, via a mechanism independent of Ca2+influx and K+efflux. Cytofluorometric measurements of Annexin-V binding and 7AAD uptake demonstrated that P2X7 activation induced EOC13 cell death. The ROS scavenger N-acetyl-L-cysteine impaired both P2X7-induced EOC13 ROS formation and cell death, suggesting that ROS mediate P2X7-induced EOC13 death. In conclusion, P2X7 activation induces the uptake of organic cations, ROS formation, and death in EOC13 microglia.

scholarly journals Roles of Reactive Oxygen Species and Mitochondria in Seed Germination

2021 ◽  
Vol 12 ◽  
Author(s):  
Muhammad Awais Farooq ◽  
Xiaomeng Zhang ◽  
Muhammad Mubashar Zafar ◽  
Wei Ma ◽  
Jianjun Zhao
Keyword(s):  
Reactive Oxygen Species ◽  
Heat Shock ◽  
Seed Germination ◽  
Seed Dormancy ◽  
Energy Demand ◽  
Crop Production ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species

Seed germination is crucial for the life cycle of plants and maximum crop production. This critical developmental step is regulated by diverse endogenous [hormones, reactive oxygen species (ROS)] and exogenous (light, temperature) factors. Reactive oxygen species promote the release of seed dormancy by biomolecules oxidation, testa weakening and endosperm decay. Reactive oxygen species modulate metabolic and hormone signaling pathways that induce and maintain seed dormancy and germination. Endosperm provides nutrients and senses environmental signals to regulate the growth of the embryo by secreting timely signals. The growing energy demand of the developing embryo and endosperm is fulfilled by functional mitochondria. Mitochondrial matrix-localized heat shock protein GhHSP24.7 controls seed germination in a temperature-dependent manner. In this review, we summarize comprehensive view of biochemical and molecular mechanisms, which coordinately control seed germination. We also discuss that the accurate and optimized coordination of ROS, mitochondria, heat shock proteins is required to permit testa rupture and subsequent germination.

Down-regulated Reactive Oxygen Species by Heat Shock Protein 90 in 3-Hydroxykynurenine-induced SKN-SH Cell Death

2004 ◽  
Vol 17 (3) ◽  
pp. 231
Author(s):  
Dae Seong Kim ◽  
Myoung Woo Lee ◽  
Yoo Hun Noh ◽  
Do Yeon Lee ◽  
Hyun Jung Lee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Reactive Oxygen ◽  
Heat Shock Protein 90 ◽  
Oxygen Species

scholarly journals NTRC and Chloroplast-Generated Reactive Oxygen Species Regulate Pseudomonas syringae pv. tomato Disease Development in Tomato and Arabidopsis

2012 ◽  
Vol 25 (3) ◽  
pp. 294-306 ◽  
Author(s):  
Yasuhiro Ishiga ◽  
Takako Ishiga ◽  
Tamding Wangdi ◽  
Kirankumar S. Mysore ◽  
Srinivasa Rao Uppalapati
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Function Analysis ◽  
Virulent Strain ◽  
Reactive Oxygen ◽  
Forward Genetics ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Oxygen Species

Coronatine (COR)-producing pathovars of Pseudomonas syringae, including pvs. tomato, maculicola, and glycinea, cause important diseases on tomato, crucifers, and soybean, respectively, and produce symptoms with necrotic lesions surrounded by chlorosis. The chlorosis is mainly attributed to COR. However, the significance of COR-induced chlorosis in localized lesion development and the molecular basis of disease-associated cell death is largely unknown. To identify host (chloroplast) genes that play a role in COR-mediated chlorosis, we used a forward genetics approach using Nicotiana benthamiana and virus-induced gene silencing and identified a gene which encodes 2-Cys peroxiredoxin (Prxs) that, when silenced, produced a spreading hypersensitive or necrosis-like phenotype instead of chlorosis after COR application in a COI1-dependent manner. Loss-of-function analysis of Prx and NADPH-dependent thioredoxin reductase C (NTRC), the central players of a chloroplast redox detoxification system, resulted in spreading accelerated P. syringae pv. tomato DC3000 disease-associated cell death with enhanced reactive oxygen species (ROS) accumulation in a COR-dependent manner in tomato and Arabidopsis. Consistent with these results, virulent strain DC3000 suppressed the expression of Prx and NTRC in Arabidopsis and tomato during pathogenesis. However, interestingly, authentic COR suppressed the expression of Prx and NTRC in tomato but not in Arabidopsis, suggesting that COR in conjunction with other effectors may modulate ROS and cell death in different host species. Taken together, these results indicated that NTRC or Prx function as a negative regulator of pathogen-induced cell death in the healthy tissues that surround the lesions, and COR-induced chloroplast-localized ROS play a role in enhancing the disease-associated cell death.

scholarly journals Shikonin Induced Program Cell Death through Generation of Reactive Oxygen Species in Renal Cancer Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1831
Author(s):  
Ming-Feng Tsai ◽  
Shih-Ming Chen ◽  
Ann-Zhi Ong ◽  
Yi-Hsuan Chung ◽  
Pei-Ni Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Proliferation ◽  
Cell Death ◽  
Cell Viability ◽  
Renal Cancer ◽  
Reactive Oxygen ◽  
Treated Group ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Acridine Orange Staining

Shikonin mitigated tumor cell proliferation by elevating reactive oxygen species (ROS) levels. Herein, we investigated the effects of shikonin on renal cancer cell (RCC) cell proliferation. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that shikonin dose-dependently reduced the proliferation of Caki-1 and ACHN cells. Shikonin remarkably triggered necrosis and apoptosis in Caki-1 and ACHN cells in proportion to its concentration. Moreover, necrostatin-1 recovered cell viability in the presence of shikonin. Elevated ROS levels and mitochondrial dysfunction were also found in shikonin treatment groups. Pretreatment with N-acetyl cysteine remarkably mitigated shikonin-induced cell death and ROS generation. Western blot analysis revealed that shikonin reduced pro-PARP, pro-caspase-3, and Bcl-2 expression and increased cleavage PARP expression. Enhanced autophagy was also found in the shikonin-treated group as evidenced by acridine orange staining. Moreover, light chain 3B (LC3B)-II accumulation and enhanced p62 expression indicated that autophagy occurred in the shikonin-treated group. LC3B knockdown considerably recovered cell viability in the presence of shikonin. Shikonin treatment elevated p38 activity in a dose-dependent manner. In conclusion, our results revealed that shikonin triggered programmed cell death via the elevation of ROS level and p38 activity in different types of RCC cells. These findings suggested that shikonin may be a potential anti-RCC agent.

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