Phytoglobins regulate nitric oxide-dependent abscisic acid synthesis and ethylene-induced program cell death in developing maize somatic embryos

Planta ◽  
2018 ◽  
Vol 247 (6) ◽  
pp. 1277-1291 ◽  
Author(s):  
Karuna Kapoor ◽  
Mohamed M. Mira ◽  
Belay T. Ayele ◽  
Tran-Nguyen Nguyen ◽  
Robert D. Hill ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Abscisic Acid ◽  
Somatic Embryos ◽  
Acid Synthesis ◽  
Program Cell Death

Interaction between reactive oxygen species and nitric oxide in drought-induced abscisic acid synthesis in root tips of wheat seedlings

2001 ◽  
Vol 28 (10) ◽  
pp. 1055 ◽  
Author(s):  
Zhiguang Zhao ◽  
Guocang Chen ◽  
Chenglie Zhang
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Abscisic Acid ◽  
Reactive Oxygen ◽  
Acid Synthesis ◽  
Oxygen Species ◽  
Root Tips ◽  
Wheat Seedlings ◽  
Acid Accumulation ◽  
Oxide Synthase

Abscisic acid accumulation and oxidative stress are two common responses of plants to environmental stresses. However, little is known about their relationships. The purpose of this article is to investigate the effects of reactive oxygen species and nitric oxide on the plant hormone abscisic acid synthesis in root tips of wheat (Triticum aestivum L.) seedlings under drought stress. Detached root tips were subjected to drought stress by naturally evaporating until 20% of their fresh weights were lost. The activities of superoxide synthases and nitric oxide synthase (EC 1.14.13.39) increased after 20 min of treatment and abscisic acid began to accumulate 60 min later. The induction of abscisic acid by drought was strongly blocked by pretreating the root tips with reactive oxygen species eliminators tiron or ascorbate acid, and with nitric oxide synthase inhibitor Nω-nitro-L-arginine or nitric oxide eliminator 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide. Consistent with these results, reactive oxygen species generators diethyldithiocarbamic acid, xanthine–xanthine oxidase and triazole or nitric oxide donor sodium nitroprusside can also induce abscisic acid accumulation in root tips of wheat seedlings. While potentiated by reactive oxygen species, the effect of sodium nitroprusside on abscisic acid accumulation was blocked by 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide. Based on these results, we suggest that reactive oxygen species and nitric oxide play important roles in drought-induced abscisic acid synthesis in plant, they may be the signals through which the plant can ‘sense’ the drought condition.

Apoptotic cell death triggered by nitric oxide in pancreatic beta-cells

Diabetes ◽  
1995 ◽  
Vol 44 (7) ◽  
pp. 733-738 ◽  
Author(s):  
H. Kaneto ◽  
J. Fujii ◽  
H. G. Seo ◽  
K. Suzuki ◽  
T. Matsuoka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Effects of Exogenous Abscisic Acid,Nitric Oxide and Hydrogen Peroxide on Stomatal Movement in Petals and Leaves ofZephyranthes candida

2013 ◽  
Vol 31 (3) ◽  
pp. 278
Author(s):  
Wen-Qi XIE ◽  
Jin-Ping ZHANG ◽  
Jian-Yi TAN ◽  
Xiao-Li XUAN ◽  
Yong-Fei WANG ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Abscisic Acid ◽  
Stomatal Movement

Nitric Oxide Exposure of CC531 Rat Colon Carcinoma Cells Induces γ-glutamyltransferase which May Counteract Glutathione Depletion and Cell Death

2003 ◽  
Vol 37 (1) ◽  
pp. 99-107 ◽  
Author(s):  
Nils-Erik Huseby ◽  
Nana Asare ◽  
Silje Wetting ◽  
Idun Merete Mikkelsen ◽  
Bente Mortensen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Colon Carcinoma ◽  
Carcinoma Cells ◽  
Glutathione Depletion ◽  
Rat Colon ◽  
Colon Carcinoma Cells

scholarly journals Cold Atmospheric Pressure Plasma-Activated Medium Induces Selective Cell Death in Human Hepatocellular Carcinoma Cells Independently of Singlet Oxygen, Hydrogen Peroxide, Nitric Oxide and Nitrite/Nitrate

2021 ◽  
Vol 22 (11) ◽  
pp. 5548
Author(s):  
Yan Li ◽  
Tianyu Tang ◽  
Haejune Lee ◽  
Kiwon Song
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Singlet Oxygen ◽  
Atmospheric Pressure ◽  
Atmospheric Pressure Plasma ◽  
Proliferative Effect ◽  
Huh7 Cells ◽  
Anti Cancer ◽  
Cold Atmospheric Pressure Plasma ◽  
Nitrite Nitrate

Cold atmospheric pressure plasma (CAP) and plasma-activated medium (PAM) induce cell death in diverse cancer cells and may function as powerful anti-cancer agents. The main components responsible for the selective anti-cancer effects of CAP and PAM remain elusive. CAP or PAM induces selective cell death in hepatocellular carcinoma cell lines Hep3B and Huh7 containing populations with cancer stem cell markers. Here, we investigated the major component(s) of CAP and PAM for mediating the selective anti-proliferative effect on Hep3B and Huh7 cells. The anti-proliferative effect of CAP was mediated through the medium; however, the reactive oxygen species scavenger N-acetyl cysteine did not suppress PAM-induced cell death. Neither high concentrations of nitrite or nitrite/nitrate nor a low concentration of H2O2 present in the PAM containing sodium pyruvate affected the viability of Hep3B and Huh7 cells. Inhibitors of singlet oxygen, superoxide anions, and nitric oxide retained the capacity of PAM to induce anti-cancer effects. The anti-cancer effect was largely blocked in the PAM prepared by placing an aluminum metal mesh, but not a dielectric PVC mesh, between the plasma source and the medium. Hence, singlet oxygen, hydrogen peroxide, nitric oxide, and nitrite/nitrate are not the main factors responsible for PAM-mediated selective death in Hep3B and Huh7 cells. Other factors, such as charged particles including various ions in CAP and PAM, may induce selective anti-cancer effects in certain cancer cells.

An Insight into the Role of Apoptosis and Autophagy in Nitric Oxide–Induced Articular Chondrocyte Cell Death

Cartilage ◽  
2020 ◽  
pp. 194760352097676
Author(s):  
Ekkapol Akaraphutiporn ◽  
Takafumi Sunaga ◽  
Eugene C. Bwalya ◽  
Wang Yanlin ◽  
Mwale Carol ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Western Blot ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Interleukin 1 ◽  
Chondrocyte Apoptosis ◽  
Protective Mechanism ◽  
Autophagic Flux ◽  
Qpcr Analysis

Objective To investigate the role and characterize the molecular mechanisms regulating apoptosis and autophagy in nitric oxide (NO)–induced chondrocyte cell death. Design Cell apoptosis and autophagy were evaluated in chondrocytes treated with sodium nitroprusside (SNP) combined with the presence or absence of interleukin-1 beta (IL-1β) and nutrient-deprived conditions. The concentration of nitrite was determined by Griess reaction. Activation of apoptosis and autophagy were determined by immunocytochemistry, Western blot, and quantitative real-time polymerase chain reaction (qPCR) analysis. Flow cytometry and MTT assay were used to assess cell viability. Results Cotreatment of chondrocytes with SNP and IL-1β under nutrient-deprived condition potentially enhanced the effect of NO-induced cell death. Immunocytochemistry, Western blot, and qPCR analysis indicated that treatment of chondrocytes with SNP significantly reduced autophagic activity, autophagic flux, and multiple autophagy-related (Atg) genes expression. These findings were associated with an increase in ERK, Akt, and mTOR phosphorylation, whereas autophagy induction through mTOR/p70S6K inhibition by rapamycin significantly suppressed NO-induced cell apoptosis. Furthermore, the cleavage of poly(ADP-ribose) polymerase (PARP) and caspase-3 activation in response to apoptosis was weakly detected. These results corresponded with a significant increase in apoptosis-inducing factor (AIF) expression, suggesting the involvement of the caspase-independent pathway. Conclusions These results demonstrate that in chondrocyte cultures with cells induced into an osteoarthritis state, NO inhibits autophagy and induces chondrocyte apoptosis mainly, but not completely through the caspase-independent pathway. Our data suggest that autophagy is a protective mechanism in the pathogenesis of osteoarthritis and could be proposed as a therapeutic target for degenerative joint diseases.

scholarly journals Nitric Oxide-induced Activation of the Type 1 Ryanodine Receptor Is Critical for Epileptic Seizure-induced Neuronal Cell Death

EBioMedicine ◽  
2016 ◽  
Vol 11 ◽  
pp. 253-261 ◽  
Author(s):  
Yoshinori Mikami ◽  
Kazunori Kanemaru ◽  
Yohei Okubo ◽  
Takuya Nakaune ◽  
Junji Suzuki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Ryanodine Receptor ◽  
Epileptic Seizure ◽  
Neuronal Cell Death ◽  
Neuronal Cell
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