Involvement of Protein Phosphorylation and Reactive Oxygen Species in Jasmonate-elicited Accumulation of Defense/stress-related Proteins in Rice Seedlings

2003 ◽  
Vol 3 (11) ◽  
pp. 994-1009 ◽  
Author(s):  
Randeep Rakwal . ◽  
Md. Monowar Karim Kh . ◽  
Setsuko Komatsu .
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Phosphorylation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rice Seedlings ◽  
Related Proteins

scholarly journals SIRT1/SIRT3 Modulates Redox Homeostasis during Ischemia/Reperfusion in the Aging Heart

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 858
Author(s):  
Jingwen Zhang ◽  
Di Ren ◽  
Julia Fedorova ◽  
Zhibin He ◽  
Ji Li
Keyword(s):  
Reactive Oxygen Species ◽  
Ischemia Reperfusion ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Primary Source ◽  
Cardiac Metabolism ◽  
Oxygen Species ◽  
Age Related ◽  
Ros Formation ◽  
Related Proteins

Ischemia/reperfusion (I/R) injury is the central cause of global death in cardiovascular diseases, which is characterized by disorders such as angina, stroke, and peripheral vascular disease, finally causing severe debilitating diseases and death. The increased rates of morbidity and mortality caused by I/R are parallel with aging. Aging-associated cardiac physiological structural and functional deterioration were found to contribute to abnormal reactive oxygen species (ROS) production during I/R stress. Disturbed redox homeostasis could further trigger the related signaling pathways that lead to cardiac irreversible damages with mitochondria dysfunction and cell death. It is notable that sirtuin proteins are impaired in aged hearts and are critical to maintaining redox homeostasis via regulating substrate metabolism and inflammation and thus preserving cardiac function under stress. This review discussed the cellular and functional alterations upon I/R especially in aging hearts. We propose that mitochondria are the primary source of reactive oxygen species (ROS) that contribute to I/R injury in aged hearts. Then, we highlight the cardiomyocyte protection of the age-related proteins Sirtuin1 (SIRT1) and Sirtuin1 (SIRT3) in response to I/R injury, and we discuss their modulation of cardiac metabolism and the inflammatory reaction that is involved in ROS formation.

Proteomic analysis of reactive oxygen species (ROS)-related proteins in rice roots

2007 ◽  
Vol 27 (2) ◽  
pp. 363-375 ◽  
Author(s):  
Sang Gon Kim ◽  
Sun Tae Kim ◽  
Sun Young Kang ◽  
Yiming Wang ◽  
Wook Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Proteomic Analysis ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rice Roots ◽  
Related Proteins

scholarly journals Pardaxin Activates Excessive Mitophagy and Mitochondria-Mediated Apoptosis in Human Ovarian Cancer by Inducing Reactive Oxygen Species

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1883
Author(s):  
Yen-Po Chen ◽  
Po-Chang Shih ◽  
Chien-Wei Feng ◽  
Chang-Cheng Wu ◽  
Kuan-Hao Tsui ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ovarian Cancer ◽  
Reactive Oxygen ◽  
New Drugs ◽  
Oxygen Species ◽  
Preclinical Development ◽  
Skov3 Cells ◽  
Ic50 Values ◽  
Induced Apoptosis ◽  
Related Proteins

Most ovarian cancer (OC) patients are diagnosed with stage III or higher disease, resulting in a poor prognosis. Currently, paclitaxel combined with carboplatin shows the best treatment outcome for OC. However, no effective drug is available for patients that do not respond to treatment; thus, new drugs for OC are needed. We evaluated the antimicrobial peptide, pardaxin, in PA-1 and SKOV3 cells. Pardaxin induced apoptosis as determined by MTT and TUNEL assays, as well as activation of caspases-9/3, Bid, t-Bid, and Bax, whereas Bcl-2 was downregulated. The IC50 values for pardaxin were 4.6–3.0 μM at 24 and 48 h. Mitochondrial and intracellular reactive oxygen species (ROS) were overproduced and associated with disrupted mitochondrial membrane potential and respiratory capacity. Additionally, the mitochondrial network was fragmented with downregulated fusogenic proteins, MFN1/2 and L-/S-OPA1, and upregulated fission-related proteins, DRP1 and FIS1. Autophagy was also activated as evidenced by increased expression of autophagosome formation-related proteins, Beclin, p62, and LC3. Enhanced mitochondrial fragmentation and autophagy indicate that mitophagy was activated. ROS-induced cytotoxicity was reversed by the addition of N-acetylcysteine, confirming ROS overproduction as a contributor. Taken together, pardaxin demonstrated promising anticancer activity in OC cells, which warrants further preclinical development of this compound.

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