Reactive Oxygen and Nitrogen Species: Oxidative Damage and Antioxidative Defense Mechanism in Plants under Abiotic Stress

2021 ◽  
pp. 71-99
Author(s):  
Amrina Shafi ◽  
Farhana Hassan ◽  
Firdous A. Khanday
2012 ◽  
Vol 2012 ◽  
pp. 1-26 ◽  
Author(s):  
Pallavi Sharma ◽  
Ambuj Bhushan Jha ◽  
Rama Shanker Dubey ◽  
Mohammad Pessarakli

Reactive oxygen species (ROS) are produced as a normal product of plant cellular metabolism. Various environmental stresses lead to excessive production of ROS causing progressive oxidative damage and ultimately cell death. Despite their destructive activity, they are well-described second messengers in a variety of cellular processes, including conferment of tolerance to various environmental stresses. Whether ROS would serve as signaling molecules or could cause oxidative damage to the tissues depends on the delicate equilibrium between ROS production, and their scavenging. Efficient scavenging of ROS produced during various environmental stresses requires the action of several nonenzymatic as well as enzymatic antioxidants present in the tissues. In this paper, we describe the generation, sites of production and role of ROS as messenger molecules as well as inducers of oxidative damage. Further, the antioxidative defense mechanisms operating in the cells for scavenging of ROS overproduced under various stressful conditions of the environment have been discussed in detail.


2014 ◽  
Vol 64 ◽  
pp. 618-625 ◽  
Author(s):  
Lilian R.B. Mariutti ◽  
Eliseu Rodrigues ◽  
Renan C. Chisté ◽  
Eduarda Fernandes ◽  
Adriana Z. Mercadante

2015 ◽  
Vol 67 (5) ◽  
pp. 1259-1274 ◽  
Author(s):  
Panagiota Filippou ◽  
Chrystalla Antoniou ◽  
Toshihiro Obata ◽  
Katrien Van Der Kelen ◽  
Vaggelis Harokopos ◽  
...  

2012 ◽  
Vol 214 (1) ◽  
pp. 11-20 ◽  
Author(s):  
P Newsholme ◽  
E Rebelato ◽  
F Abdulkader ◽  
M Krause ◽  
A Carpinelli ◽  
...  

Growing evidence indicates that the regulation of intracellular reactive oxygen species (ROS) and reactive nitrogen species (RNS) levels is essential for maintaining normal β-cell glucose responsiveness. While long-term exposure to high glucose induces oxidative stress in β cells, conflicting results have been published regarding the impact of ROS on acute glucose exposure and their role in glucose stimulated insulin secretion (GSIS). Although β cells are considered to be particularly vulnerable to oxidative damage, as they express relatively low levels of some peroxide-metabolizing enzymes such as catalase and glutathione (GSH) peroxidase, other less known GSH-based antioxidant systems are expressed in β cells at higher levels. Herein, we discuss the key mechanisms of ROS/RNS production and their physiological function in pancreatic β cells. We also hypothesize that specific interactions between RNS and ROS may be the cause of the vulnerability of pancreatic β cells to oxidative damage. In addition, using a hypothetical metabolic model based on the data available in the literature, we emphasize the importance of amino acid availability for GSH synthesis and for the maintenance of β-cell function and viability during periods of metabolic disturbance before the clinical onset of diabetes.


2008 ◽  
Vol 120 (41) ◽  
pp. 8014-8018 ◽  
Author(s):  
Adi Haber ◽  
Atif Mahammed ◽  
Bianca Fuhrman ◽  
Nina Volkova ◽  
Raymond Coleman ◽  
...  

2020 ◽  
Vol 60 (1) ◽  
pp. 010504
Author(s):  
Keisuke Takashima ◽  
Ahmad Shahir bin Ahmad Nor ◽  
Sugihiro Ando ◽  
Hideki Takahashi ◽  
Toshiro Kaneko

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.


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