Cadmium stress-induced oxidative stress and role of nitric oxide in rice (Oryza sativa L.)

2011 ◽  
Vol 33 (5) ◽  
pp. 1737-1747 ◽  
Author(s):  
Piyalee Panda ◽  
Shwetosmita Nath ◽  
Th. Thorny Chanu ◽  
Gauri Dutta Sharma ◽  
Sanjib Kumar Panda
Agronomy ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1014 ◽  
Author(s):  
Ernestina Solórzano ◽  
Francisco J. Corpas ◽  
Salvador González-Gordo ◽  
José M. Palma

Arsenic (As) is a highly toxic metalloid for all forms of life including plants. Rice is the main food source for different countries worldwide, although it can take up high amounts of As in comparison with other crops, showing toxic profiles such as decreases in plant growth and yield. The induction of oxidative stress is the main process underlying arsenic toxicity in plants, including rice, due to an alteration of the reactive oxygen species (ROS) metabolism. The aim of this work was to gain better knowledge on how the ROS metabolism and its interaction with nitric oxide (NO) operate under As stress conditions in rice plants. Thus, physiological and ROS-related biochemical parameters in roots and shoots from rice (Oryza sativa L.) were studied under 50 μM arsenate (AsV) stress, and the involvement of the main antioxidative systems and NO in the response of plants to those conditions was investigated. A decrease of 51% in root length and 27% in plant biomass was observed with 50 μM AsV treatment, as compared to control plants. The results of the activity of superoxide dismutase (SOD) isozymes, catalase, peroxidase (POD: total and isoenzymatic), and the enzymes of the ascorbate–glutathione cycle, besides the ascorbate and glutathione contents, showed that As accumulation provoked an overall significant increase of most of them, but with different profiles depending on the plant organ, either root or shoot. Among the seven identified POD isozymes, the induction of the POD-3 in shoots under As stress could help to maintain the hydrogen peroxide (H2O2) redox homeostasis and compensate the loss of the ascorbate peroxidase (APX) activity in both roots and shoots. Lipid peroxidation was slightly increased in roots and shoots from As-treated plants. The H2O2 and NO contents were enhanced in roots and shoots against arsenic stress. In spite of the increase of most antioxidative systems, a mild oxidative stress situation appears to be consolidated overall, since the growth parameters and those from the oxidative damage could not be totally counteracted. In these conditions, the higher levels of H2O2 and NO suggest that signaling events are simultaneously occurring in the whole plant.


2019 ◽  
Vol 41 (5) ◽  
Author(s):  
Md. Tahjib-Ul-Arif ◽  
Sonya Afrin ◽  
Mohammed Arif Sadik Polash ◽  
Tahmina Akter ◽  
Shuma Rani Ray ◽  
...  

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 305
Author(s):  
Harsha Gautam ◽  
Zebus Sehar ◽  
Md Tabish Rehman ◽  
Afzal Hussain ◽  
Mohamed F. AlAjmi ◽  
...  

The effects of nitric oxide (NO) as 100 µM sodium nitroprusside (SNP, NO donor) on photosynthetic-nitrogen use efficiency (NUE), photosynthetic-sulfur use efficiency (SUE), photosynthesis, growth and agronomic traits of rice (Oryza sativa L.) cultivars, Taipie-309 (high photosynthetic-N and SUE) and Rasi (low photosynthetic-N and SUE) were investigated under high temperature stress (40 °C for 6 h). Plants exposed to high temperature stress caused significant reduction in photosynthetic activity, use efficiency of N and S, and increment in H2O2 and thiobarbituric acid reactive substance (TBARS) content. The drastic effects of high temperature stress were more pronounced in cultivar Rasi than Taipie-309. However, foliar spray of SNP decreased the high temperature induced H2O2 and TBARS content and increased accumulation of proline and activity of ascorbate–glutathione cycle that collectively improved tolerance to high temperature stress more effectively in Taipie-309. Exogenously applied SNP alleviated the high temperature induced decrease in photosynthesis through maintaining higher photosynthetic-NUE and photosynthetic-SUE, activity of ribulose 1,5 bisphosphate carboxylase/oxygenase (Rubisco), and synthesis of reduced glutathione (GSH). The use of 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxy-3-oxide (cPTIO, NO scavenger) substantiated the study that in the absence of NO oxidative stress increased, while NO increased photosynthetic-NUE and photosynthetic-SUE, net photosynthesis and plant dry mass. Taken together, the present investigation reveals that NO increased heat stress tolerance and minimized high temperature stress adversaries more effectively in cultivar Taipie-309 than Rasi by enhancing photosynthetic-NUE and SUE and strengthening the antioxidant defense system.


2010 ◽  
Vol 63 (11-12) ◽  
pp. 827-832 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic ◽  
Rada Jesic-Vukicevic

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.


1997 ◽  
Vol 19 (9-10) ◽  
pp. 599-605 ◽  
Author(s):  
H. Farghali ◽  
S. Hynie ◽  
Z. Vohnikova ◽  
K. Masek

Sign in / Sign up

Export Citation Format

Share Document