The role of oxidative stress in determining the level of viability of black poplar (Populus nigra) seeds stored at different temperatures

2015 ◽  
Vol 42 (7) ◽  
pp. 630 ◽  
Author(s):  
Ewa Marzena Kalemba ◽  
Jan Suszka ◽  
Ewelina Ratajczak

Black poplar (Populus nigra L.) is one of the most threatened tree species in Europe since up to 99% of its natural habitat has disappeared. Black poplar seeds are characterised by short longevity. It was recently demonstrated that black poplar seeds can be successfully stored at −10°C, −20°C and −196°C for at least 2 years but not at higher temperatures. In the present study, the role of oxidative stress in determining the level of viability of black poplar seeds stored at −196°C, −20°C, −10°C, −3°C and 3°C for 3 months, 1 year and 2 years was monitored. The superoxide anion radicals (O2–•) and hydrogen peroxide (H2O2) increased during storage and had an impact on membrane integrity as determined by changes in the content of fatty acids and phospholipids and increases in electrolyte leakage. The level of non-enzymatic and enzymatic components of the ascorbate-glutathione (AsA-GSH) cycle was also investigated. The level of O2–• was strongly correlated with the level of seed germination after 1 and 2 years of storage. This was accompanied by changes in the redox potential, as well as changes in the content of linoleic acid and phosphatydiloglycerol over the same period of time. In particular, the deleterious effect of H2O2 was observed after 2 years of storage when its accumulation was highly correlated with changes in the composition of fatty acids and phospholipids. Despite increased activity of AsA-GSH cycle enzymes, the level of reducing agents was insufficient and seeds exhibited large increases in the redox potential when stored at −3°C and still higher when stored at 3°C. Overall, the results of the study demonstrate that oxidative stress increases during seed storage, especially at the warmer temperatures and injures seed tissues; resulting in a loss of viability.

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1991
Author(s):  
Janine Mett

Alzheimer’s disease (AD), the most common cause of dementia in the elderly population, is closely linked to a dysregulated cerebral lipid homeostasis and particular changes in brain fatty acid (FA) composition. The abnormal extracellular accumulation and deposition of the peptide amyloid-β (Aβ) is considered as an early toxic event in AD pathogenesis, which initiates a series of events leading to neuronal dysfunction and death. These include the induction of neuroinflammation and oxidative stress, the disruption of calcium homeostasis and membrane integrity, an impairment of cerebral energy metabolism, as well as synaptic and mitochondrial dysfunction. Dietary medium chain fatty acids (MCFAs) and polyunsaturated ω-3-fatty acids (ω-3-PUFAs) seem to be valuable for disease modification. Both classes of FAs have neuronal health-promoting and cognition-enhancing properties and might be of benefit for patients suffering from mild cognitive impairment (MCI) and AD. This review summarizes the current knowledge about the molecular mechanisms by which MCFAs and ω-3-PUFAs reduce the cerebral Aβ deposition, improve brain energy metabolism, and lessen oxidative stress levels.


2006 ◽  
Vol 64 (10) ◽  
pp. 31-39 ◽  
Author(s):  
José L. Quiles ◽  
Gustavo Barja ◽  
Maurizio Battino ◽  
José Mataix ◽  
Vincenzo Solfrizzi

Nutrients ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 895 ◽  
Author(s):  
Michela Zanetti ◽  
Gianluca Gortan Cappellari ◽  
Davide Barbetta ◽  
Annamaria Semolic ◽  
Rocco Barazzoni

2012 ◽  
Vol 56 ◽  
pp. S234
Author(s):  
V. Raparelli ◽  
L. Napoleone ◽  
O. Riggio ◽  
M. Merli ◽  
F. Angelico ◽  
...  

2020 ◽  
Vol 21 (12) ◽  
pp. 4259
Author(s):  
Qinhong Wang ◽  
Rahima Zennadi

Mid-life stage adults are at higher risk of developing venous thrombosis (VT)/thromboembolism (VT/E). Aging is characterized by an overproduction of reactive oxygen species (ROS), which could evoke a series of physiological changes involved in thrombosis. Here, we focus on the critical role of ROS within the red blood cell (RBC) in initiating venous thrombosis during aging. Growing evidence has shifted our interest in the role of unjustifiably unvalued RBCs in blood coagulation. RBCs can be a major source of oxidative stress during aging, since RBC redox homeostasis is generally compromised due to the discrepancy between prooxidants and antioxidants. As a result, ROS accumulate within the RBC due to the constant endogenous hemoglobin (Hb) autoxidation and NADPH oxidase activation, and the uptake of extracellular ROS released by other cells in the circulation. The elevated RBC ROS level affects the RBC membrane structure and function, causing loss of membrane integrity, and decreased deformability. These changes impair RBC function in hemostasis and thrombosis, favoring a hypercoagulable state through enhanced RBC aggregation, RBC binding to endothelial cells affecting nitric oxide availability, RBC-induced platelet activation consequently modulating their activity, RBC interaction with and activation of coagulation factors, increased RBC phosphatidylserine exposure and release of microvesicles, accelerated aging and hemolysis. Thus, RBC oxidative stress during aging typifies an ultimate mechanism in system failure, which can affect major processes involved in the development of venous thrombosis in a variety of ways. The reevaluated concept of the critical role of RBC ROS in the activation of thrombotic events during aging will help identify potential targets for novel strategies to prevent/reduce the risk for VT/E or VT/E recurrences in mid-life stage adults.


Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2579 ◽  
Author(s):  
Bee Ling Tan ◽  
Mohd Esa Norhaizan

Cognitive dysfunction is linked to chronic low-grade inflammatory stress that contributes to cell-mediated immunity in creating an oxidative environment. Food is a vitally important energy source; it affects brain function and provides direct energy. Several studies have indicated that high-fat consumption causes overproduction of circulating free fatty acids and systemic inflammation. Immune cells, free fatty acids, and circulating cytokines reach the hypothalamus and initiate local inflammation through processes such as microglial proliferation. Therefore, the role of high-fat diet (HFD) in promoting oxidative stress and neurodegeneration is worthy of further discussion. Of particular interest in this article, we highlight the associations and molecular mechanisms of HFD in the modulation of inflammation and cognitive deficits. Taken together, a better understanding of the role of oxidative stress in cognitive impairment following HFD consumption would provide a useful approach for the prevention of cognitive dysfunction.


2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Emmanuelle Sagols ◽  
Nathalie Priymenko

In dogs with heart failure, cell oxygenation and cellular metabolism do not work properly, leading to the production of a large amount of free radicals. In the organism, these free radicals are responsible of major cellular damages: this is oxidative stress. However, a suitable food intake plays an important role in limiting this phenomenon: on the one hand, the presence of essential fatty acids in the composition of membranes decreases sensitivity of cells to free radicals and constitutes a first protection against the oxidative stress; on the other hand, coenzyme Q10, vitamin E, and polyphenols are antioxidant molecules which can help cells to neutralize these free radicals.


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