scholarly journals Antioxidant Defence Systems and Oxidative Stress in Poultry Biology: An Update

Antioxidants ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 235 ◽  
Author(s):  
Surai ◽  
Kochish ◽  
Fisinin ◽  
Kidd
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Vitamin E ◽  
Heat Shock ◽  
Redox Balance ◽  
The Body ◽  
Heme Oxygenase 1 ◽  
Antioxidant Defence ◽  
Antioxidant Defences ◽  
And Oxidative Stress

Poultry in commercial settings are exposed to a range of stressors. A growing body of information clearly indicates that excess ROS/RNS production and oxidative stress are major detrimental consequences of the most common commercial stressors in poultry production. During evolution, antioxidant defence systems were developed in poultry to survive in an oxygenated atmosphere. They include a complex network of internally synthesised (e.g., antioxidant enzymes, (glutathione) GSH, (coenzyme Q) CoQ) and externally supplied (vitamin E, carotenoids, etc.) antioxidants. In fact, all antioxidants in the body work cooperatively as a team to maintain optimal redox balance in the cell/body. This balance is a key element in providing the necessary conditions for cell signalling, a vital process for regulation of the expression of various genes, stress adaptation and homeostasis maintenance in the body. Since ROS/RNS are considered to be important signalling molecules, their concentration is strictly regulated by the antioxidant defence network in conjunction with various transcription factors and vitagenes. In fact, activation of vitagenes via such transcription factors as Nrf2 leads to an additional synthesis of an array of protective molecules which can deal with increased ROS/RNS production. Therefore, it is a challenging task to develop a system of optimal antioxidant supplementation to help growing/productive birds maintain effective antioxidant defences and redox balance in the body. On the one hand, antioxidants, such as vitamin E, or minerals (e.g., Se, Mn, Cu and Zn) are a compulsory part of the commercial pre-mixes for poultry, and, in most cases, are adequate to meet the physiological requirements in these elements. On the other hand, due to the aforementioned commercially relevant stressors, there is a need for additional support for the antioxidant system in poultry. This new direction in improving antioxidant defences for poultry in stress conditions is related to an opportunity to activate a range of vitagenes (via Nrf2-related mechanisms: superoxide dismutase, SOD; heme oxygenase-1, HO-1; GSH and thioredoxin, or other mechanisms: Heat shock protein (HSP)/heat shock factor (HSP), sirtuins, etc.) to maximise internal AO protection and redox balance maintenance. Therefore, the development of vitagene-regulating nutritional supplements is on the agenda of many commercial companies worldwide.

scholarly journals An Insight of Vitamin E as Neuroprotective Agents

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Hui-Min Yap ◽  
Kwan-Liang Lye
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Vitamin E ◽  
Neuronal Cell Death ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Neuronal Cell ◽  
Redox Balance ◽  
The Body ◽  
Neuroprotective Effects

Nervous system is the network of nerve cells that transmits nerve impulses throughout the body. It is rich in both unsaturated fats and irons, making it predominantly susceptible to oxidative stress and damage. Oxidative stress reflects the disruption of the redox balance between the formation and clearance of highly free radicals, for instance reactive oxygen species (ROS) and reactive nitrogen species (RNS). Oxidative stress will further damage the cell lipid, protein and DNA. Oxidative stress has a role in the modulation of critical cellular functions, such as apoptosis program activation, ion transport and calcium mobilization which lead to cell death. Many studies were conducted to prevent neuronal cell death caused by oxidative stress through administration of free radical scavenging antioxidant, such as vitamin E. Vitamin E is known as a chain-breaking antioxidant that showed the capability to increase the viability of neuronal cells that had undergone glutamate injury by inhibiting glutamate-induced pp60 (c-Src) kinase activation. Vitamin E occurs in 8 forms, namely ?-, ?-, ?- and ?-tocopherols and ?-, ?-, ?-and ?-tocotrienols. Tocotrienols differ from tocopherols by possessing an unsaturated isoprenoid side chain instead of a saturated phytyl tail. Tocotrienols, compared to tocopherols, are lightly studied due to the abundance of ?-tocopherol in the human body and its antioxidant properties. Nevertheless, recent studies showed that ?-tocotrienol is more effective in preventing lipid peroxidation compared to ?-tocopherol. Furthermore, tocotrienol was discovered to protect neuronal cell through antioxidant-independent activities. The tocotrienol-rich fraction (TRF) is an extract that consists of 75% tocotrienol and 25% ?-tocopherol. TRF was reported to possess potent antioxidant, anti-inflammation, anticancer and cholesterol-lowering properties. Thus, this writing highlights the significant neuroprotective effects of tocotrienol and tocopherol.

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers

2019 ◽  
Vol 22 (7) ◽  
pp. 496-501
Author(s):  
Fatemeh Ahmadi-Motamayel ◽  
Parisa Falsafi ◽  
Hamidreza Abolsamadi ◽  
Mohammad T. Goodarzi ◽  
Jalal Poorolajal
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cigarette Smoke ◽  
Total Antioxidant Capacity ◽  
The Body ◽  
Total Antioxidant ◽  
The Mean ◽  
And Oxidative Stress

Background: Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. Objective: The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Methods: Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. Results: The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Conclusion: Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Lux-biosensors for detection of SOS-response, heat shock, and oxidative stress

2010 ◽  
Vol 46 (8) ◽  
pp. 781-788 ◽  
Author(s):  
V. Yu. Kotova ◽  
I. V. Manukhov ◽  
G. B. Zavilgelskii
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Sos Response ◽  
Lux Biosensors ◽  
And Oxidative Stress

Relationship between atherogenic index and oxidative stress among patients presented with coronary artery disease in a tertiary care hospital

2020 ◽  
Vol 11 (SPL4) ◽  
pp. 2807-2813
Author(s):  
Resmi C R ◽  
Kedari G S R ◽  
Deepa P K
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Vitamin C ◽  
Density Lipoprotein ◽  
Atherogenic Index ◽  
Enzymatic Antioxidants ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Lipid Parameters ◽  
And Oxidative Stress

CAD is recognized as a multifactorial disease that is influenced by environmental and genetic factors. This study aimed to evaluate the levels of lipid parameters, oxidative stress and antioxidant markers in subjects with CAD compared to their age & sex matched controls and to analyze the relationship between atherogenic Index and oxidative stress among them 62 clinically proved CAD patients and 62 healthy age and sex matched subjects without CAD were selected for this study. 5 ml of fasting venous blood was collected from all the subjects and investigations such as FPG, lipid profile, oxidative markers Malondialdehyde (MDA), F2 isoprostanes (F2iso) and antioxidants glutathione S-transferase (GST), superoxide dismutase (SOD), vitamin-C, vitamin-E were performed. This study showed that levels of lipid parameters total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-c) and AI were significantly higher whereas high density lipoprotein cholesterol (HDL-c) were significantly low in CAD patients compared to normal controls. Oxidative stress markers MDA and F2 Isoprostanes level were significantly high, whereas enzymatic antioxidants GST and SOD and non-enzymatic antioxidants Vitamin-C and Vitamin-E levels were significantly low in CAD patients. Oxidative stress markers were found to significantly influence the AI. Results of this study showed that oxidative stress markers F2iso and MDA and antioxidants GST, VIT-C and VIT-E are found to influence the atherogenic index significantly.

Daphnetin Ameliorates Corticosterone-Induced Depressive-Like Behavior and Oxidative Stress in Mice Via Nuclear Factor Erythroid 2-Related Factor/Heme Oxygenase-1 Pathway

2021 ◽  
Vol 19 (4) ◽  
pp. 470-476
Author(s):  
Chao Liu ◽  
Chao Liang ◽  
Jie Huang
Keyword(s):  
Oxidative Stress ◽  
Consumption Rate ◽  
Tail Suspension Test ◽  
Protein Carbonyl ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Sucrose Consumption ◽  
Markers Of Oxidative Stress ◽  
Swimming Test ◽  
And Oxidative Stress

We have investigated the effect of daphnetin on depressive-like behavior and oxidative stress caused by corticosterone in mice. To this end, we have analyzed the effect of corticosterone alone and combination of corticosterone and daphnetin on three behavioral indices of depressive-like behavior - sucrose consumption rate, forced swimming test, and tail suspension test as well as biochemical markers of oxidative stress - malondialdehyde, nitrite, protein carbonyl, nonprotein sulfhydryl and glutathione contents as well as hippocampal cell apoptosis. The results support the conclusion that daphnetin diminished corticosterone induced depressive like behavior and oxidative stress by activating Nrf2/HO-1 pathway.

scholarly journals Kaempferol and Kaempferide Attenuate Oleic Acid-Induced Lipid Accumulation and Oxidative Stress in HepG2 Cells

2021 ◽  
Vol 22 (16) ◽  
pp. 8847
Author(s):  
Fangfang Tie ◽  
Jin Ding ◽  
Na Hu ◽  
Qi Dong ◽  
Zhi Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Lipid Metabolism ◽  
Western Blot ◽  
Blot Analysis ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Western Blot Analysis ◽  
Heme Oxygenase 1 ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases which lacks ideal treatment options. Kaempferol and kaempferide, two natural flavonol compounds isolated from Hippophae rhamnoides L., were reported to exhibit a strong regulatory effect on lipid metabolism, for which the mechanism is largely unknown. In the present study, we investigated the effects of kaempferol and kaempferide on oleic acid (OA)-treated HepG2 cells, a widely used in vitro model of NAFLD. The results indicated an increased accumulation of lipid droplets and triacylglycerol (TG) by OA, which was attenuated by kaempferol and kaempferide (5, 10 and 20 μM). Western blot analysis demonstrated that kaempferol and kaempferide reduced expression of lipogenesis-related proteins, including sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1). Expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer binding proteins β (C/EBPβ), two adipogenic transcription factors, was also decreased by kaempferol and kaempferide treatment. In addition, western blot analysis also demonstrated that kaempferol and kaempferide reduced expression of heme oxygenase-1 (HO-1) and nuclear transcription factor-erythroid 2-related factor 2 (Nrf2). Molecular docking was performed to identify the direct molecular targets of kaempferol and kaempferide, and their binding to SCD-1, a critical regulator in lipid metabolism, was revealed. Taken together, our findings demonstrate that kaempferol and kaempferide could attenuate OA-induced lipid accumulation and oxidative stress in HepG2 cells, which might benefit the treatment of NAFLD.

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