scholarly journals Antioxidative defense mechanisms in the aging brain

2014 ◽  
Vol 66 (1) ◽  
pp. 245-252 ◽  
Author(s):  
Zorica Jovanovic
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Current Knowledge ◽  
Aging Brain ◽  
Antioxidative Defense ◽  
Neuroprotective Effects ◽  
Age Related ◽  
Antioxidant Defense Systems ◽  
High Concentrations ◽  
The Brain

Aging is an extremely complex, multifactorial process that is characterized by a gradual and continuous loss of physiological functions and responses, particularly marked in the brain. A common hallmark in aging and age-related diseases is an increase in oxidative stress and the failure of antioxidant defense systems. Current knowledge indicates that the level of glutathione progressively declines during aging. Because nerve cells are the longest-living cells that exhibit a high consumption rate of oxygen throughout an individual?s lifetime, the brain may be especially vulnerable to oxidative damage and this vulnerability increases during aging. In addition, the brain contains high concentrations of polyunsaturated fatty acids and transition metals and low antioxidative defense mechanisms. Although aging is an inevitable event, a growing volume of data confirms that antioxidant supplementation in combination with symptomatic drug treatments reduces oxidative stress and improves cognitive function in aging and age-related diseases. The present review discusses the neuroprotective effects of antioxidants in the aging brain.

Bilirubin and Epigenetic Modifications in Metabolic and Immunometabolic Disorders

2021 ◽  
Vol 21 ◽  
Author(s):  
Mostafa Moradi Sarabi ◽  
Esmaeel Babaeenezhad ◽  
Maral Amini ◽  
Mozhgan Kaviani ◽  
Fakhraddin Naghibalhossaini
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Waste Product ◽  
Epigenetic Modifications ◽  
Mechanisms Of Toxicity ◽  
High Concentrations ◽  
The Brain

: Bilirubin is the main waste product of heme catabolism. At high concentrations, bilirubin may cause toxicity, especially in the brain, kidney, and erythrocytes. Membrane and mitochondrial dysfunction, oxidative stress, apoptosis, necrosis, endoplasmic reticulum stress, excitotoxicity, inflammation, and epigenetic modifications are the main mechanisms of toxicity triggered by bilirubin in susceptible organs. Many studies have shown that there is an interaction between bilirubin and epigenetic modifications in metabolic and immune diseases. In this review, we first outline the toxicity mediated by bilirubin and then summarize the current knowledge linking bilirubin and epigenetic modifications in metabolic and immunometabolic disorders.

Pharmacotherapeutic Potential of Garlic in Age-Related Neurological Disorders

2021 ◽  
Vol 20 ◽  
Author(s):  
Ramin Ahangar-Sirous ◽  
Mohadeseh Poudineh ◽  
Arina Ansari ◽  
Ali Nili ◽  
Seyyed Mohammad Matin Alavi Dana ◽  
...  
Keyword(s):  
Public Health ◽  
Oxidative Stress ◽  
Neurological Disorders ◽  
Allium Sativum ◽  
Aged Garlic Extract ◽  
Neuroprotective Effects ◽  
Age Related ◽  
Pathologic Features ◽  
The Common ◽  
Aged Garlic

: Age-related neurological disorders [ANDs] involve neurodegenerative diseases [NDDs] such as Alzheimer's disease [AD], the most frequent kind of dementia in elderly people, and Parkinson's disease [PD], and also other disorders like epilepsy and migraine. Although ANDs are multifactorial, Aging is a principal risk factor for them. The common and most main pathologic features among ANDs are inflammation, oxidative stress, and misfolded proteins accumulation. Since failing brains caused by ANDs impose a notable burden on public health and their incidence is increasing, a lot of works has been done to overcome them. Garlic, Allium sativum, has been used for different medical purposes globally and more than thousands of publications have reported its health benefits. Garlic and aged garlic extract are considered potent anti-inflammatory and antioxidants agents and can have remarkable neuroprotective effects. This review is aimed to summarize knowledge on the pharmacotherapeutic potential of garlic and its components in ANDs.

scholarly journals The investigation into neurotoxicity mechanisms of Nonylphenol: A narrative review

2020 ◽  
Vol 18 ◽  
Author(s):  
Mandana Lotfi ◽  
Amir Hosseyn Hasanpour ◽  
Ali Akbar Moghadamnia ◽  
Sohrab Kazemi
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Health Hazard ◽  
Learning Disorders ◽  
Inflammatory Factors ◽  
Postnatal Exposure ◽  
Memory And Learning ◽  
Nonylphenol Ethoxylate ◽  
Intracellular Calcium Ion ◽  
The Brain

Background: Nonylphenol (NP), as a chemical compound that widely used in industry, is the result of the nonylphenol ethoxylate decomposition and it is known as an estrogen-like compound. Numerous studies and researches have shown that it has many destructive functions of various organs such as the brain. This toxicant causes oxidative stress in the cortex and hippocampus cells, which are two essential regions to preserve memory and learning in the brain. Methods: This review examines recent findings to better understand the mechanisms of NP neurotoxicity. We used Scopus, Google Scholar and PubMed databases to find articles with focus on the destructive effects of NP on the oxidative stress pathway and its defense mechanisms. Results: NP has potential human health hazard associated with gestational, peri- and postnatal exposure. NP can disrupt brain homeostasis in different ways, such as activation of inflammatory factors in brain especially in hippocampus and cortex, disruption of the cell cycle, changes in neuron, dendrites and synapses morphology, disruption of extra and intracellular calcium ion balance and also memory and learning disorders

scholarly journals The aging mind: neuroplasticity in response to cognitive training

2013 ◽  
Vol 15 (1) ◽  
pp. 109-119 ◽  
Keyword(s):  
Cognitive Function ◽  
Cognitive Training ◽  
Neural Plasticity ◽  
Cognitive Effort ◽  
Aging Brain ◽  
Cognitive Domains ◽  
Training Techniques ◽  
Age Related ◽  
Strategy Change ◽  
The Brain

Is it possible to enhance neural and cognitive function with cognitive training techniques? Can we delay age-related decline in cognitive function with interventions and stave off Alzheimer's disease? Does an aged brain really have the capacity to change in response to stimulation? In the present paper, we consider the neuroplasticity of the aging brain, that is, the brain's ability to increase capacity in response to sustained experience. We argue that, although there is some neural deterioration that occurs with age, the brain has the capacity to increase neural activity and develop neural scaffolding to regulate cognitive function. We suggest that increase in neural volume in response to cognitive training or experience is a clear indicator of change, but that changes in activation in response to cognitive training may be evidence of strategy change rather than indicative of neural plasticity. We note that the effect of cognitive training is surprisingly durable over time, but that the evidence that training effects transfer to other cognitive domains is relatively limited. We review evidence which suggests that engagement in an environment that requires sustained cognitive effort may facilitate cognitive function.

Different Chilling-Induced Symptoms and the Underlying Oxidative Stress and Antioxidative Defense in the Exocarp and Mesocarp of Immature Sponge Gourd (Luffa cylindrica) Fruit

2021 ◽  
Author(s):  
Pichaya Chuenchom ◽  
Sompoch Noichinda ◽  
Kitti Bodhipadma ◽  
Chalermchai Wongs-Aree ◽  
David W. M. Leung
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Considerable Increase ◽  
Chilling Injury ◽  
Oxygen Species ◽  
Antioxidative Defense ◽  
Sponge Gourd ◽  
Lower Temperature ◽  
High Level ◽  
The Relationship

Immature sponge gourd fruit is consumed as a vegetable with a limited shelf life. Although cold storage is a simple and powerful tool for maintaining postharvest fruit quality, storage at a low temperature may not be appropriate for vegetables as some chilling injury (CI) of the immature sponge gourd fruit may occur. Therefore, this research aimed to elucidate the relationship between CI, oxidative stress, and the antioxidative defense mechanisms in the exocarp and mesocarp of immature sponge gourd fruit. After storage at 5°C for 6 days, visual CI symptoms, including browning and surface pitting, were found in the peel (exocarp) but not in the mesocarp. There were, however, more dead cells (stained by Evans blue) in the mesocarp of the fruit stored at 5°C. There was a more considerable increase in the electrolyte leakage rate in both fruit tissues held at 5°C than 25°C. The CI was correlated with malondialdehyde (MDA) levels in the tissues. The MDA of fruit exocarp at 5°C was 1.6 fold higher than that at 25°C on day 6, while the lipoxygenase (LOX) activity in mesocarp was 50% higher in fruit stored at a lower temperature. The action of ascorbate peroxidase (APX) was high in the exocarp of the fruit stored at 5°C, but there appeared to be a continuous depletion of the co-substrate or ascorbic acid. In conclusion, the CI in the exocarp was mainly associated with a high level of reactive oxygen species (ROS). In contrast, the CI in the mesocarp appeared to be primarily associated with increased lipid peroxidation by the elevated LOX activity under cold stress compared to storage at 25°C.

scholarly journals Disparate Central and Peripheral Effects of Circulating IGF-1 Deficiency on Tissue Mitochondrial Function

2019 ◽  
Vol 57 (3) ◽  
pp. 1317-1331 ◽  
Author(s):  
Gavin Pharaoh ◽  
Daniel Owen ◽  
Alexander Yeganeh ◽  
Pavithra Premkumar ◽  
Julie Farley ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Spatial Learning ◽  
Mitochondrial Function ◽  
Coupling Efficiency ◽  
Redox Status ◽  
Cellular Aging ◽  
Age Related ◽  
The Brain ◽  
Circulating Levels

AbstractAge-related decline in circulating levels of insulin-like growth factor (IGF)-1 is associated with reduced cognitive function, neuronal aging, and neurodegeneration. Decreased mitochondrial function along with increased reactive oxygen species (ROS) and accumulation of damaged macromolecules are hallmarks of cellular aging. Based on numerous studies indicating pleiotropic effects of IGF-1 during aging, we compared the central and peripheral effects of circulating IGF-1 deficiency on tissue mitochondrial function using an inducible liver IGF-1 knockout (LID). Circulating levels of IGF-1 (~ 75%) were depleted in adult male Igf1f/f mice via AAV-mediated knockdown of hepatic IGF-1 at 5 months of age. Cognitive function was evaluated at 18 months using the radial arm water maze and glucose and insulin tolerance assessed. Mitochondrial function was analyzed in hippocampus, muscle, and visceral fat tissues using high-resolution respirometry O2K as well as redox status and oxidative stress in the cortex. Peripherally, IGF-1 deficiency did not significantly impact muscle mass or mitochondrial function. Aged LID mice were insulin resistant and exhibited ~ 60% less adipose tissue but increased fat mitochondrial respiration (20%). The effects on fat metabolism were attributed to increases in growth hormone. Centrally, IGF-1 deficiency impaired hippocampal-dependent spatial acquisition as well as reversal learning in male mice. Hippocampal mitochondrial OXPHOS coupling efficiency and cortex ATP levels (~ 50%) were decreased and hippocampal oxidative stress (protein carbonylation and F2-isoprostanes) was increased. These data suggest that IGF-1 is critical for regulating mitochondrial function, redox status, and spatial learning in the central nervous system but has limited impact on peripheral (liver and muscle) metabolism with age. Therefore, IGF-1 deficiency with age may increase sensitivity to damage in the brain and propensity for cognitive deficits. Targeting mitochondrial function in the brain may be an avenue for therapy of age-related impairment of cognitive function. Regulation of mitochondrial function and redox status by IGF-1 is essential to maintain brain function and coordinate hippocampal-dependent spatial learning. While a decline in IGF-1 in the periphery may be beneficial to avert cancer progression, diminished central IGF-1 signaling may mediate, in part, age-related cognitive dysfunction and cognitive pathologies potentially by decreasing mitochondrial function.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

scholarly journals Neuroprotective Effects of Grape Seed Procyanidins on Ethanol-Induced Injury and Oxidative Stress in Rat Hippocampal Neurons

2020 ◽  
Vol 55 (4) ◽  
pp. 357-366
Author(s):  
Wenyang Jin ◽  
Mizhu Sun ◽  
Bingbing Yuan ◽  
Runzhi Wang ◽  
Hongtao Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hippocampal Neurons ◽  
Primary Cultures ◽  
Neuronal Injury ◽  
Grape Seed ◽  
Neuroprotective Effects ◽  
Dendritic Length ◽  
New Type ◽  
The Brain ◽  
And Oxidative Stress

Abstract Aims Ethanol is a small molecule capable of interacting with numerous targets in the brain, the mechanisms of which are complex and still poorly understood. Studies have revealed that ethanol-induced hippocampal neuronal injury is associated with oxidative stress. Grape seed procyanidin (GSP) is a new type of antioxidant that is believed to scavenge free radicals and be anti-inflammatory. This study evaluated the ability and mechanism by which the GSP improves ethanol-induced hippocampal neuronal injury. Methods Primary cultures of hippocampal neurons were exposed to ethanol (11, 33 and 66 mM, 1, 4, 8, 12 and 24 h) and the neuroprotective effects of GSP were assessed by evaluating the activity of superoxide dismutase (SOD), the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and cell morphology. Results Our results indicated that GSP prevented ethanol-induced neuronal injury by reducing the levels of MDA and LDH, while increasing the activity of SOD. In addition, GSP increased the number of primary dendrites and total dendritic length per cell. Conclusion Together with previous findings, these results lend further support to the significance of developing GSP as a therapeutic tool for use in the treatment of alcohol use disorders.

scholarly journals Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1871 ◽  
Author(s):  
Denis Silachev ◽  
Egor Plotnikov ◽  
Irina Pevzner ◽  
Ljubava Zorova ◽  
Anastasia Balakireva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Targeted Delivery ◽  
Cell Damage ◽  
Brain Cell ◽  
Neuroprotective Effects ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
Causes Of Mortality ◽  
High Production ◽  
The Brain

Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8% oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions. Using vital sections of the brain, SkQR1 has been shown to reduce the development of oxidative stress. Thus, the mitochondrial-targeted antioxidant derived from plant plastoquinone can effectively protect the brain of newborns both in pre-ischemic and post-stroke conditions, making it a promising candidate for further clinical studies.

scholarly journals LongShengZhi Capsule Attenuates Alzheimer-Like Pathology in APP/PS1 Double Transgenic Mice by Reducing Neuronal Oxidative Stress and Inflammation

2020 ◽  
Vol 12 ◽  
Author(s):  
Zequn Yin ◽  
Xuerui Wang ◽  
Shihong Zheng ◽  
Peichang Cao ◽  
Yuanli Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transgenic Mice ◽  
Amyloid Β ◽  
B Cell Lymphoma ◽  
Acanthopanax Senticosus ◽  
Neuroprotective Effects ◽  
Long Term Treatment ◽  
Double Transgenic Mice ◽  
The Brain

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. It may be caused by oxidative stress, inflammation, and cerebrovascular dysfunctions in the brain. LongShengZhi Capsule (LSZ), a traditional Chinese medicine, has been approved by the China Food and Drug Administration for treatment of patients with cardiovascular/cerebrovascular disease. LSZ contains several neuroprotective ingredients, including Hirudo, Astmgali Radix, Carthami Flos (Honghua), Persicae Semen (Taoren), Acori Tatarinowii Rhizoma (Shichangpu), and Acanthopanax Senticosus (Ciwujia). In this study, we aimed to determine the effect of LSZ on the AD process. Double transgenic mice expressing the amyloid-β precursor protein and mutant human presenilin 1 (APP/PS1) to model AD were treated with LSZ for 7 months starting at 2 months of age. LSZ significantly improved the cognition of the mice without adverse effects, indicating its high degree of safety and efficacy after a long-term treatment. LSZ reduced AD biomarker Aβ plaque accumulation by inhibiting β-secretase and γ-secretase gene expression. LSZ also reduced p-Tau expression, cell death, and inflammation in the brain. Consistently, in vitro, LSZ ethanol extract enhanced neuronal viability by reducing L-glutamic acid-induced oxidative stress and inflammation in HT-22 cells. LSZ exerted antioxidative effects by enhancing superoxide dismutase and glutathione peroxidase expression, reduced Aβ accumulation by inhibiting β-secretase and γ-secretase mRNA expression, and decreased p-Tau level by inhibiting NF-κB-mediated inflammation. It also demonstrated neuroprotective effects by regulating the Fas cell surface death receptor/B-cell lymphoma 2/p53 pathway. Taken together, our study demonstrates the antioxidative stress, anti-inflammatory, and neuroprotective effects of LSZ in the AD-like pathological process and suggests it could be a potential medicine for AD treatment.

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