scholarly journals Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

2014 ◽  
Vol 25 (6) ◽  
Author(s):  
Lauren E. Salminen ◽  
Robert H. Paul
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Future Research ◽  
Aging Brain ◽  
Older Individuals ◽  
Glutathione S Transferase ◽  
Antioxidant Defense Enzymes ◽  
Repair Mechanisms ◽  
The Impact ◽  
The Brain

AbstractNormal aging involves a gradual breakdown of physiological processes that leads to a decline in cognitive functions and brain integrity, yet the onset and progression of decline are variable among older individuals. While many biological changes may contribute to this degree of variability, oxidative stress is a key mechanism of the aging process that can cause direct damage to cellular architecture within the brain. Oligodendrocytes are at a high risk for oxidative damage due to their role in myelin maintenance and production and limited repair mechanisms, suggesting that white matter may be particularly vulnerable to oxidative activity. Antioxidant defense enzymes within the brain, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), are crucial for breaking down the harmful end products of oxidative phosphorylation. Previous studies have revealed that allele variations of polymorphisms that encode these antioxidants are associated with abnormalities in SOD, CAT, GPx, and GST activity in the central nervous system. This review will focus on the role of oxidative stress in the aging brain and the impact of decreased antioxidant defense on brain integrity and cognitive function. Directions for future research investigations of antioxidant defense genes will also be discussed.

scholarly journals Activities of antioxidant defense enzymes in the blood of individuals with Leu144Phe mutation

2005 ◽  
Vol 24 (2) ◽  
pp. 111-114 ◽  
Author(s):  
Aleksandra Nikolic ◽  
Zorica Stevic ◽  
Dusko Blagojevic ◽  
Zorica Saicic ◽  
Mihajlo Spasic
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Antioxidant Defense ◽  
Familial Amyotrophic Lateral Sclerosis ◽  
Defense Enzymes ◽  
Glutathione S Transferase ◽  
Zinc Superoxide Dismutase ◽  
Antioxidant Defense Enzymes ◽  
Discriminant Analyses ◽  
Lateral Sclerosis

Activities of cooper zinc superoxide dismutase (Cu,Zn SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR) and glutathione-S-transferase (GST) in the blood of familial amyotrophic lateral sclerosis patients with Leu144Phe mutation (FALS), asimptomatic carriers with Leu144Phe mutation and controls were studied. Activity of Cu,Zn SOD was significantly lower in the FALS patients and asimptomatic carriers than in controls (p<0.001). In the FALS patients GSH-Px activity was lower (p<0.01) and activity of GR was higher (p<0.001) in comparison with controls. Canonical discriminant analyses provide statistical evidence that examined groups are different in the composition of antioxidant enzymes in blood and revealed that each component confers to observed difference. Our results suggests that oxidative stress is involved in pathogenesis of FALS and the activities of antioxidant enzymes are exposed to different kind of oxidative pressure in FALS patients, asymptomatic carriers and controls.

scholarly journals Aspirin treatment does not increase microhemorrhage size in young or aged mice

2018 ◽  
Author(s):  
Sandy Chan ◽  
Morgan Brophy ◽  
Nozomi Nishimura ◽  
Chris B. Schaffer
Keyword(s):  
Femtosecond Laser Ablation ◽  
Surrounding Tissue ◽  
Aging Brain ◽  
Older Individuals ◽  
Aged Mice ◽  
Intravenous Heparin ◽  
The Impact ◽  
Old Mice ◽  
The Brain ◽  
Vessel Rupture

AbstractMicrohemorrhages are common in the aging brain and are thought to contribute to cognitive decline and the development of neurodegenerative diseases, such as Alzheimer’s disease. Chronic aspirin therapy is widespread in older individuals and decreases the risk of coronary artery occlusions and stroke. There remains a concern that such aspirin usage may prolong bleeding after a vessel rupture in the brain, leading to larger bleeds that cause more damage to the surrounding tissue. Here, we aimed to understand the influence of aspirin usage on the size of cortical microhemorrhages and explored the impact of age. We used femtosecond laser ablation to rupture arterioles in the cortex of both young (2-5 months old) and aged (18-29 months old) mice dosed on aspirin in their drinking water and measured the extent of penetration of both red blood cells and blood plasma into the surrounding tissue. We found no difference in microhemorrhage size for both young and aged mice dosed on aspirin, as compared to controls (hematoma diameter = 104 +/- 39 (97 +/- 38) μm in controls and 109 +/- 25 (101 +/- 28) μm in aspirin-treated young (aged) mice; mean +/- SD). In contrast, young mice treated with intravenous heparin had an increased hematoma diameter of 136 +/- 44 μm. These data suggest that aspirin does not increase the size of microhemorrhages, supporting the safety of aspirin usage.

Antioxidant defenses and metabolic depression in a pulmonate land snail

1995 ◽  
Vol 268 (6) ◽  
pp. R1386-R1393 ◽  
Author(s):  
M. Hermes-Lima ◽  
K. B. Storey
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Thiobarbituric Acid ◽  
Land Snail ◽  
Land Snails ◽  
Antioxidant Defenses ◽  
Glutathione S Transferase ◽  
Hypometabolic State

During arousal from estivation oxygen consumption by land snails (Otala lactea) increases severalfold. To determine whether snails prepared for an accompanying rise in the rates of oxyradical generation by altering their antioxidant defense mechanisms, changes in the activities of antioxidant enzymes and lipid peroxidation products were quantified in foot and hepatopancreas of control, 30-day estivating, and aroused snails. Compared with controls, estivating O. lactea showed significant increases in the activities of foot muscle superoxide dismutase (SOD) (increasing by 56-67%), catalase (51-72%), and glutathione S-transferase (79-108%), whereas, in hepatopancreas, SOD (57-78%) and glutathione peroxidase (93-144%) increased. Within 40 min after arousal began, hepatopancreas glutathione peroxidase activity had returned to control values, but SOD showed a further 70% increase in activity but then returned to control levels by 80 min. Estivation had no effect on total glutathione (GSH + 2 GSSG) concentrations in tissues, but GSSG content had increased about twofold in both organs of 30-day dormant snails. Lipid peoxidation (quantified as thiobarbituric acid reactive substances) was significantly enhanced at the onset of arousal from dormancy, indicating that oxidative stress and tissue damage occurred at this time. The data suggest that antioxidant defenses in snail organs are increased while snails are in the hypometabolic state as a preparation for oxidative stress during arousal.

scholarly journals Cellular Senescence and Iron Dyshomeostasis in Alzheimer’s Disease

2019 ◽  
Vol 12 (2) ◽  
pp. 93 ◽  
Author(s):  
Shashank Masaldan ◽  
Abdel Ali Belaidi ◽  
Scott Ayton ◽  
Ashley I. Bush
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hydroxyl Radicals ◽  
Iron Accumulation ◽  
Brain Iron ◽  
Dependent Cell ◽  
Cellular Dysfunction ◽  
The Impact ◽  
The Brain

Iron dyshomeostasis is a feature of Alzheimer’s disease (AD). The impact of iron on AD is attributed to its interactions with the central proteins of AD pathology (amyloid precursor protein and tau) and/or through the iron-mediated generation of prooxidant molecules (e.g., hydroxyl radicals). However, the source of iron accumulation in pathologically relevant regions of the brain and its contribution to AD remains unclear. One likely contributor to iron accumulation is the age-associated increase in tissue-resident senescent cells that drive inflammation and contribute to various pathologies associated with advanced age. Iron accumulation predisposes ageing tissue to oxidative stress that can lead to cellular dysfunction and to iron-dependent cell death modalities (e.g., ferroptosis). Further, elevated brain iron is associated with the progression of AD and cognitive decline. Elevated brain iron presents a feature of AD that may be modified pharmacologically to mitigate the effects of age/senescence-associated iron dyshomeostasis and improve disease outcome.

scholarly journals High Protein Diet Induces Oxidative Stress in Rat Cerebral Cortex and Hypothalamus

2019 ◽  
Vol 20 (7) ◽  
pp. 1547 ◽  
Author(s):  
Ewa Żebrowska ◽  
Mateusz Maciejczyk ◽  
Małgorzata Żendzian-Piotrowska ◽  
Anna Zalewska ◽  
Adrian Chabowski
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
High Protein Diet ◽  
Brain Structures ◽  
High Protein ◽  
Protein Diet ◽  
Standard Diet ◽  
The Impact

This is the first study to analyze the impact of high protein diet (HPD) on antioxidant defense, redox status, as well as oxidative damage on both a local and systemic level. Male Wistar rats were divided into two equal groups (n = 9): HPD (44% protein) and standard diet (CON; 24.2% protein). After eight weeks, glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase-1 (SOD-1), reduced glutathione (GSH), uric acid (UA), total antioxidant (TAC)/oxidant status (TOS) as well as advanced glycation end products (AGE), 4-hydroxynonenal (4-HNE), and malondialdehyde (MDA) were analyzed in the serum/plasma, cerebral cortex, and hypothalamus of HPD and CON rats. HPD resulted in higher UA concentration and activity of GPx and CAT in the hypothalamus, whereas in the cerebral cortex these parameters remained unchanged. A significantly lower GSH content was demonstrated in the plasma and hypothalamus of HPD rats when compared to CON rats. Both brain structures expressed higher content of 4-HNE and MDA, whereas AGE was increased only in the hypothalamus of HPD animals. Despite the enhancement in antioxidant defense in the hypothalamus, this mechanism does not protect the hypothalamus from oxidative damage in rats. Hypothalamus is more susceptible to oxidative stress caused by HPD.

scholarly journals Pineal Proteins Upregulate Specific Antioxidant Defense Systems in the Brain

2009 ◽  
Vol 2 (2) ◽  
pp. 88-92 ◽  
Author(s):  
Vijay K. Bharti ◽  
R. S. Srivastava
Keyword(s):  
Oxidative Stress ◽  
Pineal Gland ◽  
Antioxidant Defense ◽  
Bubalus Bubalis ◽  
Female Rats ◽  
Antioxidant Systems ◽  
Secretory Product ◽  
Defense Systems ◽  
Antioxidant Defense Systems ◽  
The Brain

The neuroendocrine functions of the pineal affect a wide variety of glandular and nervous system processes. Beside melatonin (MEL), the pineal gland secretes and expresses certain proteins essential for various physiological functions. It has been suggested that the pineal gland may also have an antioxidant role due to secretory product other than MEL. Therefore, the present study was designed to study the effect of buffalo (Bubalus bubalis) pineal proteins (PP) on the antioxidant defense system in the brain of female rats. The twenty-four rats were taken in present study and were divided into four groups: control (0 day), control (28 day), vehicle control and buffalo PP. The PP was injected 100 µg/kg BW intraperitoneal (i.p.) daily for 28 days. The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione reductase (GR) and reduced glutathione (GSH) concentration and the levels of lipid peroxidation (LPO) in the brain tissue were measured to assess the antioxidant systems. These enzymes protect from adverse effects of free radicals and help in amelioration of oxidative stress. Buffalo pineal proteins administration did not cause any effect on brain LPO, whereas GPx, GR and GSH were significantly (p < 0.05) decreased. However, SOD and CAT activities were increased to significant levels than the control in PP treated rats. Our study herein suggested that buffalo (Bubalus bubalis) pineal proteins upregulates specific antioxidant defense systems and can be useful in control of various oxidative stress-induced neuronal diseases.

Brain stem oxidative stress and its associated signaling in the regulation of sympathetic vasomotor tone

2012 ◽  
Vol 113 (12) ◽  
pp. 1921-1928 ◽  
Author(s):  
Samuel H. H. Chan ◽  
Julie Y. H. Chan
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Brain Stem ◽  
Ventrolateral Medulla ◽  
Future Research ◽  
Vasomotor Tone ◽  
Cellular Mechanisms ◽  
Neurogenic Hypertension ◽  
The Impact ◽  
Sympathetic Vasomotor Tone

There is now compelling evidence from studies in humans and animals that overexcitation of the sympathetic nervous system plays an important role in the pathogenesis of cardiovascular diseases. An excellent example is neurogenic hypertension, in which central sympathetic overactivation is involved in the development, staging, and progression of the disease, and one of the underlying mechanisms involves oxidative stress in key brain stem sites that are engaged in the regulation of sympathetic vasomotor tone. Using the rostral ventrolateral medulla (RVLM) and nucleus tractus solitarii (NTS) as two illustrative brain stem neural substrates, this article provides an overview of the impact of reactive oxygen species and antioxidants on RVLM and NTS in the pathogenesis of neurogenic hypertension. This is followed by a discussion of the redox-sensitive signaling pathways, including several kinases, ion channels, and transcription factors that underpin the augmentation in sympathetic vasomotor tone. In addition, the emerging view that brain stem oxidative stress is also causally related to a reduction in sympathetic vasomotor tone and hypotension during brain stem death, methamphetamine intoxication, and temporal lobe status epilepticus will be presented, along with the causal contribution of the oxidant peroxynitrite formed by a reaction between nitric oxide synthase II (NOS II)-derived nitric oxide and superoxide. Also discussed as a reasonable future research direction is dissection of the cellular mechanisms and signaling cascades that may underlie the contributory role of nitric oxide generated by different NOS isoforms in the differential effects of oxidative stress in the RVLM or NTS on sympathetic vasomotor tone.

scholarly journals Exogenous thiourea modulates antioxidant defence and glyoxalase systems in lentil genotypes under arsenic stress

2016 ◽  
Vol 2 ◽  
pp. 9 ◽  
Author(s):  
Dibyendu Talukdar
Keyword(s):  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Imaging Study ◽  
Dry Weight ◽  
Crop Productivity ◽  
Mitigation Strategies ◽  
Grain Legume ◽  
Glutathione S Transferase ◽  
Study Results ◽  
Antioxidant Defense Enzymes

<p>Arsenic (As) is a wide-spread toxic and carcinogenic metalloid, affecting crop productivity worldwide. Lentil, an edible grain legume, is increasingly exposed to soil arsenic contamination. However, our understandings regarding mechanistic details and mitigation strategies against arsenic toxicity in edible legume are extremely poor. Main purpose of the present study was to investigate the As-effects and its mitigation by thiourea (TU), a sulfhydryl bioregulator, in lentil. Four widely grown lentil genotypes were grown in nutrient media, supplemented with 30 μM sodium arsenate (As), As + 6.5 mM TU and As + 13 mM TU, keeping an untreated control for 10 d. As severely affected plant dry weight by accumulating in shoots and roots. However, TU application sequestered As in crop roots and prevented up-ward translocation of As. TU coordinately modulated glyoxalase system I and II (Gly I and II) and ascorbate (AsA)-glutathione (GSH) redox, and antioxidant defense enzymes in both leaves and roots of four genotypes. Elevation of Gly system prevented toxic methyl glyoxal overaccumulation whereas stimulated AsA-GSH cycle enzymes and Glutathione s-transferase and catalase effectively scavenged H<sub>2</sub>O<sub>2</sub> and prevented reactive oxygen species (ROS) -mediated onset of oxidative damage in four genotypes, as was evident from ROS-imaging study. Results suggested exogenous TU stimulated the Gly and antioxidant defense in fine tune against As-induced oxidative damage in lentil genotypes.</p>

scholarly journals Characteristics of lipid peroxidation processes and factors of the antioxidant defense system in chronic atrophic gastritis and gastric cancer

2022 ◽  
Vol 20 (4) ◽  
pp. 63-70
Author(s):  
O. V. Smirnova ◽  
V. V. Tsukanov ◽  
A. A. Sinyakov ◽  
O. L. Moskalenko ◽  
N. G. Elmanova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Control Group ◽  
Defense System ◽  
Glutathione S Transferase

Background. The problem of gastric cancer remains unresolved throughout the world, while chronic atrophic gastritis (CAG) increases the likelihood of its development by 15 times. In the Russian Federation, the incidence of gastric cancer (GC) is among the highest, with it prevailing among males. One of the leading mechanisms in molecular pathology of membranes is lipid peroxidation (LPO). The severity of oxidative membrane damage depends on concomitant diseases, contributing to emergence and progression of pathological processes and development of cancer. Currently, the problem of LPO is unsolved in biological systems.The aim of this study was to investigate the state of LPO and antioxidant defense system in CAG and GC. Materials and methods. The parameters were studied in 45 patients with CAG and 50 patients with GC. The control group included 50 practically healthy volunteers without gastrointestinal complaints, who did not have changes in the gastric mucosa according to the fibroesophagogastroduodenoscopy (FEGDS) findings.Results. In patients with CAG, an increase in malondialdehyde, superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase was found in the blood plasma compared with the control group. In patients with CAG, lipid peroxidation was activated, and the malondialdehyde level increased by 3.5 times relative to normal values. At the same time, the body fought against oxidative stress by increasing the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase. All patients with GC showed pronounced oxidative stress in the blood plasma in the form of a 45-fold increase in malondialdehyde. The activity of the main antioxidant enzyme superoxide dismutase was reduced in GC. Catalase was activated, which indicated pronounced oxidative stress, significant damage to blood vessels, and massive cell death. Glutathione-related enzymes (glutathione S-transferase and glutathione peroxidase) and the antioxidant protein ceruloplasmin were activated, which also indicated significant oxidative stress and severe intoxication in patients with GC.Conclusion. Depending on the stage and type of cancer, an in-depth study of lipid peroxidation and factors of the antioxidant defense system can be used to correct therapy and prevent cancer and can serve as markers of progression and prognosis in gastric cancer. 

scholarly journals Oxidative Stress and Reproductive Function in the Aging Male

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 282
Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Defense ◽  
Structural Integrity ◽  
Germ Line ◽  
Reproductive Function ◽  
Antioxidant Defense System ◽  
Male Reproduction ◽  
Paternal Age ◽  
Theories Of Aging ◽  
The Impact

With the delay of parenthood becoming more common, the age at which men father children is on the rise. While the effects of advanced maternal age have been well documented, only recently have studies started to focus on the impact of advanced paternal age (APA) in the context of male reproduction. As men age, the antioxidant defense system gradually becomes less efficient and elevated levels of reactive oxygen species (ROS) accumulate in spermatozoa; this can impair their functional and structural integrity. In this review, we present an overview of how oxidative stress is implicated in male reproductive aging by providing a summary of the sources and roles of ROS, the theories of aging, and the current animal and human studies that demonstrate the impacts of APA on the male germ line, the health of progeny and fertility, and how treatment with antioxidants may reverse these effects.

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