TY - JOUR. T1 - Protective effects of L-arginine on pulmonary oxidative stress and antioxidant defenses during exhaustive exercise in rats. AU - Lin, Wan Teng. AU - Yang, Suh-Ching. AU - Chen, Kung Tung. AU - Huang, Chi Chang. AU - Lee, Ning Yuean. PY - 2005/8. Y1 - 2005/8. N2 - Aim: To assess the effects of L-arginine (L-Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. Methods: Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L-Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2% L-Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione ...
We show that RES increase the expression of FoxO1A, FoxO3A, and FoxO4 under chronic oxidative stress conditions (Fig. 2). This response is consistent with a homeostatic response to protect lens epithelial cells. Baur et al. 28 found that RES extended lifespan in a high-fat diet mouse model and that it appeared to be dependent on activation of Sir2. It was further demonstrated that the Sir2 homolog SIRT1 controls the cellular response to stress by regulating the FoxO family. 29 SIRT1 and the FoxO transcription factor FoxO3 form a complex in cells in response to oxidative stress. In our study, we found that RES increased expression of FoxO3A and also enhanced the expression of FoxO1A and FoxO4 under chronic oxidative stress conditions, suggesting that FoxO1A and FoxO4 may also be involved in the protective effects of RES (Fig. 2). This is further supported by the finding that knockdown of individual FoxOs by FoxO siRNAs decreases the protective effects of RES against acute oxidative stress. A ...
Markovitch, D., Tyrrell, R. M. and Thompson, D., 2005. Heme oxygenase-1 expression in human lymphocytes and resistance to oxidative stress following exercise. FASEB Journal, 19 (4), A131-A131.. ...
This is a phase II intervention to propose a new melanoma chemoprevention agent. The investigators believe oxidative stress/damage in nevi is a probable indication for melanoma risk, and propose that reduced melanoma risk in humans can be inferred by protection of nevi from ultraviolet light (UV)-induced oxidative changes. The investigators will 1) evaluate whether administration of NAC around the time of UV exposure will reduce melanoma risk in high-risk patient populations with genetic susceptibility to UV-induced oxidative stress, and 2) examine key genetic variants that will identify which individuals are most likely to benefit from chemoprotection ...
TY - JOUR. T1 - Reduced coupling of oxidative phosphorylation In Vivo precedes electron transport chain defects due to mild oxidative stress in mice. AU - Siegel, Michael P.. AU - Kruse, Shane E.. AU - Knowels, Gary. AU - Salmon, Adam. AU - Beyer, Richard. AU - Xie, Hui. AU - van Remmen, Holly. AU - Smith, Steven R.. AU - Marcinek, David J.. PY - 2011/11/22. Y1 - 2011/11/22. N2 - Oxidative stress and mitochondrial function are at the core of many degenerative conditions. However, the interaction between oxidative stress and in vivo mitochondrial function is unclear. We used both pharmacological (2 week paraquat (PQ) treatment of wild type mice) and transgenic (mice lacking Cu, Zn-superoxide dismutase (SOD1 -/-)) models to test the effect of oxidative stress on in vivo mitochondrial function in skeletal muscle. Magnetic resonance and optical spectroscopy were used to measure mitochondrial ATP and oxygen fluxes and cell energetic state. In both models of oxidative stress, coupling of oxidative ...
TY - JOUR. T1 - Longevity is associated with increased vascular resistance to high glucose-induced oxidative stress and inflammatory gene expression in Peromyscus leucopus. AU - Labinskyy, Nazar. AU - Mukhopadhyay, Partha. AU - Toth, Janos. AU - Szalai, Gabor. AU - Veres, Monika. AU - Losonczy, Gyorgy. AU - Pinto, John T.. AU - Pacher, Pal. AU - Ballabh, Praveen. AU - Podlutsky, Andrej. AU - Austad, Steven N.. AU - Csiszar, Anna. AU - Ungvari, Zoltan. PY - 2009/4/1. Y1 - 2009/4/1. N2 - Vascular aging is characterized by increased oxidative stress and proinflammatory pheno- typic alterations. Metabolic stress, such as hyperglycemia in diabetes, is known to increase the production of ROS and promote inflammatory gene expression, accelerating vascular aging. The oxidative stress hypothesis of aging predicts that vascular cells of long-lived species exhibit lower steady-state production of ROS and/or superior resistance to the prooxidant effects of metabolic stress. We tested this hypothesis using ...
The pathogenesis of hepatic encephalopathy (HE) is multifactorial and often associated with the development of brain oedema. In addition to ammonia playing a central role, systemic oxidative stress is believed to aggravate the neuropsychological effects of ammonia in patients with chronic liver disease (CLD). The aim of this study was to (i) induce systemic oxidative stress in hyperammonaemic portacaval anastomosed (PCA) rats by inhibiting the antioxidant glutathione using Dimethyl maleate (DEM) and (ii) investigate whether a synergistic relationship between ammonia and oxidative stress contributes to the pathogenesis of brain oedema in CLD. ...
BioAssay record AID 704663 submitted by ChEMBL: Antioxidant activity in tetracycline-removed human MC65 cells assessed as suppression of oxidative stress at 0.1 uM after 48 hrs by DCFH-DA assay.
Objective: To investigate the role of oxidative stress and antioxidants in depression. Data Sources: We searched the literature without language restrictions through MEDLINE/PubMed, Cochrane Library, Fisterra, and Galenicom from database inception until December 31, 2013, supplemented by a hand search of relevant articles. Search terms included (1) oxidative stress, antioxidant*, nitrosative stress, nitrative stress, nitro-oxidative stress, free radical*, and names of individual oxidative stress markers/antioxidants and (2) depression and related disorders and antidepressant. Study Selection: Included were studies in patients with depression comparing antioxidant or oxidative stress markers with those in healthy controls before and after antidepressant treatment. Data Extraction: Two authors independently extracted the data for antioxidant or oxidative stress markers. Standardized mean differences (SMDs) +/- 95% confidence intervals (CIs) for results from |= 3 studies were calculated. Data Synthesis:
Neuronal Cell Protective Effect of Dendropanax morbifera Extract against High Glucose-Induced Oxidative Stress - Dendropanax morbifera;antioxidant;oxidative stress;high glucose;neuroprotective effect;
In the pathogenesis of renal fibrosis, oxidative stress (OS) enhances the production of reactive oxygen species (ROS) leading to sustained cell growth, inflammation, excessive tissue remodelling and accumulation, which results in the development and acceleration of renal damage. In our previous work (128) we established protein DJ-1 (PARK7) as an important ROS scavenger and key player in renal cell response to OS. In the present study we investigated the impact of profibrogenic agonists on DJ-1 and shed light on the role of this protein in renal fibrosis. Treatment of renal fibroblasts and epithelial cells with the profibrogenic agonist ANG II or PDGF resulted in a significant up-regulation of DJ-1 expression parallel to an increase in the expression of fibrosis markers. Monitoring of DJ-1 expression in kidney extract and tissue sections from renal fibrosis mice model (Col4a3-deficient) revealed a disease grad dependent regulation of the protein. Overexpression of DJ-1 prompted cell resistance ...
The nuclear factor E2-related factor 2 (Nrf2) plays an important role in cellular protection against cancer, renal, pulmonary, cardiovascular and neurodegenerative diseases where oxidative stress and inflammation are common conditions. The Nrf2 regulates the expression of detoxifying enzymes by reco …
Cells, particularly mechano-sensitive musculoskeletal cells such as tenocytes, routinely encounter oxidative stress. Oxidative stress can not only stimulate tissue repair, but also cause damage leading to tissue degeneration. As diabetes is associated with increased oxidative damage as well as increased risk of tendon degeneration, the aim of this study was to determine if extracellular glucose levels alter the response of tendon cells to oxidative stress. Primary human tenocytes were cultured in either high (17.5 mM) or low (5 mM) glucose and treated with 100 μM hydrogen peroxide. In low glucose, peroxide-treated cells remained fully viable and collagen synthesis was increased, suggesting an anabolic response. In high glucose, however, peroxide treatment led to increased bim-mediated apoptosis. The activities of both forkhead box O (FOXO1) and p53 were required for upregulation of bim RNA expression in high glucose. We found that both p53-mediated inhibition of the bim repressor micro RNA (miR17-92)
There was a statistically significant difference in oxidative stress status between men and women who were CAD(−) (−0.424 ± 1.3 vs. 0.64 ± 1.1 arbitrary units, respectively), but the CAD(+) women had oxidative stress levels almost three times those of the CAD(+) men (2.45 ± 2.5 vs. 0.9 ± 1.6 arbitrary units, respectively). After adjustment in the multivariate model, age and oxidative stress status in women and diabetes and age in men remained as statistically significant predictors of positive CAD findings.. Conclusion(s): ...
Oxidative stress biomarkers, in vivo heart rate (f(H)), and contraction dynamics of ventricle strips of bullfrog (Lithobates catesbeiana) tadpoles were evaluated after 48 h of exposure to a sub-lethal concentration (1 ppm) of the herbicide Roundup Original (R) (glyphosate 41%). The activities of the antioxidant enzymes superoxide dismutase and catalase were increased in the liver and decreased in muscle, while oxidative damage to lipids increased above control values in both tissues, showing that the generation of reactive oxygen species and oxidative stress are involved in the toxicity induced by Roundup (R). Additionally, tadpoles hyperactivity was associated with tachycardia in vivo, probably due to a stress-induced adrenergic stimulation. Ventricle strips of Roundup (R)-exposed tadpoles (R-group) presented a faster relaxation and also a higher cardiac pumping capacity at the in vivo contraction frequency, indicating that bullfrog tadpoles were able to perform cardiac mechanistic adjustments ...
Hyperglycaemia-induced oxidative stress plays an important role in cardiomyocyte cell death leading to cardiac dysfunction. Autophagy is an intracellular bulk degradation process and can be induced by stressors such as nutrient depletion and acute ischemia, to promote cell survival. Oxidative stress is an important regulator of autophagy in various pathophysiological conditions such as ischemia/reperfusion injury and hypoxia. The role of autophagy in the oxidative stress tolerance of cardiac cells exposed to simultaneous hyperglycemia and hypoxia has not been studied. The aim of the present study is to determine the role of autophagy in cardiac cells in response to combined hyperglycemia and hypoxia. H9c2 rat cardiac cell lines were grown in DMEM supplemented with standard (5.6 mM), moderately high (25 mM) and high (33 mM) glucose concentrations. The cells were then exposed to hypoxia condition (1% oxygen, O2) for 24h and 48h using the hypoxia chamber. Cell viability and oxidative stress was ...
Keywords: Reactive Oxygen Species, NADPH, Ischemic strokes, cerebral ischemia, Superoxide Dismutase, Glutathione Peroxidase. Abstract: The mechanisms leading to cellular damage from ischemia-reperfusion (I/R) injury are complex and multi-factorial. Accumulating evidence suggests an important role for oxidative stress in the regulation of neuro-inflammation following stroke. Gene expression studies have revealed that the increase in oxygen radicals post-ischemia triggers the expression of a number of pro-inflammatory genes. These genes are regulated by the transcription factor, nuclear factor-kappa-B (NF-??B) which is redox-sensitive. It is hypothesised that changes in the oxidative state may modulate alterations in the neuro-inflammatory response following an I/R injury. Furthermore, NF-??B is involved in the transcriptional regulation of adhesion molecules, which play an important role in leukocyte-endothelium interactions. Recent studies have demonstrated that adhesion molecule-mediated ...
TY - JOUR. T1 - Skin fragility in obese diabetic mice. T2 - Possible involvement of elevated oxidative stress and upregulation of matrix metalloproteinases. AU - Ibuki, Ai. AU - Akase, Tomoko. AU - Nagase, Takashi. AU - Minematsu, Takeo. AU - Nakagami, Gojiro. AU - Horii, Motoko. AU - Sagara, Hiroshi. AU - Komeda, Takashi. AU - Kobayashi, Masayuki. AU - Shimada, Tsutomu. AU - Aburada, Masaki. AU - Yoshimura, Kotaro. AU - Sugama, Junko. AU - Sanada, Hiromi. PY - 2012/3. Y1 - 2012/3. N2 - The purpose of this study was to test the hypothesis that obese diabetic mice exhibit marked skin fragility, which is caused by increased oxidative stress and increased matrix metalloproteinase (MMP) gene expression in the subcutaneous adipose tissue. Scanning electron microscopy of skin samples from Tsumura-Suzuki obese diabetic (TSOD) mice revealed thinner collagen bundles, and decreased density and convolution of the collagen fibres. Furthermore, skin tensile strength measurements confirmed that the dorsal ...
This paper discusses the scientific evidence that has been collected regarding the influence of physical activity on oxidative stress. One of the bodys responses to exercise or physical activity is increased levels of free radicals. Physical activity can increase the formation of free radicals in the body thereby increasing oxidative stress. Oxidative stress is a condition that occurs because of an imbalance between the production of free radicals with antioxidant defense systems in the body. MDA (Malondialdehyde) is one of the indicators used to determine oxidative stress in humans. MDA is the result of lipid peroxidation in the body due to free radicals. Increased conditions of oxidative stress have implications for muscle damage and if it lasts in the long run will lead to various diseases such as hypertension, atherosclerosis, diabetes, heart failure, stroke, and other chronic diseases. It is recommended that the understanding of this should be understood by all sports actors, both ...
NIEHS Grant P30ES006096 An NIEHS grantee and colleagues report that biomarkers of oxidative stress are associated with hip fracture in postmenopausal women. If additional studies confirm these results, the biomarkers could help improve prediction of hip fracture, which is associated with substantial cost and a high risk of disability and death.. Oxidative stress occurs when the body insufficiently responds to reactive oxygen species. Environmental factors such as radiation and pollutants can add to the natural level of reactive oxygen species and overcome the bodys defenses. Studies in people have suggested that oxidative stress might be a risk factor for osteoporosis, but its relationship with fracture risk is poorly understood. To find out more, the researchers prospectively assessed oxidative stress by measuring fluorescent oxidation products (FlOP) in 996 women from the Nurses Health Study who were 60 or older at baseline blood collection between 1989 and 1990. FlOPs are markers of global ...
Hyperglycemia and oxidative stress are conditions directly related to the metabolic syndrome (MetS), whose prevalence is increasing worldwide. This study aimed to evaluate the effectiveness of a new weight-loss dietary pattern on improving the oxidative stress status on patients suffering MetS with hyperglycemia. Seventy-nine volunteers were randomly assigned to two low-calorie diets (−30% Energy): the control diet based on the American Health Association criteria and the RESMENA diet based on a different macronutrient distribution (30% proteins, 30% lipids, 40% carbohydrates), which was characterized by an increase of the meal frequency (seven-times/day), low glycemic load, high antioxidant capacity (TAC) and high n-3 fatty acids content. Dietary records, anthropometrical measurements, biochemical parameters and oxidative stress biomarkers were analyzed before and after the six-month-long study. The RESMENA (Metabolic Syndrome Reduction in Navarra) diet specifically reduced the android fat mass and
Not surprisingly, the body can also suffer from reductive stress which frequently goes unmentioned. Reductive stress is achieved when the concentrations of reducing agents exceeds that of oxidizing agents. This is commonly encountered with the metabolism of ethanol. It is therefore possible for "Health Fanatics" to overdose on anti-oxidants and push the body into reductive stress instead of the oxidative stress they are steadfastly trying to avoid. Exercise can have positive or negative effects with regard to Redox effects on the body according to how it is performed. Exercise increases oxidative stress due to metabolic processes but when exercise is undertaken on a regular basis the body up-regulates its own anti-oxidant capacity to cope with the increased demand. This improved anti-oxidant activity clearly has additional benefits when we are not exercising but are under oxidative stress in other ways. Intermittent exercise will increase the oxidative stress burden on the body but is not ...
Vision problems…. "Being able to stimulate the bodys own endogenous production of glutathione is the most significant breakthrough in natural medicine that Ive seen in 3o years.". Glutathione is the bodys most important defense against free radicals, chemical toxins, radiation, heavy metals, pollution and oxidative stress.. Oxidative stress is the damage caused to our cells as the result of normal oxidative processes occurring all the time in our bodies.. If you cut an apple in half the exposed sliced parts will soon turn brown. This is an example of oxidative stress. It is the same process which causes metals to rust. A healthy body will keep the damaging effects of oxidative stress at bay. However, cells are damaged when the effects of oxidative stress overwhelm the bodys ability to protect itself.. Someone who spends too much time in the sun will have damaged skin due to the effects of free radicals and oxidative stress. In a sense, oxidative stress causes the body to "rust" and cause ...
An imbalance between the production of reactive oxygen species (ROS) and the detoxification of their reactive intermediates causes oxidative stress. Cells must respond to this imbalance before the highly reactive molecules damage cellular structures, particularly DNA. Severe and prolonged oxidative stress can trigger apoptosis and necrosis. Numerous pathological conditions have an oxidative stress component, including cardiovascular diseases, neurodegenerative diseases such as Alzheimers disease, and chronic inflammation. Signaling pathways downstream of ROS detection, such as PKC, PI3K, and MAPK, phosphorylate the transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2). This transcription factor binds the antioxidant response element (ARE) within the promoters of genes encoding antioxidant enzymes and detoxifying enzymes. Key Nrf2 target genes include antioxidants such as glutathione peroxidases (GPx) and genes involved in superoxide metabolism. These genes reduce oxidative ...
AbstractBackground:Although oxidative stress-related diseases mostly affect neonates with extremely low birthweight, healthy preterm and term newborns may also be at risk of oxidative damage. There have been studies concerning factors that affect the level of oxidative stress biomarkers in term and
SIGNIFICANCE. Oxidative stress is considered to be an important component of various diseases. A vast number of methods have been developed and used in virtually all diseases to measure the extent and nature of oxidative stress, ranging from oxidation of DNA to proteins, lipids, and free amino acids. Recent Advances: An increased understanding of the biology behind diseases and redox biology has led to more specific and sensitive tools to measure oxidative stress markers, which are very diverse and sometimes very low in abundance.. CRITICAL ISSUES. The literature is very heterogeneous. It is often difficult to draw general conclusions on the significance of oxidative stress biomarkers, as only in a limited proportion of diseases have a range of different biomarkers been used, and different biomarkers have been used to study different diseases. In addition, biomarkers are often measured using nonspecific methods, while specific methodologies are often too sophisticated or laborious for routine ...
In certain situations, free radicals can be generated in an exaggerated manner and can injure tissues and organs by interacting with lipids, proteins, or DNA. So, oxidative stress has been implicated in a large number of human diseases. To survive, the human body has developed a complex, efficient, and highly adaptive antioxidant defense system. The eye is also protected against oxidative stress by several mechanisms involving antioxidant enzymes such as catalase (CAT) and superoxide dismutase (SOD), as well as by low-molecular-weight antioxidants such as glutathion (GSH) and ascorbate.. Primary open-angle glaucoma (POAG) is a chronic, slowly progressive optic neuropathy, characterized by excavation of the optic nerve head (ONH) and a distinctive pattern of visual field (VF) defects. The disease is multifactorial in origin, so that besides more extensively investigated factors oxidative stress has also been proposed as a contributing factor in the etiology of glaucomatous optic neuropathy. ...
Oxidative stress is involved in the initiation and progression of atherosclerosis, and hyperglycemia is known to increase oxidative stress, which injures the endothelium and accelerates atherosclerosis. To clarify the relation between oxidative stress, diabetes mellitus (DM), and acute myocardial infarction (AMI), we evaluated and compared time-specific oxidative stress after AMI in patients with and without DM by simple measurement of derivatives of reactive oxygen metabolites (d-ROMs) levels as indices of reactive oxygen species production. Sixty-eight AMI patients were enrolled (34 non-DM patients and 34 DM patients). Using the FRAS4 free radical analytical system, we measured d-ROMs levels in each patient at two time points: 1 and 2 weeks after AMI onset. d-ROM levels decreased significantly between week 1 and week 2 (from 475.4 ± 119.4 U.CARR to 367.7 ± 87.9 U.CARR, p | 0.001) in the non-DM patients but did not change in the DM patients (from 463.1 ± 109.3 U.CARR to 461.7 ± 126.8 U.CARR, p = 0
The Gene Ontology (GO) project is a collaborative effort to address the need for consistent descriptions of gene products across databases. You can use this browser to view terms, definitions, and term relationships in a hierarchical display. Links to summary annotated gene data at MGI are provided in Term Detail reports.
Alzheimers disease (AD) is a devastating neurodegenerative disorder which is thought to affect 26.6 million individuals worldwide. There is growing concern over a worldwide dementia epidemic that is predicted to develop over the coming decades. The evidence thus far suggests that increased levels of oxidative stress and vascular risk factors are two major contributors, amongst others, to AD development. The thesis aimed to investigate markers of oxidative stress in AD plasma. Moreover, the oxidative status of specific proteins was investigated using both hypothesis driven and proteomic approaches. Results presented in this thesis suggest that global plasma protein oxidation levels are not different when AD and control subjects are compared, but that individual plasma proteins are specific targets for oxidative modification in AD. The thesis explores different methodologies to assess oxidative changes in AD. In addition it demonstrates that emerging novel and powerful mass spectrometry ...
Open access preprint on Evaluation of hemolytic activity and oxidative stress biomarkers in erythrocytes after exposure to bioactive glass nanoceramics
In the past few years there has been the increased recognition that the effects of oxidative stress are not limited to the damage of cellular constituents. There is now evidence that reactive oxygen species (ROS) can alter cell function by acting upon the intermediates, or second messengers, in signal transductions. Such effects on signaling mechanisms probably account for the role of oxidative stress in inflammation, aging, and cancer. This volume brings together internationally recognized researchers in both the major areas covered by the book, oxidative stress and signal transduction. The work is organized in three sections. The first deals with the immediate cellular responses to oxidative stress and the production of second messengers. The second details the connection between second messengers and the gene. The third part looks more closely at the level of the gene.
Abstract: After the onset of a stroke, blood flows disrupted in areas affected by vascular occlusion limit the delivery of oxygen and metabolic substrates to neurons causing ATP reduction and energy depletion. The glucose and oxygen deficit that occurs after severe vascular occlusion is the origin of the mechanisms that lead to cell death and cerebral injury caused of oxidative stress. Oxidative stress constitutes mechanism of injury of many types of disease processes. On oxidative stress occurs on the increase in ROS and RNS. This paper will discuss about cerebral ischemia that causes activation of ROS and RNS, also themechanisms that play a role in cell death after cerebral ischemia, for example the role of phospholipase, Haber-Weiss reaction, and lipid peroxidation. It is also described about anti-oxidants to fight free radicals, for examples glutathione peroxidase, catalase and superoxide dismutase. ...
During physiological aerobic metabolism, the epidermis undergoes significant oxidative stress as a result of the production of reactive oxygen species (ROS). To maintain a balanced oxidative state, cells have developed protective antioxidant systems, and preliminary studies suggest that the transcriptional factor p63 is involved in cellular oxidative defence. Supporting this hypothesis, the ΔNp63α isoform of p63 is expressed at high levels in the proliferative basal layer of the epidermis. Here we identify the CYGB gene as a novel transcriptional target of ΔNp63 that is involved in maintaining epidermal oxidative defence. The CYGB gene encodes cytoglobin, a member of the globin protein family, which facilitates the diffusion of oxygen through tissues and acts as a scavenger for nitric oxide or other ROS. By performing promoter activity assays and chromatin immunoprecipitation, reverse transcriptase quantitative PCR and western blotting analyses, we confirm the direct regulation of CYGB by ΔNp63α.
Free radicals are biological kleptomaniacs, and no amount of psycho-therapy is going to quell their desire to steal. In the case of skin aging, they are taking electrons. When free radicals steal electrons from other molecules, the result is damage to delicate skin components and further inflammation. Inflammation promotes oxidative stress, and oxidative stress promotes inflammation in an ongoing vicious cycle.. Oxidative Stress: When oxygen is used to produce energy in the human body, one of the byproducts is the creation of highly reactive molecules called free radicals. They are highly reactive because each of them is an unpaired molecule looking for a partner. They can interact with and damage structural fats, proteins, and even delicate genetic components in a process called oxidative stress.. The generation of free radicals is never going to stop. And approximately 3 percent of oxygen used in the metabolic processes of our cells is converted to free radicals. So why bother to worry about ...
Aging is associated with increased oxidative stress. Muscle levels of oxidative stress are further elevated with exercise. The purpose of this study was to determine if dietary antioxidant supplementation would improve muscle function and cellular markers of oxidative stress in response to chronic repetitive loading in aging. The dorsiflexors of the left limb of aged and young adult Fischer 344 Br
TY - CHAP. T1 - Exploring the effect of redox enzyme modulation on the biology of mouse aging. AU - Salmon, Adam. AU - Richardson, Arlan. AU - Pérez, Viviana I.. PY - 2014/5/1. Y1 - 2014/5/1. N2 - The oxidative stress theory of aging has been the most studied and tested mechanistic theory of why organisms age. However, most recent data on this theory suggest that broadly altering levels of oxidative stress or accumulation of oxidative damage has limited effects on the regulation of lifespan in mammals. This has led to the proposition that aging may be regulated through oxidation-induced changes to cellular redox state and redox signaling rather than through general oxidative stress mechanisms. Redox regulation of cell survival and homeostasis through modulating the pathways necessary for gene regulation, protein activation and deactivation, and apoptosis might then amplify minor alterations in oxidative stress to have drastic effects on an organism. In this chapter, we discuss the evidence that ...
... , Krishnamurthy N, Chinmoy Ghosh , Sumathi M E, Ashakiran S, Dayanand C D
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Most schemes for TGs role in acute and chronic neurodegeneration have centered around the ability of these enzymes to cross-link mutated and/or accumulated proteins in a host of diseases, including AD, HD, and PD (Caccamo et al., 2010). And while this model unifies diseases associated with proteotoxicity, it fails to account for the benefits of molecular or pharmacological TG deletion in ischemic (Hwang et al., 2009; Colak et al., 2011) or hemorrhagic stroke (Okauchi et al., 2009). Indeed, exciting new data on the role of TG in autophagosome formation (DEletto et al., 2009), in inhibiting axonal transport of growth factors such as BDNF (Borrell-Pagès et al., 2006), in repressing adaptive gene expression (McConoughey et al., 2010), and on influencing nuclear actin dynamics (Munsie et al., 2011) have focused attention on biological roles of these fascinating enzymes other than cross-linking. Here, we demonstrate that TG is a necessary component of oxidative stress-induced death signaling in ...
Title: Anti-Atherosclerotic Molecules Targeting Oxidative Stress and Inflammation. VOLUME: 15 ISSUE: 27. Author(s):A. Adameova, Y. J. Xu, T. A. Duhamel, P. S. Tappia, L. Shan and N. S. Dhalla. Affiliation:Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center, 351 Tache Avenue, Winnipeg, Canada R2H 2A6.. Keywords:Atherosclerosis, inflammation, oxidative stress, statins, fibrates, novel anti-atherosclerotic drugs. Abstract: The accumulation of lipids within arteries remains to be the initial impulse for the pathogenesis of atherosclerosis; however, both inflammation and oxidative stress are considered to play a critical role in this process. Several lipid lowering drugs are used as the first line therapy in atherosclerosis; however, different agents have been found to exhibit beneficial effects which are independent of their lipid lowering activity. Both statins and fibrates have been reported to exert anti-inflammatory and anti-oxidative effects in addition to their ...
In this manuscript we have further defined the mechanisms underlying the protective effects of GM-CSF for the alveolar epithelium in the setting of oxidative stress. We found that treatment of AEC in vitro with GM-CSF resulted in increased tolerance of oxidative stress following exposure to hyperoxia or H2O2, manifest as preserved mitochondrial activity and decreased cellular injury and death. Intracellular events associated with this effect included activation of Akt, increased expression of Mcl-1, and phosphorylation of GSK3. Compared with the MLE-12 cell line, primary murine AEC in vitro were more resistant to oxidative injury, and demonstrated constitutive expression of GM-CSF and activation of Akt. Silencing GM-CSF expression in primary AEC increased the vulnerability of these cells to oxidant injury.. A wide variety of insults that lead to acute lung injury involve oxidative stress in the lung, often as a result of endogenously generated reactive oxygen species from inflammatory cells or ...
Title: Oxidative Stress and Antioxidants in Exercise. VOLUME: 8 ISSUE: 7. Author(s):C. Leeuwenburgh and J. W. Heinecke. Affiliation:University of Florida, Biochemistry of Aging Laboratory, College of Health and Human Performance, P.O. Box 118206, Gainesville, FL 32611, USA.. Keywords:Oxidative Stress, Antioxidants, hydrogen peroxide, nitric oxide, Electron Spin Resonance, Gas Chromatography-Mass Spectrometry. Abstract: Increased aerobic metabolism during exercise is a potential source of oxidative stress. In muscle, mitochondria are one important source of reactive intermediates that include superoxide,hydrogen peroxide, and possibly hydroxyl radical . The recent discovery that mitochondria may generate nitric oxide also has implications for oxidant production and mitochondrial function. In this review, we critically examine the concept that production of reactive intermediates increases during exercise. Because the health benefits of regular exercise are well-documented, we also examine ...
M2 peptide is under clinical investigation as a target for universal flu vaccines. Studies have shown that Abs induced by M2 vaccines can provide cross-strain protection against flu A virus challenge. Because of the high level expression of M2 protein on the cell surface of flu virus infected cells and minimal neutralizing activities of M2 Abs in vitro, Ab-mediated cytotoxicity by NK cells has been implicated as a protection mechanism by M2 peptide vaccines. However, the studies were mostly based on the observations using M2 immune sera. Thus, to better understand immune protection mechanisms by M2 vaccines, we generated 4 mAbs. Although all mAbs showed little antiviral activity in vitro, adoptive transfer of 2 of 4 mAbs could confer protection against lethal flu A virus challenge in naïve mice. More importantly, the protection was not affected by depletion of NK cells in mice. Further characterizations revealed that the 2 protective mAbs recognize core epitopes located at the N-terminal 10 ...
Malaria is a significant public health problem in more than 100 countries and causes an estimated 200 million new infections every year. Despite the significant effort to eradicate this dangerous disease, lack of complete knowledge of its physiopathology compromises the success in this enterprise. In this paper we review oxidative stress mechanisms involved in the disease and discuss the potential benefits of antioxidant supplementation as an adjuvant antimalarial strategy.
The generation of ROS induced by oxidative stress is involved in the pathogenesis of neurodegenerative disorders, cancers, and inflammatory diseases. Since excessive oxidative stress induces serious cell damage and finally leads to cell death, the inhibition of excessive oxidative stress may prevent various disorders [31-33]. The role of AR protein in a variety of disorders has been widely investigated. Several studies have shown that expression of AR protein protects against ROS formation and plays an important role as an antioxidant in neuronal cell [9-11]. On the other hand, some studies have demonstrated that inhibition of AR dramatically prevents production of LPS-induced cytokines, and inflammatory mediator proteins in Raw 264.7 cells, suggesting that inhibitors of AR could be used for therapeutic agent in inflammation [34]. Thus, the AR protein shows contradictory effects depending on cell type or disease. Therefore, we examined whether AR protein has a protective effect against oxidative ...
The clinical significance of oxidative stress and its role in hypertension was recently reviewed by Touyz,18 and so the current discussion is limited to the interaction between ET-1, Ang II, and superoxide.. Studies from Ortiz et al have shown that the slow pressor response to Ang II is associated with increases in ET, as well as isoprostanes, a marker of lipid oxidation and an index of oxidative stress.9 These effects could be prevented with bosentan, suggesting a role for ET in mediating the increase in oxidative stress in this model. They went on to demonstrate that antioxidant treatment with the superoxide dismutase mimetic, tempol, or the combination of vitamins C and E reduced Ang II-induced changes in ET expression.14 Acute administration of tempol also has antihypertensive effects in rats chronically infused with Ang II.15 Long-term treatment with tempol will lower arterial pressure in several models of hypertension associated with increases in ET production, including chronic Ang II, ...
The NanoVi Pro™ device works by triggering oxidative response, which is the bodys way of counteracting oxidative stress damage caused by free radicals. While free radicals are generally damaging, the final phase of certain free radicals acts as a signal for oxidative response. The excitation units inside NanoVi™ devices produce the same emission as the final phase of the radical. This mimics a biological process that triggers the bodys response to oxidative stress. Once triggered, oxidative response helps protect against and repair damage. Since the metabolism of oxygen and other factors constantly creates free radicals, strong oxidative response is essential to good health and vitality.. ...
Plants reconfigure their metabolic network under stress conditions. Changes of mitochondrial metabolism such as tricarboxylic acid (TCA) cycle and amino acid metabolism are reported in Arabidopsis roots but the exact molecular basis underlying this remains unknown. We here hypothesise the reassembly of enzyme protein complexes to be a molecular mechanism for metabolic regulation and tried in the present study to find out mitochondrial protein complexes which change their composition under oxidative stress by the combinatorial approach of proteomics and metabolomics. Arabidopsis seedlings were treated with menadione to induce oxidative stress. The inhibition of several TCA cycle enzymes and the oxidised NADPH pool indicated the onset of oxidative stress. In blue native/SDS-PAGE analysis of mitochondrial protein complexes the intensities of 18 spots increased and those of 13 spots decreased in menadione treated samples suggesting these proteins associate with, or dissociate from, protein complexes. Some
Under normal cellular conditions there is a constant balancing act between the creation of reactive oxygen species (ROS) and their elimination by the antioxidant system including enzymes such as superoxide dismutase, glutathione peroxidase, and catalase. Abnormally low levels of ROS can impede cellular signaling and some normal intracellular reactions, while overly high levels of ROS create oxidative stress which can lead to the improper oxidation of lipids, proteins and DNA resulting eventually resulting in apoptosis, necrosis, and other cellular damage.. It has been demonstrated that acute hypoxia induces increased production of ROS in the brain by altering the activity of the cytochrome chain responsible for mitochondrial oxidative phosphorylation. This results in a decrease in ATP synthesis and an increase in ROS while decreasing the activity of the normal cellular antioxidant system. The resulting oxidative stress initiates apoptosis, which contributes significantly to the neuronal cell ...