Mechanical ventilation promotes redox status alterations in the diaphragm

2006 ◽  
Vol 101 (4) ◽  
pp. 1017-1024 ◽  
Author(s):  
D. J. Falk ◽  
K. C. DeRuisseau ◽  
D. L. Van Gammeren ◽  
M. A. Deering ◽  
A. N. Kavazis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Superoxide Dismutase ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Diaphragm Muscle ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Oxidant Production ◽  
The Impact

Oxidative stress is an important mediator of diaphragm muscle atrophy and contractile dysfunction during prolonged periods of controlled mechanical ventilation (MV). To date, specific details related to the impact of MV on diaphragmatic redox status remain unknown. To fill this void, we tested the hypothesis that MV-induced diaphragmatic oxidative stress is the consequence of both an elevation in intracellular oxidant production in conjunction with a decrease in the antioxidant buffering capacity. Adult rats were assigned to one of two experimental groups: 1) control or 2) 12 h of MV. Compared with controls, diaphragms from MV animals demonstrated increased oxidant production, diminished total antioxidant capacity, and decreased glutathione levels. Heme oxygenase-1 (HO-1) mRNA and protein levels increased (23.0- and 5.1-fold, respectively) following MV. Thioredoxin reductase-1 and manganese superoxide dismutase mRNA levels were also increased in the diaphragm following MV (2.4- and 1.6-fold, respectively), although no change was detected in the levels of either protein. Furthermore, copper-zinc superoxide dismutase and glutathione peroxidase mRNA were not altered following MV, although protein content decreased −1.3- and −1.7-fold, respectively. We conclude that MV promotes increased oxidant production and impairment of key antioxidant defenses in the diaphragm; collectively, these changes contribute to the MV-induced oxidative stress in this key inspiratory muscle.

Dietary Salvia hispanica L. reduces cardiac oxidative stress of dyslipidemic insulin-resistant rats

2020 ◽  
Vol 45 (7) ◽  
pp. 761-768 ◽  
Author(s):  
Agustina Creus ◽  
Adriana Chicco ◽  
Silvina M. Álvarez ◽  
María S. Giménez ◽  
Yolanda Bolzón de Lombardo
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Defenses ◽  
Related Factor ◽  
Mrna Levels ◽  
Salvia Hispanica ◽  
Insulin Resistant ◽  
Beneficial Effects ◽  
Chia Seed ◽  
Salvia Hispanica L

Salvia hispanica L., commonly known as chia seed, has beneficial effects upon some signs of metabolic syndrome (MS), such as dyslipidemia and insulin resistance. However, its action on cardiac oxidative stress associated with MS remains unknown. The goal of this study was to analyze the possible beneficial effects of chia seed (variety Salba) upon the oxidative stress of left ventricle heart muscle (LV) of a well-established dyslipidemic insulin-resistant rat model induced by feeding them a sucrose-rich diet (SRD). Male Wistar rats received an SRD for 3 months. After that, for 3 additional months, half of the animals continued with the SRD, while the other half received the SRD containing chia as the source of dietary fat instead corn oil (SRD+chia). In the LV of SRD-fed rats, chia seed improved/reverted the depleted activity of antioxidant enzymes glutathione peroxidase, superoxide dismutase (SOD), and catalase, and ameliorated manganese superoxide dismutase messenger RNA (mRNA) levels increasing the expression of the nuclear factor erythroid 2-related factor 2 (Nrf2). Improved the glutathione redox estate, reactive oxygen species, and thiobarbituric acid reactive substances contents normalizing the p47NOX subunit mRNA level. Furthermore, chia normalized hypertension and plasma levels of pro-inflammatory cytokines and oxidative stress biomarkers. The findings show that chia seed intake impacts positively upon oxidative imbalance of LV of dyslipidemic insulin-resistant rats. Novelty Healthy effects of chia seed involve an improvement of cardiac antioxidant defenses through Nrf2 induction. Chia seed intake reduces cardiac oxidative stress markers of dyslipidemic insulin-resistant rats. Dietary chia seed restores cardiac unbalanced redox state of dyslipidemic insulin-resistant rats.

Increased Superoxide Levels, HO-1 and Fyn Protein Expression in Bcr/abl Overexpressing Cells: Implications for Adaptation and Survival in an Oxidatively Challenging Environment.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4403-4403
Author(s):  
Joya Chandra ◽  
Kechen Ban
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Disease Progression ◽  
Mapk Pathway ◽  
Antioxidant Properties ◽  
Antioxidant Defenses ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Ros Production ◽  
Challenging Environment

Abstract The bcr/abl oncogene is present in the majority of CML and in a subset of ALL patients. In addition to anti-apoptotic properties, proliferative advantages and growth factor independence, the presence of the Bcr/abl kinase raises intracellular levels of reactive oxygen species (ROS). Increased ROS in CML have been linked to DNA damage and DNA repair deficiencies with implications for promoting genomic instability and secondary mutations associated with disease progression. Here we show that superoxide is the specific ROS entity that is elevated when Bcr/abl is overexpressed in an IL-3 dependent pre-B cell line, BaF3. Strikingly, treatment with classical oxidants, such as hydrogen peroxide or tert-butyl peroxide, demonstrated an inherent resistance to oxidative stress induced apoptosis in Bcr/abl-containing cells, suggesting that antioxidant defenses activated by Bcr/abl as a response to the increased endogenous ROS production may promote survival in Bcr/abl positive populations. In an effort to characterize the redox environment in Bcr/abl containing cells, we examined several antioxidant enzymes that are known downstream substrates of c-abl or bcr/abl, including peroxiredoxin, catalase and heme oxygenase-1 (HO-1). Of these, HO-1 protein expression was three fold higher in Bcr/abl transductants, consistent with a reported role for HO-1 as a Bcr/abl dependent survival factor. Interestingly, the Src family kinase, Fyn, which can be activated by oxidative stress, was increased four fold in Bcr/abl overexpressing cells. This is consistent with reported microarray data in which fyn mRNA levels are higher in Philadelphia positive leukemias than non-Philapdelphia positive leukemias. Other components of ROS responsive signaling pathways were also interrogated including the Mapk pathway and Akt pathway, with no difference noted between parental and Bcr/abl overexpressing cells. Our data suggest a relationship between Bcr/abl-induced superoxide elevation, resistance to oxidative stress, elevation of HO-1 (which has antioxidant properties) and elevated Fyn (a putative downstream target for ROS production). These redox alterations and their consequences may equip Bcr/abl positive cells with a survival and/or proliferative advantage in an oxidatively challenging environment, thus promoting disease progression and blast crisis.

scholarly journals Evidence Around the Impact of Pulmonary Rehabilitation and Exercise on Redox Status in COPD: A Systematic Review

2021 ◽  
Vol 3 ◽  
Author(s):  
Alastair Watson ◽  
Tom M. A. Wilkinson ◽  
Anna Freeman
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Pulmonary Rehabilitation ◽  
Redox Status ◽  
Risk Of Bias ◽  
Antioxidant Defenses ◽  
Current Evidence ◽  
High Quality ◽  
Exercise Interventions ◽  
The Impact

Introduction: Oxidative stress is increasingly recognized as a significant factor in the pathogenesis of chronic obstructive pulmonary disease (COPD). Pulmonary rehabilitation, a major component of which is prescribed exercise, is essential in COPD care. Regular exercise has been proposed to increase antioxidant defenses and overall enhance the ability of the body to counteract oxidative stress. However, the mechanisms through which it improves COPD outcomes remain unclear.Objectives: We aimed to appraise the current evidence around the impact of pulmonary rehabilitation on redox status, compared with other exercise interventions, to gain an understanding of optimal exercise interventions to modify this pathophysiological mechanism.Methods: We performed a systematic review through searching CENTRAL, MEDLINE, PubMed, Scopus, and Web of Science. Results were independently reviewed and relevant studies were selected by two independent assessors. Studies were assessed by two independent people using the modified RoB 2 tool and discrepancies were resolved through discussion.Results: We identified 1,710 records and 1,117 records after duplicate removal. Six studies were included in the final analysis. The evidence available was low quality and four studies had high risk of bias and two studies had unclear risk of bias. Studies were small (15–56 participants); only two included details of randomization and patient cohorts were of varying ages and poorly described. Differences in smoking status and previous exercise levels, which are known to impact redox status, were not well documented. Studies were not standardized and used different exercise doses and measured different outcomes. One study reported lower malondialdehyde levels, a marker of lipid peroxidation, after pulmonary rehabilitation, compared with control. However, one study saw no difference following whole-body vibration training and another study showed higher malondialdehyde levels following supervised modified arm swing exercise compared with control.Conclusion: Understanding the impact of exercise on oxidative stress in COPD could lead to tailored exercise programs and modification of pathological mechanisms. However, we identify a lack of high-quality evidence to determine this. Larger, standardized, and high quality randomized controlled trials (RCTs) are essential, which use carefully clinically characterized and controlled cohorts to determine the relative impact of different exercise interventions on redox status to guide COPD management. We propose an idealized RCT design, which could be used to try and meet this need.

Assessment of Superoxide Dismutase and Catalase Evolution in Different Stages of an Experimental Endometriosis

2017 ◽  
Vol 68 (6) ◽  
pp. 1381-1383
Author(s):  
Allia Sindilar ◽  
Carmen Lacramioara Zamfir ◽  
Eusebiu Viorel Sindilar ◽  
Alin Constantin Pinzariu ◽  
Eduard Crauciuc ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Reproductive Function ◽  
Female Rats ◽  
Oxygen Species ◽  
Efficient Treatment ◽  
Endometrial Cells ◽  
Gynecological Disorder ◽  
The Impact

Endometriosis is described as a gynecological disorder characterized by the presence of endometrial tissue outside the uterus; extensively explored because of its increasing incidency, with an indubitable diagnostic only after invasive surgery, with no efficient treatment, it has still many aspects to be elucidated. A growing body of facts sustain oxidative stress as a crucial factor between the numerous incriminated factors implicated in endometriosis ethiopathogeny. Reactive oxygen species(ROS) act to decline reproductive function. Our study intends to determine if an experimental model of endometriosis may be useful to assess the impact of oxidative stress on endometrial cells; we have used a murine model of 18 adult Wistar female rats. A fragment from their left uterine horn was implanted in the abdominal wall. After 4 weeks, a laparatomy was performed, 5 endometrial implants were removed, followed by biochemical tissue assay of superoxide dismutase(SOD) and catalase(CAT). At the end of the experiment, the rats were sacrificed, the implants were removed for histopathological exam and biochemical assay of antioxidant enzymes. The results revealed decreased levels of antioxidant enzymes, pointing on significant oxidative stress involvement.

scholarly journals Effect of Bacillus spp. and Brevibacillus sp. on the Photosynthesis and Redox Status of Solanum lycopersicum

Horticulturae ◽  
2021 ◽  
Vol 7 (2) ◽  
pp. 24
Author(s):  
Marino Costa-Santos ◽  
Nuno Mariz-Ponte ◽  
Maria Celeste Dias ◽  
Luísa Moura ◽  
Guilhermina Marques ◽  
...  
Keyword(s):  
Solanum Lycopersicum ◽  
Intercellular Co2 Concentration ◽  
Redox Status ◽  
Antioxidant Defenses ◽  
Photosynthetic Parameters ◽  
Plant Growth Promoting Bacteria ◽  
Potted Plants ◽  
Chlorophylls A And B ◽  
Bacillus Spp ◽  
The Impact

Plant-growth-promoting bacteria (PGPB) are gaining attention as a sustainable alternative to current agrochemicals. This study evaluated the impact of three Bacillus spp. (5PB1, 1PB1, FV46) and one Brevibacillus sp. (C9F) on the important crop tomato (Solanum lycopersicum) using the model cv. ‘MicroTom’. The effects of these isolates were assessed on (a) seedlings’ growth and vigor, and (b) adult potted plants. In potted plants, several photosynthetic parameters (chlorophylls (a and b), carotenoids and anthocyanins contents, transpiration rate, stomatal conductance, net CO2 photosynthetic rate, and intercellular CO2 concentration, and on chlorophyll fluorescence yields of light- and dark-adapted leaves)), as well as soluble sugars and starch contents, were quantified. Additionally, the effects on redox status were evaluated. While the growth of seedlings was, overall, not influenced by the strains, some effects were observed on adult plants. The Bacillus safensis FV46 stimulated the content of pigments, compared to C9F. Bacillus zhangzhouensis 5PB1 increased starch levels and was positively correlated with some parameters of the photophosphorylation and the gas exchange phases. Interestingly, Bacillus megaterium 1PB1 decreased superoxide (O2−) content, and B. safensis FV46 promoted non-enzymatic antioxidant defenses, increasing total phenol content levels. These results, conducted on a model cultivar, support the theory that these isolates differently act on tomato plant physiology, and that their activity depends on the age of the plant, and may differently influence photosynthesis. It would now be interesting to analyze the influence of these bacteria using commercial cultivars.

scholarly journals Imaging NAD(H) Redox Alterations in Cryopreserved Alveolar Macrophages from Ozone-Exposed Mice and the Impact of Nutrient Starvation during Long Lag Times

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 767
Author(s):  
He N. Xu ◽  
Joanna Floros ◽  
Lin Z. Li ◽  
Shaili Amatya
Keyword(s):  
Oxidative Stress ◽  
Alveolar Macrophages ◽  
Redox State ◽  
Redox Status ◽  
Nutrient Starvation ◽  
Ozone Exposure ◽  
Reduced Form ◽  
Time Period ◽  
Lag Times ◽  
The Impact

Employing the optical redox imaging technique, we previously identified a significant redox shift of nicotinamide adenine dinucleotide (NAD and the reduced form NADH) in freshly isolated alveolar macrophages (AM) from ozone-exposed mice. The goal here was twofold: (a) to determine the NAD(H) redox shift in cryopreserved AM isolated from ozone-exposed mice and (b) to investigate whether there is a difference in the redox status between cryopreserved and freshly isolated AM. We found: (i) AM from ozone-exposed mice were in a more oxidized redox state compared to that from filtered air (FA)-exposed mice, consistent with the results obtained from freshly isolated mouse AM; (ii) under FA exposure, there was no significant NAD(H) redox difference between fresh AM that had been placed on ice for 2.5 h and cryopreserved AM; however, under ozone exposure, fresh AM were more oxidized than cryopreserved AM; (iii) via the use of nutrient starvation and replenishment and H2O2-induced oxidative stress of an AM cell line, we showed that this redox difference between cryopreserved and freshly isolated AM is likely the result of the double “hit”, i.e., the ozone-induced oxidative stress plus nutrient starvation that prevented freshly isolated AM from a full recovery after being on ice for a prolonged time period. The cryopreservation technique we developed eliminates/minimizes the effects of oxidative stress and nutrient starvation on cells. This method can be adopted to preserve lung macrophages from animal models or clinical patients for further investigations.

scholarly journals Sesamin Modulates Tyrosine Hydroxylase, Superoxide Dismutase, Catalase, Inducible No Synthase and Interleukin-6 Expression in Dopaminergic Cells Under Mpp+-Induced Oxidative Stress

2008 ◽  
Vol 1 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Vicky Lahaie-Collins ◽  
Julie Bournival ◽  
Marilyn Plouffe ◽  
Julie Carange ◽  
Maria-Grazia Martinoli
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Tyrosine Hydroxylase ◽  
Protein Expression ◽  
Pc12 Cells ◽  
Interleukin 6 ◽  
Estrogen Receptor Alpha ◽  
Strong Increase ◽  
Mrna Levels ◽  
Neuronal Pc12 Cells

Oxidative stress is regarded as a mediator of nerve cell death in several neurodegenerative disorders, such as Parkinson's disease. Sesamin, a lignan mainly found in sesame oil, is currently under study for its anti-oxidative and possible neuroprotective properties. We used 1-methyl-4-phenyl-pyridine (MPP+) ion, the active metabolite of the potent parkinsonism-causing toxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine, to produce oxidative stress and neurodegeneration in neuronal PC12 cells, which express dopamine, as well as neurofilaments. Our results show that picomolar doses of sesamin protected neuronal PC12 cells from MPP+-induced cellular death, as revealed by colorimetric measurements and production of reactive oxygen species. We also demonstrated that sesamin acted by rescuing tyrosine hydroxylase levels from MPP+-induced depletion. Sesamin, however, did not modulate dopamine transporter levels, and estrogen receptor-alpha and -beta protein expression. By examining several parameters of cell distress, we found that sesamin also elicited a strong increase in superoxide dismutase activity as well as protein expression and decreased catalase activity and the MPP+stimulated inducible nitric oxide synthase protein expression, in neuronal PC12 cells. Finally, sesamin possessed significant anti-inflammatory properties, as disclosed by its potential to reduce MPP+-induced interleukin-6 mRNA levels in microglia. From these studies, we determined the importance of the lignan sesamin as a neuroprotective molecule and its possible role in complementary and/or preventive therapies of neurodegenerative diseases.

The Impact of Concomitant Chronic Pancreatitis on Prooxidant-antioxidant Status and Other Conditions in Osteoarthritis

2016 ◽  
pp. 75-78
Author(s):  
Liliia Babynets ◽  
Tetiana Maevska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Chronic Pancreatitis ◽  
Functional Capacity ◽  
Antioxidant Status ◽  
Activation Parameters ◽  
Tissue Destruction ◽  
The Impact ◽  
Stress Accumulation

The study proved that patients with combined progress of osteoarthritis and chronic pancreatitis have reliable top-level activation of lipid peroxidation in terms of malonyc aldehyde and tissue destruction in terms of oxyproline, weakening of the antioxidant level (in terms of superoxide dismutase and SH-groups) and activation parameters of catalase and ceruloplasmin (p<0,05). The authentic predictority of patients biological age, duration of combined clinical courses, the functional capacity of the pancreas in terms of fecal α-elastase, structural state by ultrasound criteria for progression effects of oxidative stress, accumulation oxyproline activation parameters catalase and ceruloplasmin, which statistically was reflected by the presence of mainly moderate of significant correlations between these groups of indicators have been identified.

scholarly journals Ventilator-induced diaphragm dysfunction in critical illness

2018 ◽  
Vol 243 (17-18) ◽  
pp. 1331-1339 ◽  
Author(s):  
Yung-Yang Liu ◽  
Li-Fu Li
Keyword(s):  
Oxidative Stress ◽  
Mechanical Ventilation ◽  
Muscle Atrophy ◽  
Structural Damage ◽  
Molecular Mechanisms ◽  
Substantial Reduction ◽  
Mechanical Stretch ◽  
Janus Kinase ◽  
Diaphragm Muscle ◽  
Diaphragm Dysfunction

Mechanical ventilation is an essential intervention for intensive care unit patients with acute lung injury. However, the use of controlled mechanical ventilation in both animal and human models causes ventilator-induced diaphragm dysfunction, wherein a substantial reduction in diaphragmatic force-generating capacity occurs, along with structural injury and atrophy of diaphragm muscle fibers. Although diaphragm dysfunction, noted in most mechanically ventilated patients, is correlated with poor clinical outcome, the specific pathophysiology underlying ventilator-induced diaphragm dysfunction requires further elucidation. Numerous factors may underlie this condition in humans as well as animals, such as increased oxidative stress, calcium-activated calpain and caspase-3, the ubiquitin–proteasome system, autophagy–lysosomal pathway, and proapoptotic proteins. All these alter protein synthesis and degradation, thus resulting in muscle atrophy and impaired contractility and compromising oxidative phosphorylation and upregulating glycolysis associated with impaired mitochondrial function. Furthermore, infection combined with mechanical stretch may induce multisystem organ failure and render the diaphragm more sensitive to ventilator-induced diaphragm dysfunction. Herein, several major cellular mechanisms associated with autophagy, apoptosis, and mitochondrial biogenesis—including toll-like receptor 4, nuclear factor-κB, Src, class O of forkhead box, signal transducer and activator of transcription 3, and Janus kinase—are reviewed. In addition, we discuss the potential therapeutic strategies used to ameliorate ventilator-induced diaphragm dysfunction and thus prevent delay in the management of patients under prolonged duration of mechanical ventilation. Impact statement Mechanical ventilation (MV) is life-saving for patients with acute respiratory failure but also causes difficult liberation of patients from ventilator due to rapid decrease of diaphragm muscle endurance and strength, which is termed ventilator-induced diaphragmatic damage (VIDD). Numerous studies have revealed that VIDD could increase extubation failure, ICU stay, ICU mortality, and healthcare expenditures. However, the mechanisms of VIDD, potentially involving a multistep process including muscle atrophy, oxidative loads, structural damage, and muscle fiber remodeling, are not fully elucidated. Further research is necessary to unravel mechanistic framework for understanding the molecular mechanisms underlying VIDD, especially mitochondrial dysfunction and increased mitochondrial oxidative stress, and develop better MV strategies, rehabilitative programs, and pharmacologic agents to translate this knowledge into clinical benefits.

scholarly journals Mineral Micronutrients in Asthma

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4001
Author(s):  
Dominika Zajac
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Air Pollution ◽  
Defense Mechanisms ◽  
Redox Status ◽  
Chronic Inflammatory Disease ◽  
Modern World ◽  
Medical Issues ◽  
Persistent Inflammation ◽  
The Impact

Asthma represents one of the most common medical issues in the modern world. It is a chronic inflammatory disease characterized by persistent inflammation of the airways and disturbances in redox status, leading to hyperresponsiveness of bronchi and airway obstruction. Apart from classical risk factors such as air pollution, family history, allergies, or obesity, disturbances of the levels of micronutrients lead to impairments in the defense mechanisms of the affected organism against oxidative stress and proinflammatory stimuli. In the present review, the impact of micronutrients on the prevalence, severity, and possible risk factors of asthma is discussed. Although the influence of classical micronutrients such as selenium, copper, or zinc are well known, the effects of those such as iodine or manganese are only rarely mentioned. As a consequence, the aim of this paper is to demonstrate how disturbances in the levels of micronutrients and their supplementation might affect the course of asthma.

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