scholarly journals Long-Term Cd Exposure Alters the Metabolite Profile in Stem Tissue of Medicago sativa

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2707
Author(s):  
Annelie Gutsch ◽  
Sophie Hendrix ◽  
Gea Guerriero ◽  
Jenny Renaut ◽  
Stanley Lutts ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Medicago Sativa ◽  
Stress Responses ◽  
Anthropogenic Activities ◽  
Cellular Damage ◽  
Stem Tissue ◽  
Cd Stress ◽  
Cd Exposure

As a common pollutant, cadmium (Cd) is one of the most toxic heavy metals accumulating in agricultural soils through anthropogenic activities. The uptake of Cd by plants is the main entry route into the human food chain, whilst in plants it elicits oxidative stress by unbalancing the cellular redox status. Medicago sativa was subjected to chronic Cd stress for five months. Targeted and untargeted metabolic analyses were performed. Long-term Cd exposure altered the amino acid composition with levels of asparagine, histidine and proline decreasing in stems but increasing in leaves. This suggests tissue-specific metabolic stress responses, which are often not considered in environmental studies focused on leaves. In stem tissue, profiles of secondary metabolites were clearly separated between control and Cd-exposed plants. Fifty-one secondary metabolites were identified that changed significantly upon Cd exposure, of which the majority are (iso)flavonoid conjugates. Cadmium exposure stimulated the phenylpropanoid pathway that led to the accumulation of secondary metabolites in stems rather than cell wall lignification. Those metabolites are antioxidants mitigating oxidative stress and preventing cellular damage. By an adequate adjustment of its metabolic composition, M. sativa reaches a new steady state, which enables the plant to acclimate under chronic Cd stress.

scholarly journals Impairment between Oxidant and Antioxidant Systems: Short- and Long-term Implications for Athletes’ Health

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1353 ◽  
Author(s):  
Cristina Nocella ◽  
Vittoria Cammisotto ◽  
Fabio Pigozzi ◽  
Paolo Borrione ◽  
Chiara Fossati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Physical Activity ◽  
Exercise Training ◽  
Muscle Damage ◽  
Neurological Diseases ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Oxidative Balance

The role of oxidative stress, an imbalance between reactive oxygen species production (ROS) and antioxidants, has been described in several patho-physiological conditions, including cardiovascular, neurological diseases and cancer, thus impacting on individuals’ lifelong health. Diet, environmental pollution, and physical activity can play a significant role in the oxidative balance of an organism. Even if physical training has proved to be able to counteract the negative effects caused by free radicals and to provide many health benefits, it is also known that intensive physical activity induces oxidative stress, inflammation, and free radical-mediated muscle damage. Indeed, variations in type, intensity, and duration of exercise training can activate different patterns of oxidant–antioxidant balance leading to different responses in terms of molecular and cellular damage. The aim of the present review is to discuss (1) the role of oxidative status in athletes in relation to exercise training practice, (2) the implications for muscle damage, (3) the long-term effect for neurodegenerative disease manifestations, (4) the role of antioxidant supplementations in preventing oxidative damages.

scholarly journals Cloning, Functional Characterization and Response to Cadmium Stress of the Thioredoxin-like Protein 1 Gene from Phascolosoma esculenta

2021 ◽  
Vol 23 (1) ◽  
pp. 332
Author(s):  
Jiajie Meng ◽  
Xinming Gao ◽  
Shengyu Luo ◽  
Chenwen Lin ◽  
Chen Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Functional Characterization ◽  
Radical Scavenging ◽  
Cadmium Stress ◽  
Coelomic Fluid ◽  
Molecular Response ◽  
Cd Stress ◽  
Phylogenetic Tree Analysis ◽  
Multiple Sequence ◽  
Cd Exposure

Cadmium (Cd) is a heavy metal toxicant and is widely distributed in aquatic environments. It can cause excessive production of reactive oxygen species (ROS) in the organism, which in turn leads to a series of oxidative damages. Thioredoxin (Trx), a highly conserved disulfide reductase, plays an important role in maintaining the intracellular redox homeostasis in eukaryotes and prokaryotes. Phascolosoma esculenta is an edible marine worm, an invertebrate that is extensively found on the mudflats of coastal China. To explore the molecular response of Trx in mudflat organisms under Cd stress, we identified a new Trx isoform (Trx-like protein 1 gene) from P. esculenta for the first time, designated as PeTrxl. Molecular and structural characterization, as well as multiple sequence and phylogenetic tree analysis, demonstrated that PeTrxl belongs to the Trx superfamily. PeTrxl transcripts were found to be ubiquitous in all tissues, and the highest expression level occurred in the coelomic fluid. Exposure to three sublethal concentrations of Cd resulted in the upregulation and then downregulation of PeTrxl expression levels over time in coelomic fluid of P. esculenta. The significant elevation of PeTrxl expression after 12 and 24 h of Cd exposure at 6 and 96 mg/L, respectively, might reflect its important role in the resistance to Cd stress. Recombinant PeTrxl (rPeTrxl) showed prominent dose-dependent insulin-reducing and ABTS free radical-scavenging abilities. After exposure to 96 mg/L Cd for 24 h, the ROS level increased significantly in the coelomic fluid, suggesting that Cd induced oxidative stress in P. esculenta. Furthermore, the injection of rPeTrxl during Cd exposure significantly reduced the ROS in the coelomic fluid. Our data suggest that PeTrxl has significant antioxidant capacity and can protect P. esculenta from Cd-induced oxidative stress.

scholarly journals Persistent Oxidative Stress and Inflammasome Activation in CD14highCD16− Monocytes From COVID-19 Patients

2022 ◽  
Vol 12 ◽  
Author(s):  
Silvia Lucena Lage ◽  
Eduardo Pinheiro Amaral ◽  
Kerry L. Hilligan ◽  
Elizabeth Laidlaw ◽  
Adam Rupert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Stress Responses ◽  
Inflammasome Activation ◽  
Strongly Correlated ◽  
Long Term Outcomes ◽  
Caspase 1 ◽  
Mitochondrial Superoxide

The poor outcome of the coronavirus disease-2019 (COVID-19), caused by SARS-CoV-2, is associated with systemic hyperinflammatory response and immunopathology. Although inflammasome and oxidative stress have independently been implicated in COVID-19, it is poorly understood whether these two pathways cooperatively contribute to disease severity. Herein, we found an enrichment of CD14highCD16− monocytes displaying inflammasome activation evidenced by caspase-1/ASC-speck formation in severe COVID-19 patients when compared to mild ones and healthy controls, respectively. Those cells also showed aberrant levels of mitochondrial superoxide and lipid peroxidation, both hallmarks of the oxidative stress response, which strongly correlated with caspase-1 activity. In addition, we found that NLRP3 inflammasome-derived IL-1β secretion by SARS-CoV-2-exposed monocytes in vitro was partially dependent on lipid peroxidation. Importantly, altered inflammasome and stress responses persisted after short-term patient recovery. Collectively, our findings suggest oxidative stress/NLRP3 signaling pathway as a potential target for host-directed therapy to mitigate early COVID-19 hyperinflammation and also its long-term outcomes.

scholarly journals Persistent oxidative stress and inflammasome activation in CD14highCD16- monocytes from COVID-19 patients

2021 ◽  
Author(s):  
Silvia Lucena Lage ◽  
Eduardo Pinheiro Amaral ◽  
kerry L. Hilligan ◽  
Elizabeth Laidlaw ◽  
Adam Rupert ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Stress Responses ◽  
Inflammasome Activation ◽  
Strongly Correlated ◽  
Long Term Outcomes ◽  
Caspase 1 ◽  
Mitochondrial Superoxide

The poor outcome of the coronavirus disease-2019 (COVID-19), caused by SARS-CoV-2, is associated with systemic hyperinflammatory response and immunopathology. Although inflammasome and oxidative stress have independently been implicated in COVID-19, it is poorly understood whether these two pathways cooperatively contribute to disease severity. Herein, we found an enrichment of CD14highCD16- monocytes displaying inflammasome activation evidenced by caspase-1/ASC-speck formation in severe COVID-19 patients when compared to mild ones and healthy controls, respectively. Those cells also showed aberrant levels of mitochondrial superoxide (MitoSOX) and lipid peroxidation, both hallmarks of the oxidative stress response, which strongly correlated with caspase-1 activity. In addition, we found that NLRP3 inflammasome-derived IL-1β secretion by SARS-CoV-2-exposed monocytes in vitro was partially dependent on lipid peroxidation. Importantly, altered inflammasome and stress responses persisted after short-term patient recovery. Collectively, our findings suggest oxidative stress/NLRP3 signaling pathway as a potential target for host-directed therapy to mitigate early COVID-19 hyperinflammation as well as its long-term outcomes.

scholarly journals Oxidative Stress: A Double Edged Sword

BioSight ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 4-12
Author(s):  
Kausar Abbas ◽  
Ufaque Batool ◽  
Abdul Shakoor Memon ◽  
Sana Soomro
Keyword(s):  
Oxidative Stress ◽  
Human Health ◽  
Stress Responses ◽  
Structural Defects ◽  
Radical Species ◽  
Biological Stress ◽  
Nutrition Deficiency ◽  
Harmful Effects ◽  
Aging Factor

Oxidative stress (OS) in simple words is defined as a state of imbalance between antioxidant and pro-oxidants defenses. The purpose of this article is to find out the connection of oxidative stress and free radical species with different aspects of human health. Owing to its harmful effects on proteins and nucleic acids, oxidative stress causes chronic diseases such as cardiovascular and neurodegenerative diseases, diabetes and cancer. It highlights the impacts of antioxidants and pro-oxidants particularly on fertility and infertility. It also focuses on the adverse effects caused by the long-term exposure to pro-oxidant factors leading to structural defects of mitochondrial DNA. As modern life style consists of more reliance on the processed foods and lack of physical activity, a nutrition deficiency, which is common in the present lifestyle, is also one of the reasons for oxidative stress to cause inflammation. However, this review also focuses on how diet affects and triggers inflammation. Redox mechanism with potential threats to health of mankind is discussed, how mere stress can provoke biological stress responses leading to development of disease or metabolic errors. Methods for reduction of oxidative stress are discussed in this review. It also highlights mitochondria as an aging factor as many ROS, particularly mitochondria ROS contribute directly to aging in human body. We will be discussing the recent findings in the oxidative stress field and its negative and positive impacts on human health.

Biomarkers Associated with Atrial Fibrosis and Remodeling

2019 ◽  
Vol 26 (5) ◽  
pp. 780-802 ◽  
Author(s):  
Polychronis Dilaveris ◽  
Christos-Konstantinos Antoniou ◽  
Panagiota Manolakou ◽  
Eleftherios Tsiamis ◽  
Konstantinos Gatzoulis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Atrial Fibrillation ◽  
Stress Responses ◽  
Volume Overload ◽  
Current Evidence ◽  
Electrical Remodeling ◽  
Atrial Remodeling ◽  
Atrial Fibrosis ◽  
Oxidative Stress Responses

Atrial fibrillation is the most common rhythm disturbance encountered in clinical practice. Although often considered as solely arrhythmic in nature, current evidence has established that atrial myopathy constitutes both the substrate and the outcome of atrial fibrillation, thus initiating a vicious, self-perpetuating cycle. This myopathy is triggered by stress-induced (including pressure/volume overload, inflammation, oxidative stress) responses of atrial tissue, which in the long term become maladaptive, and combine elements of both structural, especially fibrosis, and electrical remodeling, with contemporary approaches yielding potentially useful biomarkers of these processes. Biomarker value becomes greater given the fact that they can both predict atrial fibrillation occurrence and treatment outcome. This mini-review will focus on the biomarkers of atrial remodeling (both electrical and structural) and fibrosis that have been validated in human studies, including biochemical, histological and imaging approaches.

scholarly journals Nucleoredoxin guards against oxidative stress by protecting antioxidant enzymes

2017 ◽  
Vol 114 (31) ◽  
pp. 8414-8419 ◽  
Author(s):  
Sophie Kneeshaw ◽  
Rumana Keyani ◽  
Valérie Delorme-Hinoux ◽  
Lisa Imrie ◽  
Gary J. Loake ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Oxygen Species ◽  
Optimal Activity ◽  
Substrate Interaction ◽  
Wide Range ◽  
Scavenging Enzymes ◽  
Reduced State

Cellular accumulation of reactive oxygen species (ROS) is associated with a wide range of developmental and stress responses. Although cells have evolved to use ROS as signaling molecules, their chemically reactive nature also poses a threat. Antioxidant systems are required to detoxify ROS and prevent cellular damage, but little is known about how these systems manage to function in hostile, ROS-rich environments. Here we show that during oxidative stress in plant cells, the pathogen-inducible oxidoreductase Nucleoredoxin 1 (NRX1) targets enzymes of major hydrogen peroxide (H2O2)-scavenging pathways, including catalases. Mutant nrx1 plants displayed reduced catalase activity and were hypersensitive to oxidative stress. Remarkably, catalase was maintained in a reduced state by substrate-interaction with NRX1, a process necessary for its H2O2-scavenging activity. These data suggest that unexpectedly H2O2-scavenging enzymes experience oxidative distress in ROS-rich environments and require reductive protection from NRX1 for optimal activity.

scholarly journals Changes in the Proteome of Medicago sativa Leaves in Response to Long-Term Cadmium Exposure Using a Cell-Wall Targeted Approach

2018 ◽  
Vol 19 (9) ◽  
pp. 2498 ◽  
Author(s):  
Annelie Gutsch ◽  
Salha Zouaghi ◽  
Jenny Renaut ◽  
Ann Cuypers ◽  
Jean-Francois Hausman ◽  
...  
Keyword(s):  
Cell Wall ◽  
Medicago Sativa ◽  
Protein Identification ◽  
Molecular Mechanisms ◽  
Time Of Flight ◽  
Cell Wall Protein ◽  
Wall Structure ◽  
Cd Exposure ◽  
Targeted Approach

Accumulation of cadmium (Cd) shows a serious problem for the environment and poses a threat to plants. Plants employing various cellular and molecular mechanisms to limit Cd toxicity and alterations of the cell wall structure were observed upon Cd exposure. This study focuses on changes in the cell wall protein-enriched subproteome of alfalfa (Medicago sativa) leaves during long-term Cd exposure. Plants grew on Cd-contaminated soil (10 mg/kg dry weight (DW)) for an entire season. A targeted approach was used to sequentially extract cell wall protein-enriched fractions from the leaves and quantitative analyses were conducted with two-dimensional difference gel electrophoresis (2D DIGE) followed by protein identification with matrix-assisted laser desorption/ionization (MALDI) time-of-flight/time of flight (TOF/TOF) mass spectrometry. In 212 spots that showed a significant change in intensity upon Cd exposure a single protein was identified. Of these, 163 proteins are predicted to be secreted and involved in various physiological processes. Proteins of other subcellular localization were mainly chloroplastic and decreased in response to Cd, which confirms the Cd-induced disturbance of the photosynthesis. The observed changes indicate an active defence response against a Cd-induced oxidative burst and a restructuring of the cell wall, which is, however, different to what is observed in M. sativa stems and will be discussed.

scholarly journals Characterization of Stress Responses in a Drosophila Model of Werner Syndrome

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1868
Author(s):  
Derek G. Epiney ◽  
Charlotte Salameh ◽  
Deirdre Cassidy ◽  
Luhan T. Zhou ◽  
Joshua Kruithof ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Stress Responses ◽  
Werner Syndrome ◽  
Stress Sensitivity ◽  
Cellular Damage ◽  
Age Related ◽  
Increased Risk ◽  
Early Aging ◽  
Risk Of Cancer

As organisms age, their resistance to stress decreases while their risk of disease increases. This can be shown in patients with Werner syndrome (WS), which is a genetic disease characterized by accelerated aging along with increased risk of cancer and metabolic disease. WS is caused by mutations in WRN, a gene involved in DNA replication and repair. Recent research has shown that WRN mutations contribute to multiple hallmarks of aging including genomic instability, telomere attrition, and mitochondrial dysfunction. However, questions remain regarding the onset and effect of stress on early aging. We used a fly model of WS (WRNexoΔ) to investigate stress response during different life stages and found that stress sensitivity varies according to age and stressor. While larvae and young WRNexoΔ adults are not sensitive to exogenous oxidative stress, high antioxidant activity suggests high levels of endogenous oxidative stress. WRNexoΔ adults are sensitive to stress caused by elevated temperature and starvation suggesting abnormalities in energy storage and a possible link to metabolic dysfunction in WS patients. We also observed higher levels of sleep in aged WRNexoΔ adults suggesting an additional adaptive mechanism to protect against age-related stress. We suggest that stress response in WRNexoΔ is multifaceted and evokes a systemic physiological response to protect against cellular damage. These data further validate WRNexoΔ flies as a WS model with which to study mechanisms of early aging and provide a foundation for development of treatments for WS and similar diseases.

Sign in / Sign up

Export Citation Format

Share Document