scholarly journals The Type and Source of Reactive Oxygen Species Influences the Outcome of Oxidative Stress in Cultured Cells

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1075
Author(s):  
Steffi Goffart ◽  
Petra Tikkanen ◽  
Craig Michell ◽  
Trevor Wilson ◽  
Jaakko L. O. Pohjoismäki
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Cultured Cells ◽  
Cellular Processes ◽  
Different Types ◽  
Measured Effect ◽  
Experimental Approaches ◽  
Different Sources

Oxidative stress can be modeled using various different experimental approaches, such as exposing the cells or organisms to oxidative chemicals. However, the actual effects of these chemicals, outside of the immediate measured effect, have attracted relatively little attention. We show here that three commonly used oxidants, menadione, potassium bromate, and hydrogen peroxide, while known to function differently, also elicit different types of responses in HEK293T cells. Menadione and bromate exposure mainly trigger an integrated stress response, whereas hydrogen peroxide affects cellular processes more diversely. Interestingly, acute oxidative stress does not universally cause notable induction of DNA repair or antioxidant defense mechanisms. We also provide evidence that cells with previous experience of oxidative stress show adaptive changes in their responses when the stress is renewed. Our results urge caution when comparing studies where different sources of oxidative stress have been used or when generalizing the findings of these studies to other oxidant types or tissues.

scholarly journals The type and source of reactive oxygen species influences the outcome of oxidative stress in cultured cells

2021 ◽  
Author(s):  
Steffi Goffart ◽  
Petra Tikkanen ◽  
Craig Michell ◽  
Trevor Wilson ◽  
Jaakko L.O. Pohjoismäki
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Cultured Cells ◽  
Oxygen Species ◽  
Different Types ◽  
Measured Effect ◽  
Experimental Approaches ◽  
Different Sources

AbstractOxidative stress can be modeled using various different experimental approaches, such as exposing the cells or organisms to oxidative chemicals. However, the actual effects of these chemicals, outside of the immediate measured effect, have attracted relatively little attention. We show here that three commonly used oxidants, menadione, potassium bromate and hydrogen peroxide, while known to function differently, also elicit different types of responses in cultured cells. While cells response to menadione and bromate exposure mainly by an integrated stress response, hydrogen peroxide has more indirect effects. Primary oxidative stress does not induce DNA repair or antioxidant defense mechanisms. However, cells with previous experience of oxidative stress show adaptive changes when the stress is renewed. Our results urge caution when comparing studies using different sources of oxidative stress or generalizing the findings of these studies to different tissue or oxidant types.

scholarly journals Oxidative stress and antioxidant defense in Brassicaceae plants under abiotic stresses

2021 ◽  
Vol 5 (1) ◽  
pp. 232-244
Author(s):  
Faiçal Brini ◽  
◽  
Walid Saibi
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Environmental Stress ◽  
Signaling Pathway ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Enzymatic Antioxidants ◽  
Ros Production ◽  
Cellular Processes

Brassicaceae plants, as an important source of primary and secondary metabolites, are becoming a research model in plant science. Plants have developed different ways to ward off environmental stress factors. This is lead to the activation of various defense mechanisms resulting in a qualitative and/or quantitative change in plant metabolite production. Reactive oxygen species (ROS) is being continuously produced in cell during normal cellular processes. Under stress conditions, there are excessive production of ROS causing progressive oxidative damage and ultimately cell death. Despite their destructive activity, ROS are considered as important secondary messengers of signaling pathway that control metabolic fluxes and a variety of cellular processes. Plant response to environmental stress depends on the delicate equilibrium between ROS production, and their scavenging. This balance of ROS level is required for performing its dual role of acting as a defensive molecule in signaling pathway or a destructive molecule. Efficient scavenging of ROS produced during various environmental stresses requires the action of several non-enzymatic as well as enzymatic antioxidants present in the tissues. In this review, we describe the ROS production and its turnover and the role of ROS as messenger molecules as well as inducers of oxidative damage in Brassicaceae plants. Further, the antioxidant defense mechanisms comprising of enzymatic and non-enzymatic antioxidants have been discussed. Keywords: Abiotic stress, Antioxidant defence, Brassicaceae, Oxidative stress, ROS

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 Oxidative Stress and Nucleic Acid Oxidation in Patients with Chronic Kidney Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Chih-Chien Sung ◽  
Yu-Chuan Hsu ◽  
Chun-Chi Chen ◽  
Yuh-Feng Lin ◽  
Chia-Chao Wu
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Nucleic Acid ◽  
Kidney Disease ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Enzyme Inhibitor ◽  
Alpha Tocopherol ◽  
Acid Oxidation ◽  
Clinical Biomarkers

Patients with chronic kidney disease (CKD) have high cardiovascular mortality and morbidity and a high risk for developing malignancy. Excessive oxidative stress is thought to play a major role in elevating these risks by increasing oxidative nucleic acid damage. Oxidative stress results from an imbalance between reactive oxygen/nitrogen species (RONS) production and antioxidant defense mechanisms and can cause vascular and tissue injuries as well as nucleic acid damage in CKD patients. The increased production of RONS, impaired nonenzymatic or enzymatic antioxidant defense mechanisms, and other risk factors including gene polymorphisms, uremic toxins (indoxyl sulfate), deficiency of arylesterase/paraoxonase, hyperhomocysteinemia, dialysis-associated membrane bioincompatibility, and endotoxin in patients with CKD can inhibit normal cell function by damaging cell lipids, arachidonic acid derivatives, carbohydrates, proteins, amino acids, and nucleic acids. Several clinical biomarkers and techniques have been used to detect the antioxidant status and oxidative stress/oxidative nucleic acid damage associated with long-term complications such as inflammation, atherosclerosis, amyloidosis, and malignancy in CKD patients. Antioxidant therapies have been studied to reduce the oxidative stress and nucleic acid oxidation in patients with CKD, including alpha-tocopherol, N-acetylcysteine, ascorbic acid, glutathione, folic acid, bardoxolone methyl, angiotensin-converting enzyme inhibitor, and providing better dialysis strategies. This paper provides an overview of radical production, antioxidant defence, pathogenesis and biomarkers of oxidative stress in patients with CKD, and possible antioxidant therapies.

scholarly journals Quantification and Mechanisms of Oxidative Stress in Chronic Disease

Proceedings ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 18 ◽  
Author(s):  
Davies
Keyword(s):  
Oxidative Stress ◽  
Chronic Disease ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Cell Function ◽  
Critical Role ◽  
Extracellular Proteins ◽  
Oxidation Chemistry ◽  
Redox Equilibria

There is now strong evidence that the redox environment inside cells is very different to that outside the cell, and that many extracellular environments are both more oxidizing and also subject to extensive oxidation. This difference in redox environments results in significant changes in oxidation chemistry and biology, altered redox equilibria, and antioxidant defense mechanisms. It is also increasingly apparent that oxidation events both inside and outside cells (extracellular oxidation) play a critical role in driving many diseases. Many extracellular proteins are highly abundant, long-lived and relatively poorly protected against damage. They can therefore accumulate high levels of modification during ageing and chronic disease, resulting in their use as biomarkers of long-term oxidative stress. Furthermore, increasing evidence supports the hypothesis that oxidized extracellular matrix materials play a key role in determining cell function and fate.

Impairment of antioxidant defense mechanisms in elderly women without increase in oxidative stress markers: “A weak equilibrium”

Lipids ◽  
1999 ◽  
Vol 34 (S1) ◽  
pp. S289-S289 ◽  
Author(s):  
J. P. Cristol ◽  
M. Abderrazick ◽  
F. Favier ◽  
F. Michel ◽  
J. Castel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Elderly Women ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Weak Equilibrium

Nitric Oxide-Mediated Modulation of Functional Iron Status in Iron-Deficient Maize Plants

2019 ◽  
Vol 5 (02) ◽  
pp. 78-83
Author(s):  
Rajesh Kumar Tewari
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Antioxidant Defense ◽  
Zea Mays L ◽  
Iron Status ◽  
Leaf Tissue ◽  
Sod Activity ◽  
Iron Deficient ◽  
Maize Plants

Nitric oxide is reported to alleviate Fe-deficiency effects, possibly by enhancing the functional Fe status of plants. Study describes changes in leaf tissue Fe status and consequent modulation of oxidative stress and antioxidant defense in Fe-deficient maize (Zea mays L.) plants supplied with NO. Supply of sodium nitroprusside (SNP), but not of sodium ferrocyanide (SF), caused regreening of leaves, syntheses of chlorophylls and carotenoids and increased activities of hydrogen peroxide-scavenging heme-Fe enzymes and lipid peroxidation, decreased SOD activity and hydrogen peroxide concentration. Though SNP or SF appears to donate Fe and increase leaf active Fe, the later did not induce increases in chlorophyll and carotenoids, and therefore NO appears to have a role in Fe nutrition irrespective of total or active Fe status of plants.

scholarly journals Enhancing the Adaptability of the Deep-Sea Bacterium Shewanella piezotolerans WP3 to High Pressure and Low Temperature by Experimental Evolution under H 2 O 2 Stress

2017 ◽  
Vol 84 (5) ◽  
Author(s):  
Zhe Xie ◽  
Huahua Jian ◽  
Zheng Jin ◽  
Xiang Xiao
Keyword(s):  
Oxidative Stress ◽  
Low Temperature ◽  
Experimental Evolution ◽  
Deep Sea ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Direct Evidence ◽  
Defense Responses ◽  
Content Type ◽  
In Cells

ABSTRACT Oxidative stresses commonly exist in natural environments, and microbes have developed a variety of defensive systems to counteract such events. Although increasing evidence has shown that high hydrostatic pressure (HHP) and low temperature (LT) induce antioxidant defense responses in cells, there is no direct evidence to prove the connection between antioxidant defense mechanisms and the adaptation of bacteria to HHP and LT. In this study, using the wild-type (WT) strain of a deep-sea bacterium, Shewanella piezotolerans WP3, as an ancestor, we obtained a mutant, OE100, with an enhanced antioxidant defense capacity by experimental evolution under H 2 O 2 stress. Notably, OE100 exhibited better tolerance not only to H 2 O 2 stress but also to HHP and LT (20 MPa and 4°C, respectively). Whole-genome sequencing identified a deletion mutation in the oxyR gene, which encodes the transcription factor that controls the oxidative stress response. Comparative transcriptome analysis showed that the genes associated with oxidative stress defense, anaerobic respiration, DNA repair, and the synthesis of flagella and bacteriophage were differentially expressed in OE100 compared with the WT at 20 MPa and 4°C. Genetic analysis of oxyR and ccpA2 indicated that the OxyR-regulated cytochrome c peroxidase CcpA2 significantly contributed to the adaptation of WP3 to HHP and LT. Taken together, these results confirmed the inherent relationship between antioxidant defense mechanisms and the adaptation of a benthic microorganism to HHP and LT. IMPORTANCE Oxidative stress exists in various niches, including the deep-sea ecosystem, which is an extreme environment with conditions of HHP and predominantly LT. Although previous studies have shown that HHP and LT induce antioxidant defense responses in cells, direct evidence to prove the connection between antioxidant defense mechanisms and the adaptation of bacteria to HHP and LT is lacking. In this work, using the deep-sea bacterium Shewanella piezotolerans WP3 as a model, we proved that enhancement of the adaptability of WP3 to HHP and LT can benefit from its antioxidant defense mechanism, which provided useful insight into the ecological roles of antioxidant genes in a benthic microorganism and contributed to an improved understanding of microbial adaptation strategies in deep-sea environments.

scholarly journals Tocotrienol-Rich Fraction Ameliorates Antioxidant Defense Mechanisms and Improves Replicative Senescence-Associated Oxidative Stress in Human Myoblasts

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Shy Cian Khor ◽  
Wan Zurinah Wan Ngah ◽  
Yasmin Anum Mohd Yusof ◽  
Norwahidah Abdul Karim ◽  
Suzana Makpol
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radical ◽  
Glutathione Peroxidase ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Replicative Senescence ◽  
Ros Generation ◽  
Tocotrienol Rich Fraction

During aging, oxidative stress affects the normal function of satellite cells, with consequent regeneration defects that lead to sarcopenia. This study aimed to evaluate tocotrienol-rich fraction (TRF) modulation in reestablishing the oxidative status of myoblasts during replicative senescence and to compare the effects of TRF with other antioxidants (α-tocopherol (ATF) andN-acetyl-cysteine (NAC)). Primary human myoblasts were cultured to young, presenescent, and senescent phases. The cells were treated with antioxidants for 24 h, followed by the assessment of free radical generation, lipid peroxidation, antioxidant enzyme mRNA expression and activities, and the ratio of reduced to oxidized glutathione. Our data showed that replicative senescence increased reactive oxygen species (ROS) generation and lipid peroxidation in myoblasts. Treatment with TRF significantly diminished ROS production and decreased lipid peroxidation in senescent myoblasts. Moreover, the gene expression of superoxide dismutase(SOD2), catalase(CAT),and glutathione peroxidase(GPX1)was modulated by TRF treatment, with increased activity of superoxide dismutase and catalase and reduced glutathione peroxidase in senescent myoblasts. In comparison to ATF and NAC, TRF was more efficient in heightening the antioxidant capacity and reducing free radical insults. These results suggested that TRF is able to ameliorate antioxidant defense mechanisms and improves replicative senescence-associated oxidative stress in myoblasts.

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