scholarly journals Antioxidants: Positive or Negative Actors?

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 124 ◽  
Author(s):  
Bahare Salehi ◽  
Miquel Martorell ◽  
Jack Arbiser ◽  
Antoni Sureda ◽  
Natália Martins ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Current Knowledge ◽  
Disease Onset ◽  
Reactive Oxygen ◽  
Population Based ◽  
Reactive Species ◽  
Oxygen Species ◽  
A Cell ◽  
Nuanced Understanding ◽  
Definition Of

The term “antioxidant” is one of the most confusing definitions in biological/medical sciences. In chemistry, “antioxidant” is simply conceived “a compound that removes reactive species, mainly those oxygen-derived”, while in a cell context, the conceptual definition of an antioxidant is poorly understood. Indeed, non-clinically recommended antioxidants are often consumed in large amounts by the global population, based on the belief that cancer, inflammation and degenerative diseases are triggered by high oxygen levels (or reactive oxygen species) and that through blocking reactive species production, organic unbalances/disorders can be prevented and/or even treated. The popularity of these chemicals arises in part from the widespread public mistrust of allopathic medicine. In fact, reactive oxygen species play a dual role in dealing with different disorders, since they may contribute to disease onset and/or progression but may also play a key role in disease prevention. Further, the ability of the most commonly used supplements, such as vitamins C, E, selenium, and herbal supplements to decrease pathologic reactive oxygen species is not clearly established. Hence, the present review aims to provide a nuanced understanding of where current knowledge is and where it should go.

scholarly journals Decrease in generation of reactive oxygen species by neutrophils from patients with infectious mononucleosis: role of suppressor T lymphocytes

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 994-999
Author(s):  
Y Niwa ◽  
T Sakane ◽  
Y Miyachi ◽  
T Kanoh ◽  
K Somiya
Keyword(s):  
Reactive Oxygen Species ◽  
T Lymphocytes ◽  
Infectious Mononucleosis ◽  
Disease Onset ◽  
Reactive Oxygen ◽  
Control Group ◽  
Ros Generation ◽  
Oxygen Species ◽  
Suppressor T Lymphocytes ◽  
Subsets Of T Lymphocytes

We assessed the generation of reactive oxygen species (ROS: O2-, H2O2, OH . , chemiluminescence) by neutrophils and monocytes from six patients with infectious mononucleosis, ten patients with other viral diseases, and ten normal controls. Neutrophils from infectious mononucleosis patients showed markedly decreased generation of all reactive oxygen species, compared with the two control groups; this abnormality persisted for four to eight weeks after disease onset. Monocytes from these patients generated normal levels of ROS. Normal neutrophils incubated with T lymphocytes from infectious mononucleosis patients generated significantly less of each ROS than did those incubated with T cells from either control group. T cell-mediated suppression of ROS generation required both OKT4+ cells from infectious mononucleosis patients and OKT8+ cells from either patients or normals. We conclude that the generation of reaction oxygen species in neutrophils is suppressed in patients with infectious mononucleosis, at least in part, by interacting subsets of T lymphocytes.

Reactive oxygen species generated by renal ischemia and reperfusion trigger protection against subsequent renal ischemia and reperfusion injury in mice

2010 ◽  
Vol 298 (1) ◽  
pp. F158-F166 ◽  
Author(s):  
Jinu Kim ◽  
Hee-Seong Jang ◽  
Kwon Moo Park
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
A Cell ◽  
Copper Zinc ◽  
And Oxidative Stress

Ischemic preconditioning by a single event of ischemia and reperfusion (SIRPC) dramatically protects renal function against ischemia and reperfusion (I/R) induced several weeks later. We recently reported that reactive oxygen species (ROS) and oxidative stress were sustained in a kidney that had functionally recovered from I/R injury, thus suggesting an association between SIRPC and ROS and oxidative stress. However, the role of ROS in SIRPC remains to be clearly elucidated. To assess the involvement of ROS in SIRPC, mice were subjected to SIRPC (30 min of bilateral renal ischemia and 8 days of reperfusion) and then exposed to I/R injury. Thirty minutes of bilateral renal ischemia in the non-SIRPC mice resulted in a marked increase in plasma creatinine levels 4 and 24 h after reperfusion, which was not observed in the I/R in the SIRPC mice. SIRPC resulted in increases in the levels of kidney superoxide. Administrations of manganese(III) tetrakis(1-methyl-4-pyridyl) porphyrin [MnTMPyP; a cell-permeable superoxide dismutase (SOD) mimetic] and N-acetylcysteine (NAc; a ROS scavenger) to SIRPC mice blocked the SIRPC-induced increase in superoxide levels and removed ∼48–64% of the functional protection of the SIRPC kidney. Additionally, these administrations significantly inhibited I/R-induced increases in superoxide formation, hydrogen peroxide production, and lipid peroxidation, along with the inhibition of I/R-induced reductions in the expression and activity of manganese SOD, copper-zinc SOD, and catalase. Furthermore, administrations of MnTMPyP or NAc inhibited the SIRPC-induced increase in inducible nitric oxide synthase expression but did not inhibit the SIRPC-induced increases in heat shock protein-25 expression. In conclusion, the renoprotection afforded by SIRPC was triggered by ROS generated by SIRPC.

Mild Therapeutic Hypothermia for Postischemic Vasoconstriction in the Perfused Rat Liver 

1999 ◽  
Vol 90 (4) ◽  
pp. 1103-1111 ◽  
Author(s):  
Harvey A. Zar ◽  
Koichi Tanigawa ◽  
Young-Myeong Kim ◽  
Jack R. Lancaster
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lactate Dehydrogenase ◽  
Vascular Resistance ◽  
Mild Hypothermia ◽  
Reactive Oxygen ◽  
Thiobarbituric Acid ◽  
Reactive Species ◽  
Oxygen Species ◽  
No Reflow

Background Mild hypothermia, a promising therapy being evaluated for various clinical situations, may suppress the formation of reactive oxygen species during reperfusion and may ameliorate microcirculatory perfusion failure (the "no-reflow phenomenon"). Methods Isolated rat livers underwent 30 min of perfusion, 2.5 h of ischemia, and 3 h of reperfusion. The temperature was maintained at 34 degrees C (mild hypothermia, n = 5) or 38 degrees C (normothermia, n = 6) for all three periods by perfusion of a modified Krebs Henseleit solution, air surface cooling, or both. A third group of livers was normothermic before and during ischemia and mildly hypothermic during reperfusion (reperfusion hypothermia, n = 6). Control livers had 3 h of perfusion at normothermia. Chemiluminescence (a measure of the generation of reactive oxygen species) and hepatic vascular resistance were monitored simultaneously to evaluate the effect of temperature on the formation of reactive oxygen species and the development of no reflow. Also measured were thiobarbituric acid reactive species and lactate dehydrogenase, as indicators of oxidative stress and cell injury. Results Mild hypothermia decreased formation of reactive oxygen species and postischemic increases in vascular resistance. Reperfusion hypothermia also decreased postischemic increases in vascular resistance, but not as effectively as did mild hypothermia. Levels of thiobarbituric acid reactive species were lower for reperfusion hypothermia than for mild hypothermia at only 0 and 30 min of reperfusion. Lactate dehydrogenase was significant only at 0 min of reperfusion for the normothermic group. Oxygen consumption did not change. Conclusion The prevention of hepatic vascular injury by suppression of oxidative stress may be an important protective mechanism of mild hypothermia.

scholarly journals Glutathione Metabolism in Plants under Stress: Beyond Reactive Oxygen Species Detoxification

Metabolites ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 641
Author(s):  
Sonia Dorion ◽  
Jasmine C. Ouellet ◽  
Jean Rivoal
Keyword(s):  
Reactive Oxygen Species ◽  
Current Knowledge ◽  
Reactive Oxygen ◽  
Covalent Modification ◽  
Regulatory Function ◽  
Glutathione Metabolism ◽  
Oxygen Species ◽  
Post Translational Modification ◽  
Stress Regulation ◽  
Recent Developments

Glutathione is an essential metabolite for plant life best known for its role in the control of reactive oxygen species (ROS). Glutathione is also involved in the detoxification of methylglyoxal (MG) which, much like ROS, is produced at low levels by aerobic metabolism under normal conditions. While several physiological processes depend on ROS and MG, a variety of stresses can dramatically increase their concentration leading to potentially deleterious effects. In this review, we examine the structure and the stress regulation of the pathways involved in glutathione synthesis and degradation. We provide a synthesis of the current knowledge on the glutathione-dependent glyoxalase pathway responsible for MG detoxification. We present recent developments on the organization of the glyoxalase pathway in which alternative splicing generate a number of isoforms targeted to various subcellular compartments. Stress regulation of enzymes involved in MG detoxification occurs at multiple levels. A growing number of studies show that oxidative stress promotes the covalent modification of proteins by glutathione. This post-translational modification is called S-glutathionylation. It affects the function of several target proteins and is relevant to stress adaptation. We address this regulatory function in an analysis of the enzymes and pathways targeted by S-glutathionylation.

scholarly journals Signaling Toward Reactive Oxygen Species-Scavenging Enzymes in Plants

2021 ◽  
Vol 11 ◽  
Author(s):  
Petr Dvořák ◽  
Yuliya Krasylenko ◽  
Adam Zeiner ◽  
Jozef Šamaj ◽  
Tomáš Takáč
Keyword(s):  
Reactive Oxygen Species ◽  
Antioxidant Enzymes ◽  
Environmental Conditions ◽  
Antioxidant Defense ◽  
Current Knowledge ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Negative Consequences ◽  
Ros Scavenging ◽  
Enzymatic Antioxidant

Reactive oxygen species (ROS) are signaling molecules essential for plant responses to abiotic and biotic stimuli as well as for multiple developmental processes. They are produced as byproducts of aerobic metabolism and are affected by adverse environmental conditions. The ROS content is controlled on the side of their production but also by scavenging machinery. Antioxidant enzymes represent a major ROS-scavenging force and are crucial for stress tolerance in plants. Enzymatic antioxidant defense occurs as a series of redox reactions for ROS elimination. Therefore, the deregulation of the antioxidant machinery may lead to the overaccumulation of ROS in plants, with negative consequences both in terms of plant development and resistance to environmental challenges. The transcriptional activation of antioxidant enzymes accompanies the long-term exposure of plants to unfavorable environmental conditions. Fast ROS production requires the immediate mobilization of the antioxidant defense system, which may occur via retrograde signaling, redox-based modifications, and the phosphorylation of ROS detoxifying enzymes. This review aimed to summarize the current knowledge on signaling processes regulating the enzymatic antioxidant capacity of plants.

scholarly journals  Metals as a cause of oxidative stress in fish: a review

2011 ◽  
Vol 56 (No. 11) ◽  
pp. 537-546 ◽  
Author(s):  
M. Sevcikova ◽  
H. Modra ◽  
A. Slaninova ◽  
Z. Svobodova
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Metal Binding ◽  
Special Functions ◽  
Current Knowledge ◽  
Reactive Oxygen ◽  
Enzyme Inactivation ◽  
Oxygen Species ◽  
Antioxidant Defences

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  

Effect of Pyridone Carboxylic Acid Anti-microbials on the Generation of Reactive Oxygen Species In Vitro

1996 ◽  
Vol 24 (4) ◽  
pp. 345-351 ◽  
Author(s):  
H Akamatsu ◽  
Y Niwa ◽  
H Sasaki ◽  
Y Matoba ◽  
Y Asada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Human Neutrophils ◽  
Oxygen Species ◽  
Oxidase System ◽  
Superoxide Radical Anion ◽  
A Cell ◽  
Inflammatory Action

The effects of ofloxacin, ciprofloxacin and balofloxacin on the reactive oxygen species (ROS) levels generated by human neutrophils was examined in vitro; ROS generated in a cell-free, xanthine–xanthine oxidase system was also assessed. The species investigated were superoxide radical anion (O2−), hydrogen peroxide (H2O2) and hydroxyl radical (OH·). Both ofloxacin and ciprofloxacin markedly decreased the levels of O2−, H2O2 and OH· generated by human neutrophils. On the other hand, these drugs did not affect any of the ROS examined in the xanthine-xanthine oxidase system. Balofloxacin showed no significant effect on ROS generated by either system. The present study indicates that ofloxacin and ciprofloxacin may exert an anti-inflammatory action by reducing the potent ROS species excessively generated by neutrophils at the sites of inflammation.

scholarly journals Detection of Oxidative Stress Induced by Nanomaterials in Cells—The Roles of Reactive Oxygen Species and Glutathione

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4710
Author(s):  
Jan Čapek ◽  
Tomáš Roušar
Keyword(s):  
Reactive Oxygen Species ◽  
Current Knowledge ◽  
Reactive Oxygen ◽  
Glutathione Depletion ◽  
Oxygen Species ◽  
Cellular Processes ◽  
Cellular Pathways ◽  
Antioxidant Mechanisms ◽  
Harmful Effects ◽  
In Cells

The potential of nanomaterials use is huge, especially in fields such as medicine or industry. Due to widespread use of nanomaterials, their cytotoxicity and involvement in cellular pathways ought to be evaluated in detail. Nanomaterials can induce the production of a number of substances in cells, including reactive oxygen species (ROS), participating in physiological and pathological cellular processes. These highly reactive substances include: superoxide, singlet oxygen, hydroxyl radical, and hydrogen peroxide. For overall assessment, there are a number of fluorescent probes in particular that are very specific and selective for given ROS. In addition, due to the involvement of ROS in a number of cellular signaling pathways, understanding the principle of ROS production induced by nanomaterials is very important. For defense, the cells have a number of reparative and especially antioxidant mechanisms. One of the most potent antioxidants is a tripeptide glutathione. Thus, the glutathione depletion can be a characteristic manifestation of harmful effects caused by the prooxidative-acting of nanomaterials in cells. For these reasons, here we would like to provide a review on the current knowledge of ROS-mediated cellular nanotoxicity manifesting as glutathione depletion, including an overview of approaches for the detection of ROS levels in cells.

scholarly journals Effect of ClAlPcS2 photodynamic and sonodynamic therapy on hela cells

2019 ◽  
pp. S375-S384 ◽  
Author(s):  
S. Binder ◽  
B Hosikova ◽  
Z. Mala ◽  
L. Zarska ◽  
H. Kolarova
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Hela Cells ◽  
Cell Damage ◽  
Combined Therapy ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Sonodynamic Therapy ◽  
A Cell

Photodynamic therapy (PDT) uses photosensitive substance to provoke a cytotoxic reaction causing a cell damage or cell death. The substances, photosensitizers, are usually derivates of porphyrine or phtalocyanine. Photosensitizers must be activated by light in order to produce reactive oxygen species, mainly singlet oxygen. Sonodynamic therapy (SDT) utilizes ultrasound to enhance a cytotoxic effects of compounds called sonosensitizers. In this study we investigated photodynamic and sonodynamic effect of chloraluminium phtalocyanine disulfonate (ClAlPcS(2)) on HeLa cells. DNA damage, cell viability and reactive oxygen species (ROS) production were assessed to find whether the combination of PDT and SDT inflicts HeLa cells more than PDT alone. We found that the combined therapy increases DNA fragmentation, enhances ROS production and decreases cell survival. Our results indicate that ClAlPcS(2) can act as a sonosentitiser and combined with PDT causes more irreversible changes to the cells resulting in cell death than PDT alone.

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