scholarly journals Horse Oil Mitigates Oxidative Damage to Human HaCaT Keratinocytes Caused by Ultraviolet B Irradiation

2019 ◽  
Vol 20 (6) ◽  
pp. 1490
Author(s):  
Mei Piao ◽  
Kyoung Kang ◽  
Ao Zhen ◽  
Hee Kang ◽  
Young Koh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Matrix Metalloproteinase ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Ultraviolet B ◽  
Electromagnetic Spectrum ◽  
Oxygen Species ◽  
Uvb Radiation ◽  
Hacat Keratinocytes

Horse oil products have been used in skin care for a long time in traditional medicine, but the biological effects of horse oil on the skin remain unclear. This study was conducted to evaluate the protective effect of horse oil on ultraviolet B (UVB)-induced oxidative stress in human HaCaT keratinocytes. Horse oil significantly reduced UVB-induced intracellular reactive oxygen species and intracellular oxidative damage to lipids, proteins, and DNA. Horse oil absorbed light in the UVB range of the electromagnetic spectrum and suppressed the generation of cyclobutane pyrimidine dimers, a photoproduct of UVB irradiation. Western blotting showed that horse oil increased the UVB-induced Bcl-2/Bax ratio, inhibited mitochondria-mediated apoptosis and matrix metalloproteinase expression, and altered mitogen-activated protein kinase signaling-related proteins. These effects were conferred by increased phosphorylation of extracellular signal-regulated kinase 1/2 and decreased phosphorylation of p38 and c-Jun N-terminal kinase 1/2. Additionally, horse oil reduced UVB-induced binding of activator protein 1 to the matrix metalloproteinase-1 promoter site. These results indicate that horse oil protects human HaCaT keratinocytes from UVB-induced oxidative stress by absorbing UVB radiation and removing reactive oxygen species, thereby protecting cells from structural damage and preventing cell death and aging. In conclusion, horse oil is a potential skin protectant against skin damage involving oxidative stress.

scholarly journals Protein-L-isoaspartate O-methyltransferase is required for in vivo control of oxidative damage in red blood cells

Haematologica ◽  
2020 ◽  
pp. 0-0
Author(s):  
Angelo D’Alessandro ◽  
Ariel Hay ◽  
Monika Dzieciatkowska ◽  
Benjamin C. Brown ◽  
Evan J Morrison ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Reactive Oxygen ◽  
Metabolic Reprogramming ◽  
Oxygen Species ◽  
Common Amino Acid

Red blood cells have the special challenge of a large amount of reactive oxygen species (from their substantial iron load and Fenton reactions) combined with the inability to synthesize new gene products. Considerable progress has been made in elucidating the multiple pathways by which red blood cells neutralize reactive oxygen species via NADPH driven redox reactions. However, far less is known about how red blood cells repair the inevitable damage that does occur when reactive oxygen species break through anti-oxidant defenses. When structural and functional proteins become oxidized, the only remedy available to red blood cells is direct repair of the damaged molecules, as red blood cells cannot synthesize new proteins. Amongst the most common amino acid targets of oxidative damage is the conversion of asparagine and aspartate side chains into a succinimidyl group through deamidation or dehydration, respectively. Red blood cells express an L-Isoaspartyl methyltransferase (PIMT, gene name PCMT1) that can convert succinimidyl groups back to an aspartate. Herein, we report that deletion of PCMT1 significantly alters red blood cell metabolism in a healthy state, but does not impair the circulatory lifespan of red blood cells. Through a combination of genetic ablation, bone marrow transplantation and oxidant stimulation with phenylhydrazine in vivo or blood storage ex vivo, we use omics approaches to show that, when animals are exposed to oxidative stress, red blood cells from PCMT1 knockout undergo significant metabolic reprogramming and increased hemolysis. This is the first report of an essential role of PCMT1 for normal RBC circulation during oxidative stress.

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.  

scholarly journals Regulation of Reactive Oxygen Species and Antioxidant Defense in Plants under Salinity

2021 ◽  
Vol 22 (17) ◽  
pp. 9326
Author(s):  
Mirza Hasanuzzaman ◽  
Md. Rakib Hossain Raihan ◽  
Abdul Awal Chowdhury Masud ◽  
Khussboo Rahman ◽  
Farzana Nowroz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salt Stress ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Reactive Oxygen ◽  
Antioxidant Defense System ◽  
Ros Generation ◽  
Oxygen Species ◽  
Defense System

The generation of oxygen radicals and their derivatives, known as reactive oxygen species, (ROS) is a part of the signaling process in higher plants at lower concentrations, but at higher concentrations, those ROS cause oxidative stress. Salinity-induced osmotic stress and ionic stress trigger the overproduction of ROS and, ultimately, result in oxidative damage to cell organelles and membrane components, and at severe levels, they cause cell and plant death. The antioxidant defense system protects the plant from salt-induced oxidative damage by detoxifying the ROS and also by maintaining the balance of ROS generation under salt stress. Different plant hormones and genes are also associated with the signaling and antioxidant defense system to protect plants when they are exposed to salt stress. Salt-induced ROS overgeneration is one of the major reasons for hampering the morpho-physiological and biochemical activities of plants which can be largely restored through enhancing the antioxidant defense system that detoxifies ROS. In this review, we discuss the salt-induced generation of ROS, oxidative stress and antioxidant defense of plants under salinity.

scholarly journals Molecular Interactions Between Reactive Oxygen Species and Autophagy in Kidney Disease

2019 ◽  
Vol 20 (15) ◽  
pp. 3791 ◽  
Author(s):  
Gur P. Kaushal ◽  
Kiran Chandrashekar ◽  
Luis A. Juncos
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Kidney Disease ◽  
Oxidative Damage ◽  
Molecular Interactions ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Renal Diseases ◽  
Oxygen Species

Reactive oxygen species (ROS) are highly reactive signaling molecules that maintain redox homeostasis in mammalian cells. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of ROS, culminating in oxidative stress and the associated oxidative damage of cellular components. ROS and oxidative stress play a vital role in the pathogenesis of acute kidney injury and chronic kidney disease, and it is well documented that increased oxidative stress in patients enhances the progression of renal diseases. Oxidative stress activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular oxidized and damaged macromolecules and dysfunctional organelles. In this review, we report the current understanding of the molecular regulation of autophagy in response to oxidative stress in general and in the pathogenesis of kidney diseases. We summarize how the molecular interactions between ROS and autophagy involve ROS-mediated activation of autophagy and autophagy-mediated reduction of oxidative stress. In particular, we describe how ROS impact various signaling pathways of autophagy, including mTORC1-ULK1, AMPK-mTORC1-ULK1, and Keap1-Nrf2-p62, as well as selective autophagy including mitophagy and pexophagy. Precise elucidation of the molecular mechanisms of interactions between ROS and autophagy in the pathogenesis of renal diseases may identify novel targets for development of drugs for preventing renal injury.

scholarly journals Dual and Opposite Roles of Reactive Oxygen Species (ROS) in Chagas Disease: Beneficial on the Pathogen and Harmful on the Host

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Edio Maldonado ◽  
Diego A. Rojas ◽  
Sebastian Morales ◽  
Vicente Miralles ◽  
Aldo Solari
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Chagas Disease ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Parasite Growth ◽  
Oxygen Species ◽  
Chronic Stage ◽  
Mitochondrial Ros

Chagas disease is a neglected tropical disease, which affects an estimate of 6-7 million people worldwide. Chagas disease is caused by Trypanosoma cruzi, which is a eukaryotic flagellate unicellular organism. At the primary infection sites, these parasites are phagocytized by macrophages, which produce reactive oxygen species (ROS) in response to the infection with T. cruzi. The ROS produce damage to the host tissues; however, macrophage-produced ROS is also used as a signal for T. cruzi proliferation. At the later stages of infection, mitochondrial ROS is produced by the infected cardiomyocytes that contribute to the oxidative damage, which persists at the chronic stage of the disease. The oxidative damage leads to a functional impairment of the heart. In this review article, we will discuss the mechanisms by which T. cruzi is able to deal with the oxidative stress and how this helps the parasite growth at the acute phase of infection and how the oxidative stress affects the cardiomyopathy at the chronic stage of the Chagas disease. We will describe the mechanisms used by the parasite to deal with ROS and reactive nitrogen species (RNS) through the trypanothione and the mechanisms used to repair the damaged DNA. Also, a description of the events produced by ROS at the acute and chronic stages of the disease is presented. Lastly, we discuss the benefits of ROS for T. cruzi growth and proliferation and the possible mechanisms involved in this phenomenon. Hypothesis is put forward to explain the molecular mechanisms by which ROS triggers parasite growth and proliferation and how ROS is able to produce a long persisting damage on cardiomyocytes even in the absence of the parasite.

scholarly journals Quercetin and Its Mixture Increase the Stress Resistance of Caenorhabditis elegans to UV-B

2020 ◽  
Vol 17 (5) ◽  
pp. 1572
Author(s):  
Shi-ming Li ◽  
Dan Liu ◽  
Yi-lin Liu ◽  
Bin Liu ◽  
Xing-huang Chen
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Caenorhabditis Elegans ◽  
Stress Resistance ◽  
Reactive Oxygen ◽  
Species Level ◽  
Ultraviolet B ◽  
Oxygen Species ◽  
Germ Cell Apoptosis ◽  
Embryonic Lethal

Ultraviolet B (UV-B, 280–320 nm) radiation causes complex molecular reactions in cells, including DNA damage, oxidative stress, and apoptosis. This study designed a mixture consisting of quercetin, luteolin and lycopene and used Caenorhabditis elegans as a model to study the resistance of these natural chemicals to UV-B. Specifically, we have confirmed that quercetin and its mixture can increase the resistance of Caenorhabditis elegans to UV-B through lifespan test, reactive oxygen species level assay, germ cell apoptosis test, embryonic lethal test and RT-qPCR experiments. The results show that quercetin and its mixture prolonged the lifespan of UV-B-irradiated Caenorhabditis elegans and reduced abnormal levels of reactive oxygen species, embryo death, and apoptosis induced by UV-B. The protective effect of quercetin and its mixture may be attributed to its down-regulation of HUS-1, CEP-1, EGL-1 and CED-13. Therefore, the results of this research could help the development of UV-B radiation protection agents.

Oxidative Stress and Cancer

2019 ◽  
Vol 24 (40) ◽  
pp. 4771-4778 ◽  
Author(s):  
James E. Klaunig
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Proliferation ◽  
Dna Repair ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Genetic Inheritance

Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation) while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role of oxidative stress and oxidative damage in cancer initiation and progression. Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic antioxidants is important in determining the potential human cancer risk. Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and progression of cancer.

scholarly journals Viewing oxidative stress through the lens of oxidative signalling rather than damage

2017 ◽  
Vol 474 (6) ◽  
pp. 877-883 ◽  
Author(s):  
Christine H. Foyer ◽  
Alexander V. Ruban ◽  
Graham Noctor
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Photosystem Ii ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Oxidative Modification ◽  
Current View ◽  
Oxygen Species ◽  
Repair Processes

Concepts of the roles of reactive oxygen species (ROS) in plants and animals have shifted in recent years from focusing on oxidative damage effects to the current view of ROS as universal signalling metabolites. Rather than having two opposing activities, i.e. damage and signalling, the emerging concept is that all types of oxidative modification/damage are involved in signalling, not least in the induction of repair processes. Examining the multifaceted roles of ROS as crucial cellular signals, we highlight as an example the loss of photosystem II function called photoinhibition, where photoprotection has classically been conflated with oxidative damage.

scholarly journals Reactive Oxygen Species and Their Involvement in Red Blood Cell Damage in Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Krzysztof Gwozdzinski ◽  
Anna Pieniazek ◽  
Lukasz Gwozdzinski
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Molecular Weight ◽  
Blood Cell ◽  
Oxidative Damage ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Reactive Oxygen ◽  
Low Molecular Weight ◽  
Oxygen Species

Reactive oxygen species (ROS) released in cells are signaling molecules but can also modify signaling proteins. Red blood cells perform a major role in maintaining the balance of the redox in the blood. The main cytosolic protein of RBC is hemoglobin (Hb), which accounts for 95-97%. Most other proteins are involved in protecting the blood cell from oxidative stress. Hemoglobin is a major factor in initiating oxidative stress within the erythrocyte. RBCs can also be damaged by exogenous oxidants. Hb autoxidation leads to the generation of a superoxide radical, of which the catalyzed or spontaneous dismutation produces hydrogen peroxide. Both oxidants induce hemichrome formation, heme degradation, and release of free iron which is a catalyst for free radical reactions. To maintain the redox balance, appropriate antioxidants are present in the cytosol, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and peroxiredoxin 2 (PRDX2), as well as low molecular weight antioxidants: glutathione, ascorbic acid, lipoic acid, α-tocopherol, β-carotene, and others. Redox imbalance leads to oxidative stress and may be associated with overproduction of ROS and/or insufficient capacity of the antioxidant system. Oxidative stress performs a key role in CKD as evidenced by the high level of markers associated with oxidative damage to proteins, lipids, and DNA in vivo. In addition to the overproduction of ROS, a reduced antioxidant capacity is observed, associated with a decrease in the activity of SOD, GPx, PRDX2, and low molecular weight antioxidants. In addition, hemodialysis is accompanied by oxidative stress in which low-biocompatibility dialysis membranes activate phagocytic cells, especially neutrophils and monocytes, leading to a respiratory burst. This review shows the production of ROS under normal conditions and CKD and its impact on disease progression. Oxidative damage to red blood cells (RBCs) in CKD and their contribution to cardiovascular disease are also discussed.

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