scholarly journals Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Zhuhui Qiao ◽  
Xiuxiu Wang ◽  
Leihong Xiang ◽  
Chengfeng Zhang
Keyword(s):  
Oxidative Stress ◽  
Uv Light ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Degradation Pathway ◽  
Protective Role ◽  
Epidermal Keratinocytes ◽  
New Ideas ◽  
Important Regulator ◽  
Pigmentation Disorders

Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of functional melanocytes from the epidermis and follicular reservoir. Among multiple hypotheses which have been proposed in the pathogenesis of vitiligo, autoimmunity and oxidative stress-mediated toxicity in melanocytes remain most widely accepted. Macroautophagy is a lysosome-dependent degradation pathway which widely exists in eukaryotic cells. Autophagy participates in the oxidative stress response in many cells, which plays a protective role in preventing damage caused by oxidative stress. Recent studies have enrolled autophagy as an important regulator in limiting damage caused by UV light and lipid oxidation, keeping oxidative stress in a steady state in epidermal keratinocytes and maintaining normal proliferation and aging of melanocytes. Impairment of autophagy might disrupt the antioxidant defense system which renders melanocytes to oxidative insults. These findings provide supportive evidence to explore new ideas of the pathogenesis of vitiligo and other pigmentation disorders.

scholarly journals An Antioxidant Defense System in Radiation-Resistant Bacterium Deinococcus geothermalis against Oxidative Stress

2021 ◽  
Author(s):  
Chanjae Lee ◽  
Min K. Bae ◽  
Sung-Jae Lee
Keyword(s):  
Oxidative Stress ◽  
Dna Binding ◽  
Carotenoid Biosynthesis ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Primary Response ◽  
Resistant Bacterium ◽  
Loss Of Function ◽  
Deinococcus Geothermalis ◽  
Radiation Resistant

A radiation-resistant bacterium, Deinococcus geothermalis has various stress response mechanisms, including antioxidation. Features that maintain vitality at high radiation doses include the following: enzymatic scavengers of ROS such as catalase, SOD, and peroxidase; strain-specific DNA repair systems such as Deinococcal unique proteins; non-enzymatic responses such as manganese complexes, carotenoids, and DNA-binding proteins. This chapter summarizes the primary response mechanism by redox balance centered on the cystine transporter. It also reviews action characteristics of DNA-binding protein Dps and a putative LysR family protein, and effects on loss of function of the carotenoid biosynthesis genes by transposition of insertion sequences. Environmental adaptation and molecular evolution of radiation-resistant bacterium are also considered to explain the potentials of molecular behavior induced by oxidative stress.

scholarly journals Modulation of Hippocampal Antioxidant Defense System in Chronically Stressed Rats by Lithium

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Nataša Popović ◽  
Vesna Stojiljković ◽  
Snežana Pejić ◽  
Ana Todorović ◽  
Ivan Pavlović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Superoxide Dismutase ◽  
Enzyme Activities ◽  
Manganese Superoxide Dismutase ◽  
Lithium Treatment ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Preclinical Research ◽  
Protein Levels

This study examined the effects of lithium on gene expression and activity of the antioxidant enzymes copper zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) in the hippocampus of chronically stressed rats. In addition, we examined the effects of lithium on anxiety behaviors, hippocampal concentrations of dopamine (DA) and malondialdehyde (MDA), protein levels of brain-derived neurotrophic factor (BDNF), tyrosine hydroxylase (TH), dopamine transporter (DAT), and catechol-O-methyltransferase (COMT), as well as activity of monoamine oxidase (MAO) in chronically stressed rats. The investigated parameters were quantified by real-time RT-PCR, Western blot analyses, and assays of enzyme activities. We found that lithium did not change gene expression of SOD1, CAT, GPx, and GR but decreased gene expression of SOD2 in chronically stressed rats. A very important result in this study was that lithium treatment decreased the enzyme activities of SOD1 and SOD2 but increased the enzyme activities of GPx and GR in stress condition, which indicates the control of redox balance. The reduced concentration of MDA confirms this. In addition, we found that lithium treatment decreased high protein levels of BDNF and DAT in chronically stressed rats to the level found in unstressed animals. Also, lithium treatment increased the expression of TH but decreased the enzyme activity of MAO B, which contributed to the increase of hippocampal concentration of DA in chronically stressed rats to the level of unstressed animals. Finally, lithium treatment in animals exposed to chronic stress increased the time spent in open arms. Lithium-induced modulation of hippocampal antioxidant status and attenuation of oxidative stress stabilized behavior in animals with high anxiety index. In addition, reduced oxidative stress was followed by the changes of both turnover of DA and levels of BDNF protein in chronically stressed rats treated with lithium. These findings may be important in preclinical research of the effects of lithium on oxidative stress level in pathological conditions.

scholarly journals LATS1 Is a Mediator of Melanogenesis in Response to Oxidative Stress and Regulator of Melanoma Growth

2021 ◽  
Vol 22 (6) ◽  
pp. 3108
Author(s):  
Urszula Kazimierczak ◽  
Ewelina Dondajewska ◽  
Maria Zajaczkowska ◽  
Marianna Karwacka ◽  
Tomasz Kolenda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tumor Growth ◽  
Protective Role ◽  
Melanin Synthesis ◽  
Melanin Content ◽  
Melanin Production ◽  
And Oxidative Stress ◽  
Pigmentation Disorders ◽  
Melanoma Growth

The LATS1 kinase has been described as a tumor suppressor in various cancers. However, its role in melanoma has not been fully elucidated. There are several processes involved in tumorigenesis, including melanin production. Melanin content positively correlates with the level of reactive oxygen species (ROS) inside the cell. Accordingly, the purpose of the study was to assess the role of LATS1 in melanogenesis and oxidative stress and its influence on tumor growth. We have knocked down LATS1 in primary melanocytes and melanoma cells and found that its expression is crucial for melanin synthesis, ROS production, and oxidative stress response. We showed that LATS1 ablation significantly decreased the melanogenesis markers’ expression and melanin synthesis in melanocyte and melanoma cell lines. Moreover, silencing LATS1 resulted in enhanced oxidative stress. Reduced melanin content in LATS1 knocked down tumors was associated with increased tumor growth, pointing to melanin’s protective role in this process. The study demonstrated that LATS1 is highly engaged in melanogenesis and oxidative stress control and affects melanoma growth. Our results may find the implications in the diagnosis and treatment of pigmentation disorders, including melanoma.

scholarly journals Revisiting Oxidative Stress and the Use of Organic Selenium in Dairy Cow Nutrition

Animals ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 462 ◽  
Author(s):  
Peter F. Surai ◽  
Ivan I. Kochish ◽  
Vladimir I. Fisinin ◽  
Darren T. Juniper
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Molecular Mechanisms ◽  
Animal Feed ◽  
Animal Health ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
The Body ◽  
Organic Selenium ◽  
Ruminant Species

In commercial animals production, productive stress can negatively impact health status and subsequent productive and reproductive performance. A great body of evidence has demonstrated that as a consequence of productive stress, an overproduction of free radicals, disturbance of redox balance/signaling, and oxidative stress were observed. There is a range of antioxidants that can be supplied with animal feed to help build and maintain the antioxidant defense system of the body responsible for prevention of the damaging effects of free radicals and the toxic products of their metabolism. Among feed-derived antioxidants, selenium (Se) was shown to have a special place as an essential part of 25 selenoproteins identified in animals. There is a comprehensive body of research in monogastric species that clearly shows that Se bioavailability within the diet is very much dependent on the form of the element used. Organic Se, in the form of selenomethionine (SeMet), has been reported to be a much more effective Se source when compared with mineral forms such as sodium selenite or selenate. It has been proposed that one of the main advantages of organic Se in pig and poultry nutrition is the non-specific incorporation of SeMet into general body proteins, thus forming an endogenous Se reserve that can be utilized during periods of stress for additional synthesis of selenoproteins. Responses in ruminant species to supplementary Se tend to be much more variable than those reported in monogastric species, and much of this variability may be a consequence of the different fates of Se forms in the rumen following ingestion. It is likely that the reducing conditions found in the rumen are responsible for the markedly lower assimilation of inorganic forms of Se, thus predisposing selenite-fed animals to potential Se inadequacy that may in turn compromise animal health and production. A growing body of evidence demonstrates that organic Se has a number of benefits, particularly in dairy and beef animals; these include improved Se and antioxidant status and better Se transfer via the placenta, colostrum, and milk to the newborn. However, there is a paucity in the data concerning molecular mechanisms of SeMet assimilation, metabolism and selenoprotein synthesis regulation in ruminant animals, and as such, further investigation is required.

scholarly journals Fémelem-homeosztázis és oxidatív stressz patológiás folyamatokban

2019 ◽  
Vol 160 (36) ◽  
pp. 1407-1416
Author(s):  
Klára Szentmihályi
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Metal Ions ◽  
Intracellular Signaling ◽  
Metal Ion ◽  
Cell Damage ◽  
Neurological Diseases ◽  
Redox Homeostasis ◽  
Antioxidant Defense System ◽  
Redox Balance

Abstract: The author briefly summarizes the relationship between oxidative stress and changes in metal ion metabolism in pathological processes. Essential metal ions such as Ca, Mg, Fe, Cu, Zn, Se are essential in the living organisms, their metabolism and intracellular concentration are strictly regulated. Externally or intrinsically, altered metal ion metabolism can lead to metal ion accumulation or metal ion deficiency. Excess amounts of redox-active essential metals such as Fe, Cu, Co, Cr, Ni can induce free radicals under certain circumstances that cause inflammation, cell damage, and cancerous changes, although the molecular mechanism is still unclear in every detail. Changes in the metabolism of non-essential and non-variable valence metal ions also affect redox homeostasis. Despite the fact that each metal can react in a unique way and with different mechanisms, similar processes occur, where both metal deficiency and excessive metal induce oxidative stress. Antioxidant defense system is damaged, free radicals produced alter the redox balance, and redox homeostasis changed induces the production of cytokines and other transcription factors that affect the intracellular signaling pathways and affect the development of various diseases, including metabolic, cardiovascular, neurological diseases and cancer. Orv Hetil. 2019; 160(36): 1407–1416.

scholarly journals Endogenous Enzymatic Antioxidant Defense and Pathologies

2021 ◽  
Author(s):  
Atika Eddaikra ◽  
Naouel Eddaikra
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Biological Macromolecules ◽  
Metabolic Dysfunction ◽  
Enzymatic Antioxidant ◽  
Metabolic Imbalance

Oxidative stress is an important component of various diseases. It manifests as an imbalance caused by an excessive production of reactive oxygen species (ROS) which are associated with a deficit of antioxidant activity. This deficit can be the consequence of genetic factors, environmental ones, metabolic imbalance, toxicity or direct attacks by the accumulation of free radicals. These can induce metabolic dysfunction affecting biological macromolecules in their structures or activities. From a physiological perspective, the neutralization of free radicals is ensured by enzymatic, antioxidant and non-enzymatic defense systems. In the present chapter, we will focus on the endogenous enzymatic antioxidant defense system such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPxs), thioredoxin (Trx) and paraxonase which play an important role in homeostatic redox balance. Also, we will review this set of antioxidants enzymes within different pathological states such as diabetes, cancer, autoimmune diseases, cardiovascular, Alzheimer’s, Parkinson’s or parasitic diseases such as Leishmaniasis and Malaria.

scholarly journals Enhancing Salt Tolerance in Soybean by Exogenous Boron: Intrinsic Study of the Ascorbate-Glutathione and Glyoxalase Pathways

Plants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2085
Author(s):  
Hesham F. Alharby ◽  
Kamrun Nahar ◽  
Hassan S. Al-Zahrani ◽  
Khalid Rehman Hakeem ◽  
Mirza Hasanuzzaman
Keyword(s):  
Oxidative Stress ◽  
Salt Stress ◽  
Antioxidant Defense ◽  
Higher Plants ◽  
Antioxidant Defense System ◽  
Protective Role ◽  
Monodehydroascorbate Reductase ◽  
Glyoxalase System ◽  
System Components ◽  
Soybean Plants

Boron (B) performs physiological functions in higher plants as an essential micronutrient, but its protective role in salt stress is poorly understood. Soybean (Glycine max L.) is planted widely throughout the world, and salinity has adverse effects on its physiology. Here, the role of B (1 mM boric acid) in salt stress was studied by subjecting soybean plants to two levels of salt stress: mild (75 mM NaCl) and severe (150 mM NaCl). Exogenous B relieved oxidative stress by enhancing antioxidant defense system components, such as ascorbate (AsA) levels, AsA/dehydroascorbate ratios, glutathione (GSH) levels, the GSH and glutathione disulfide ratios, and ascorbate peroxidase, monodehydroascorbate reductase, and dehydroascorbate reductase activities. B also enhanced the methylglyoxal detoxification process by upregulation of the components of the glyoxalase system in salt-stressed plants. Overall, B supplementation enhanced antioxidant defense and glyoxalase system components to alleviate oxidative stress and MG toxicity induced by salt stress. B also improved the physiology of salt-affected soybean plants.

The Impact of L-Carnitine and Coenzyme Q10 as Protection Against Busulfan-Oxidative Stress in the Liver of Adult Rats

2020 ◽  
Vol 10 (5) ◽  
pp. 578-586
Author(s):  
Areeg M. Abdelrazek ◽  
Shimaa A. Haredy
Keyword(s):  
Oxidative Stress ◽  
Coenzyme Q10 ◽  
Protective Role ◽  
Albino Rats ◽  
Distilled Water ◽  
Negative Effects ◽  
Adult Rats ◽  
Stress Damage ◽  
The Impact ◽  
Liver Tissues

Background: Busulfan (Bu) is an anticancer drug with a variety of adverse effects for cancer patients. Oxidative stress has been considered as a common pathological mechanism and it has a key role in the initiation and progression of liver injury by Bu. Aim: The study aimed to evaluate the antioxidant impact of L-Carnitine and Coenzyme Q10 and their protective role against oxidative stress damage in liver tissues. Methods and Material: Thirty-six albino rats were divided equally into six groups. G1 (con), received I.P. injection of DMSO plus 1 ml of distilled water daily by oral gavages; G2 (Bu), received I.P. injection of Bu plus 1 ml of the distilled water daily; G3 (L-Car), received 1 ml of L-Car orally; G4 (Bu + L-Car) received I.P. injection of Bu plus 1 ml of L-Car, G5 (CoQ10) 1 ml of CoQ10 daily; and G6 (Bu + CoQ10) received I.P. injection of Bu plus 1 ml of CoQ10 daily. Results: The recent data showed that Bu induced significant (P<0.05) elevation in serum ALT, AST, liver GSSG, NO, MDA and 8-OHDG, while showing significant (P<0.05) decrease in liver GSH and ATP. On the other hand, L-Carnitine and Coenzyme Q10 ameliorated the negative effects prompted by Bu. Immunohistochemical expression of caspase-3 in liver tissues reported pathological alterations in Bu group while also showed significant recovery in L-Car more than CoQ10. Conclusion: L-Car, as well as CoQ10, can enhance the hepatotoxic effects of Bu by promoting energy production in oxidative phosphorylation process and by scavenging the free radicals.

scholarly journals Antia, a Natural Antioxidant Product, Attenuates Cognitive Dysfunction in Streptozotocin-Induced Mouse Model of Sporadic Alzheimer’s Disease by Targeting the Amyloidogenic, Inflammatory, Autophagy, and Oxidative Stress Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nesrine S. El Sayed ◽  
Mamdooh H. Ghoneum
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Protective Effect ◽  
Cognitive Dysfunction ◽  
Protective Role ◽  
Sporadic Alzheimer’S Disease ◽  
Stat3 Pathway ◽  
And Oxidative Stress

Background. Many neurodegenerative diseases such as Alzheimer’s disease are associated with oxidative stress. Therefore, antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases. Objective. We investigated the ability of the antioxidant Antia to exert a protective effect against sporadic Alzheimer’s disease (SAD) induced in mice. Antia is a natural product that is extracted from the edible yamabushitake mushroom, the gotsukora and kothala himbutu plants, diosgenin (an extract from wild yam tubers), and amla (Indian gooseberry) after treatment with MRN-100. Methods. Single intracerebroventricular (ICV) injection of streptozotocin (STZ) (3 mg/kg) was used for induction of SAD in mice. Antia was injected intraperitoneally (i.p.) in 3 doses (25, 50, and 100 mg/kg/day) for 21 days. Neurobehavioral tests were conducted within 24 h after the last day of injection. Afterwards, mice were sacrificed and their hippocampi were rapidly excised, weighed, and homogenized to be used for measuring biochemical parameters. Results. Treatment with Antia significantly improved mice performance in the Morris water maze. In addition, biochemical analysis showed that Antia exerted a protective effect for several compounds, including GSH, MDA, NF-κB, IL-6, TNF-α, and amyloid β. Further studies with western blot showed the protective effect of Antia for the JAK2/STAT3 pathway. Conclusions. Antia exerts a significant protection against cognitive dysfunction induced by ICV-STZ injection. This effect is achieved through targeting of the amyloidogenic, inflammatory, and oxidative stress pathways. The JAK2/STAT3 pathway plays a protective role for neuroinflammatory and neurodegenerative diseases such as SAD.

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