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 Transposition of Insertion Sequences was Triggered by Oxidative Stress in Radiation-Resistant Bacterium Deinococcus geothermalis

2019 ◽  
Vol 7 (10) ◽  
pp. 446 ◽  
Author(s):  
Chanjae Lee ◽  
Nakjun Choi ◽  
Min K. Bae ◽  
Kyungsil Choo ◽  
Sung-Jae Lee
Keyword(s):  
Oxidative Stress ◽  
Family Member ◽  
Mutant Strain ◽  
Mutant Cell ◽  
Carotenoid Biosynthesis ◽  
Wild Type ◽  
Is Element ◽  
Deinococcus Geothermalis ◽  
Key Enzyme ◽  
Radiation Resistant

During an oxidative stress-response assay on a putative Dps-like gene-disrupted Δdgeo_0257 mutant strain of radiation-resistant bacterium Deinococcus geothermalis, a non-pigmented colony was observed among the normal reddish color colonies. This non-pigmented mutant cell subsequently displayed higher sensitivity to H2O2. While carotenoid has a role in protecting as scavenger of reactive oxygen species the reddish wild-type strain from radiation and oxidative stresses, it is hypothesized that the carotenoid biosynthesis pathway has been disrupted in the mutant D. geothermalis cell. Here, we show that, in the non-pigmented mutant cell of interest, phytoene desaturase (Dgeo_0524, crtI), a key enzyme in carotenoid biosynthesis, was interrupted by transposition of an ISDge7 family member insertion sequence (IS) element. RNA-Seq analysis between wild-type and Δdgeo_0257 mutant strains revealed that the expression level of ISDge5 family transposases, but not ISDge7 family members, were substantially up-regulated in the Δdgeo_0257 mutant strain. We revealed that the non-pigmented strain resulted from the genomic integration of ISDge7 family member IS elements, which were also highly up-regulated, particularly following oxidative stress. The transposition path for both transposases is a replicative mode. When exposed to oxidative stress in the absence of the putative DNA binding protein Dgeo_0257, a reddish D. geothermalis strain became non-pigmented. This transformation was facilitated by transposition of an ISDge7 family IS element into a gene encoding a key enzyme of carotenoid biosynthesis. Further, we present evidence of additional active transposition by the ISDge5 family IS elements, a gene that was up-regulated during the stationary phase regardless of the presence of 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.

Two-dimensional proteome reference map for the radiation-resistant bacterium Deinococcus geothermalis

PROTEOMICS ◽  
2009 ◽  
Vol 10 (3) ◽  
pp. 555-563 ◽  
Author(s):  
Christina Liedert ◽  
Jörg Bernhardt ◽  
Dirk Albrecht ◽  
Birgit Voigt ◽  
Michael Hecker ◽  
...  
Keyword(s):  
Resistant Bacterium ◽  
Two Dimensional ◽  
Deinococcus Geothermalis ◽  
Radiation Resistant ◽  
Reference Map

Abstract 15092: The Yin-yang of Bmpr2 and Ces1 in the Pulmonary Endothelium Aad Its Role in Pulmonary Arterial Hypertension

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Stuti Agarwal ◽  
Ananya Chakraborty ◽  
David Condon ◽  
Salvador Tello ◽  
Karthik Suresh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Redox Balance ◽  
Tube Formation ◽  
Vascular Lesions ◽  
Mrna Levels ◽  
Loss Of Function ◽  
Pulmonary Endothelium ◽  
Pulmonary Arterial

Background/Hypothesis: Pulmonary Arterial Hypertension (PAH) is a life-threatening disease characterized by loss of pulmonary microvessels and vascular remodeling. Loss of function BMPR2 mutations contribute to pulmonary endothelial cell (EC) apoptosis and oxidative stress, but their reduced penetrance suggests need for additional modifiers. Carboxylesterase1 (CES1) is endoplasmic reticulum (ER) enzyme responsible for detoxification, proteostasis, and redox balance. Similar to BMPR2 mutations, we found that loss of CES1 is associated with oxidative stress and apoptosis. In this study, we explore a plausible link between BMPR2 pathway and CES1 regulation in promoting EC survival and angiogenesis. Methods: PECs & lung tissue from healthy donors and PAH patients were obtained from PHBI. To induce oxidative stress, we used H 2 O 2 (100 μM) & methamphetamine HCl (METH, 0.5-2mM). Both siRNA and pharmacological approaches were used to inhibit BMPR2, Nrf2, and CES1 expression. Caspase and Matrigel assays were used to assess PEC survival and tube formation, respectively. Results: RNAseq of BMPR2-mutant PECs showed significantly less CES1 expression, which correlated with reduced protein expression in PEC lysates and within lung vascular lesions. In healthy PECs, BMP9 stimulation led to increase in CES1 expression that was absent post BMPR2 knockdown. CES1 gene transcription was by BMPR2-dependent activation of Nrf2, a transcription factor responsible for antioxidant gene expression and mitochondrial biogenesis. Inhibition of Nrf2 activation by ML385 (5μM) abrogates BMP9 induced CES1 mRNA levels similar to BMPR2 knockdown. The connection between BMPR2 and CES1 was further strengthened by CES1 knockdown studies in PECs that demonstrated reduction in BMPR2 protein synthesis associated with ER stress and reduced autophagy. Finally, lung examination in CRISPR generated CES1 +/- mice demonstrated increased microvascular muscularization at normoxia compared to wild type mice. Conclusion: BMPR2 and CES1 are part of common signaling pathway that protects PECs against oxidative stress and mitochondrial damage through a positive feedback loop. Interventions that restore CES1 activity could rescue BMPR2 signaling and serve as novel PAH therapeutics.

scholarly journals Genome Plasticity by Insertion Sequences Learned From a Case of Radiation-Resistant Bacterium Deinococcus geothermalis

2021 ◽  
Vol 15 ◽  
pp. 117793222110374
Author(s):  
Chanjae Lee ◽  
Min K Bae ◽  
Nakjun Choi ◽  
Su Jeong Lee ◽  
Sung-Jae Lee
Keyword(s):  
Bacterial Genome ◽  
Single Species ◽  
Resistant Bacterium ◽  
Insertion Sequences ◽  
Genome Plasticity ◽  
Total Size ◽  
Deinococcus Geothermalis ◽  
Radiation Resistant ◽  
Is Integration ◽  
Main Chromosome

The genome of the radiation-resistant bacterium Deinococcus geothermalis contains 19 types of insertion sequences (ISs), including 93 total transposases (Tpases) in 73 full-length ISs from the main chromosome and 2 mega plasmids. In this study, 68 ISs from the D. geothermalis genome were extracted to implicate the earlier genome before its mutation by transposition of ISs. The total size of eliminated ISs from genome was 78.85 kb. From these in silico corrections of mutation by the ISs, we have become aware of some bioinformatics factualness as follows: (1) can reassemble the disrupted genes if the exact IS region was eliminated, (2) can configure the schematic clustering of major DDE type Tpases, (3) can determine IS integration order across multiple hot spots, and (4) can compare genetic relativeness by the partial synteny analysis between D. geothermalis and Deinococcus strain S9. Recently, we found that several IS elements actively transferred to other genomic sites under hydrogen peroxide-induced oxidative stress conditions, resulting in the inactivation of functional genes. Therefore, the single species genome’s mobilome study provides significant support to define bacterial genome plasticity and molecular evolution from past and present progressive transposition events.

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 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 Redox Imbalance in T Cell-Mediated Skin Diseases

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Saveria Pastore ◽  
Liudmila Korkina
Keyword(s):  
Oxidative Stress ◽  
Atopic Dermatitis ◽  
Contact Dermatitis ◽  
Skin Diseases ◽  
Redox Balance ◽  
Inflammatory Disorder ◽  
Chronic Inflammatory Disorder ◽  
Physical Chemical ◽  
Chemical Oxidants ◽  
Beneficial Outcome

The skin is permanently exposed to physical, chemical, and biological aggression by the environment. In addition, acute and chronic inflammatory events taking place in the skin are accompanied by abnormal release of pro-oxidative mediators. In this paper, we will briefly overview the homeostatic systems active in the skin to maintain the redox balance and also to counteract abnormal oxidative stress. We will concentrate on the evidence that a local and/or systemic redox dysregulation accompanies the chronic inflammatory disorder events associated to psoriasis, contact dermatitis, and atopic dermatitis. We will also discuss the fact that several well-established treatments for the therapy of chronic inflammatory skin disorders are based on the application of strong physical or chemical oxidants onto the skin, indicating that, in selected conditions, a further increase of the oxidative imbalance may lead to a beneficial outcome.

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