Role of NADPH and hydrogen peroxide in modulating oxidative stress and oocyte aging

2004 ◽  
Vol 82 ◽  
pp. S111
Author(s):  
P.T. Goud ◽  
A.P. Goud ◽  
H.M. Abu-Soud ◽  
M.P. Diamond
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oocyte Aging

scholarly journals S-Allyl Cysteine Alleviates Hydrogen Peroxide Induced Oxidative Injury and Apoptosis through Upregulation of Akt/Nrf-2/HO-1 Signaling Pathway in HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Chitra Basu ◽  
Runa Sur
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Damage ◽  
Hepg2 Cells ◽  
Liver Diseases ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Cell Viability Assay

Hydrogen peroxide (H2O2) mediated oxidative stress leading to hepatocyte apoptosis plays a pivotal role in the pathophysiology of several chronic liver diseases. This study demonstrates that S-allyl cysteine (SAC) renders cytoprotective effects on H2O2 induced oxidative damage and apoptosis in HepG2 cells. Cell viability assay showed that SAC protected HepG2 cells from H2O2 induced cytotoxicity. Further, SAC treatment dose dependently inhibited H2O2 induced apoptosis via decreasing the Bax/Bcl-2 ratio, restoring mitochondrial membrane potential (∆Ψm), inhibiting mitochondrial cytochrome c release, and inhibiting proteolytic cleavage of caspase-3. SAC protected cells from H2O2 induced oxidative damage by inhibiting reactive oxygen species accumulation and lipid peroxidation. The mechanism underlying the antiapoptotic and antioxidative role of SAC is the induction of the heme oxygenase-1 (HO-1) gene in an NF-E2-related factor-2 (Nrf-2) and Akt dependent manner. Specifically SAC was found to induce the phosphorylation of Akt and enhance the nuclear localization of Nrf-2 in cells. Our results were further confirmed by specific HO-1 gene knockdown studies which clearly demonstrated that HO-1 induction indeed played a key role in SAC mediated inhibition of apoptosis and ROS production in HepG2 cells, thus suggesting a hepatoprotective role of SAC in combating oxidative stress mediated liver diseases.

scholarly journals Cytoprotective role of vitamin E in porcine adipose-tissue-derived mesenchymal stem cells against hydrogen-peroxide-induced oxidative stress

2018 ◽  
Vol 374 (1) ◽  
pp. 111-120 ◽  
Author(s):  
Fazal Ur Rehman Bhatti ◽  
Song Ja Kim ◽  
Ae-Kyung Yi ◽  
Karen A. Hasty ◽  
Hongsik Cho
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Vitamin E

scholarly journals Regulation of Brucella abortusCatalase

2000 ◽  
Vol 68 (7) ◽  
pp. 3861-3866 ◽  
Author(s):  
Jeong-a Kim ◽  
Zengyu Sha ◽  
John E. Mayfield
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Pathogenic Bacteria ◽  
Sublethal Concentration ◽  
Subsequent Exposure ◽  
Catalase Peroxidase ◽  
Increased Sensitivity ◽  
Analysis Survival ◽  
Hostile Environments

ABSTRACT All aerobic organisms have mechanisms that protect against oxidative compounds. Catalase, peroxidase, superoxide dismutase, glutathione, and thioredoxin are widely distributed in many taxa and constitute elements of a nearly ubiquitous antioxidant metabolic strategy. Interestingly, the regulatory mechanisms that control these elements are rather different depending on the nature of the oxidative stress and the organism. Catalase is well documented to play an important role in protecting cells from oxidative stress. In particular, pathogenic bacteria seem to use this enzyme as a defensive tool against attack by the host. To investigate the significance of catalase in hostile environments, we made catalase deletion mutations in two different B. abortus strains and used two-dimensional gel analysis, survival tests, and adaptation experiments to explore the behavior and role of catalase under several oxidative stress conditions. These studies show that B. abortus strains that do not express catalase activity exhibit increased sensitivity to hydrogen peroxide. We also demonstrate that catalase expression is regulated in this species, and that preexposure to a sublethal concentration of hydrogen peroxide allows B. abortus to adapt so as to survive subsequent exposure to higher concentrations of hydrogen peroxide.

scholarly journals Manganese Homeostasis in Group A Streptococcus Is Critical for Resistance to Oxidative Stress and Virulence

mBio ◽  
2015 ◽  
Vol 6 (2) ◽  
Author(s):  
Andrew G. Turner ◽  
Cheryl-lynn Y. Ong ◽  
Christine M. Gillen ◽  
Mark R. Davies ◽  
Nicholas P. West ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Transition Metal ◽  
Metal Ion ◽  
Double Mutant ◽  
Efflux Pump ◽  
Group A Streptococcus ◽  
Wild Type ◽  
Group A

ABSTRACT Streptococcus pyogenes (group A Streptococcus [GAS]) is an obligate human pathogen responsible for a spectrum of human disease states. Metallobiology of human pathogens is revealing the fundamental role of metals in both nutritional immunity leading to pathogen starvation and metal poisoning of pathogens by innate immune cells. Spy0980 (MntE) is a paralog of the GAS zinc efflux pump CzcD. Through use of an isogenic mntE deletion mutant in the GAS serotype M1T1 strain 5448, we have elucidated that MntE is a manganese-specific efflux pump required for GAS virulence. The 5448ΔmntE mutant had significantly lower survival following infection of human neutrophils than did the 5448 wild type and the complemented mutant (5448ΔmntE::mntE). Manganese homeostasis may provide protection against oxidative stress, explaining the observed ex vivo reduction in virulence. In the presence of manganese and hydrogen peroxide, 5448ΔmntE mutant exhibits significantly lower survival than wild-type 5448 and the complemented mutant. We hypothesize that MntE, by maintaining homeostatic control of cytoplasmic manganese, ensures that the peroxide response repressor PerR is optimally poised to respond to hydrogen peroxide stress. Creation of a 5448ΔmntE-ΔperR double mutant rescued the oxidative stress resistance of the double mutant to wild-type levels in the presence of manganese and hydrogen peroxide. This work elucidates the mechanism for manganese toxicity within GAS and the crucial role of manganese homeostasis in maintaining GAS virulence. IMPORTANCE Manganese is traditionally viewed as a beneficial metal ion to bacteria, and it is also established that most bacteria can tolerate high concentrations of this transition metal. In this work, we show that in group A Streptococcus, mutation of the mntE locus, which encodes a transport protein of the cation diffusion facilitator (CDF) family, results in accumulation of manganese and sensitivity to this transition metal ion. The toxicity of manganese is indirect and is the result of a failure of the PerR regulator to respond to oxidative stress in the presence of high intracellular manganese concentrations. These results highlight the importance of MntE in manganese homeostasis and maintenance of an optimal manganese/iron ratio in GAS and the impact of manganese on resistance to oxidative stress and virulence.

Role of calreticulin in the sensitivity of myocardiac H9c2 cells to oxidative stress caused by hydrogen peroxide

2006 ◽  
Vol 290 (1) ◽  
pp. C208-C221 ◽  
Author(s):  
Yoshito Ihara ◽  
Yoshishige Urata ◽  
Shinji Goto ◽  
Takahito Kondo
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Molecular Chaperone ◽  
Vital Role ◽  
H9c2 Cells ◽  
Cardiac Physiology ◽  
Caspase 12 ◽  
A Cell ◽  
Induced Apoptosis

Calreticulin (CRT), a Ca2+-binding molecular chaperone in the endoplasmic reticulum, plays a vital role in cardiac physiology and pathology. Oxidative stress is a main cause of myocardiac apoptosis in the ischemic heart, but the function of CRT under oxidative stress is not fully understood. In the present study, the effect of overexpression of CRT on susceptibility to apoptosis under oxidative stress was examined using myocardiac H9c2 cells transfected with the CRT gene. Under oxidative stress due to H2O2, the CRT-overexpressing cells were highly susceptible to apoptosis compared with controls. In the overexpressing cells, the levels of cytoplasmic free Ca2+ ([Ca2+]i) were significantly increased by H2O2, whereas in controls, only a slight increase was observed. The H2O2-induced apoptosis was enhanced by the increase in [Ca2+]i caused by thapsigargin in control cells but was suppressed by BAPTA-AM, a cell-permeable Ca2+ chelator in the CRT-overexpressing cells, indicating the importance of the level of [Ca2+]i in the sensitivity to H2O2-induced apoptosis. Suppression of CRT by the introduction of the antisense cDNA of CRT enhanced cytoprotection against oxidative stress compared with controls. Furthermore, we found that the levels of activity of calpain and caspase-12 were elevated through the regulation of [Ca2+]i in the CRT-overexpressing cells treated with H2O2 compared with controls. Thus we conclude that the level of CRT regulates the sensitivity to apoptosis under oxidative stress due to H2O2 through a change in Ca2+ homeostasis and the regulation of the Ca2+-calpain-caspase-12 pathway in myocardiac cells.

scholarly journals Role of protein kinases JNK and p38 in regulation of mononuclear leucocytes apoptosis in oxidative stress

2008 ◽  
Vol 7 (3) ◽  
pp. 38-43 ◽  
Author(s):  
N. Yu. Chasovskikh
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Transmembrane Potential ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Stress Induction ◽  
Healthy Donors ◽  
Mononuclear Leucocytes

Programmed cell death of peripheral blood mononuclear leucocytes taken from healthy donors and cultivated with various concentration of Н2О2, selective inhibitors of JNK (SP600125), 38 (ML3403) and in case of pneumonia was investigated. Intensification of intracellular production of reactive oxy р МАРК - gen species was accompanied by the increase in number of apoptotic and TNFR1-presented cells and mononuclears with reduced value of mitochondrial transmembrane potential in a case of oxidative stress induction with 1 mM hydrogen peroxide and in blood taken from patients with pneumonia. Action of inhibitors SP600125 and ML3403 in vitro in oxidative stress conditions prevents the increase in number of annexin- positive mononuclear cells, that confirms the participation of JNK and 38 -kinases in mechanisms of oxidative stress-mediated apoptosis dysregulation.

scholarly journals Photobiomodulation Therapy Decreases Oxidative Stress in the Lung Tissue after Formaldehyde Exposure: Role of Oxidant/Antioxidant Enzymes

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Rodrigo Silva Macedo ◽  
Mayara Peres Leal ◽  
Tarcio Teodoro Braga ◽  
Éric Diego Barioni ◽  
Stephanie de Oliveira Duro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Oxidative Burst ◽  
Photobiomodulation Therapy ◽  
Heme Oxygenase 1 ◽  
New Information ◽  
Male Wistar Rats ◽  
Formaldehyde Exposure ◽  
Antioxidant Mechanisms

Formaldehyde is ubiquitous pollutant that induces oxidative stress in the lung. Several lung diseases have been associated with oxidative stress and their control is necessary. Photobiomodulation therapy (PBMT) has been highlighted as a promissory treatment, but its mechanisms need to be better investigated. Our objective was to evaluate the effects of PBMT on the oxidative stress generated by FA exposure. Male Wistar rats were submitted to FA exposure of 1% or vehicle (3 days) and treated or not with PBMT (1 and 5 h after each FA exposure). Rats treated only with laser were used as control. Twenty-four hours after the last FA exposure, we analyzed the effects of PBMT on the generation of nitrites and hydrogen peroxide, oxidative burst, glutathione reductase, peroxidase, S-transferase enzyme activities, the gene expression of nitric oxide, cyclooxygenase, superoxide dismutase, the catalase enzyme, and heme oxygenase-1. PBMT reduced the generation of nitrites and hydrogen peroxide and increased oxidative burst in the lung cells. A decreased level of oxidant enzymes was observed which were concomitantly related to an increased level of antioxidants. This study provides new information about the antioxidant mechanisms of PBMT in the lung and might constitute an important tool for lung disease treatment.

ROLE OF PREGNAN-X-RECEPTOR IN CELL RESISTANCE TO NITROSATIVE AND OXIDATIVE STRESS

2021 ◽  
Author(s):  
Yulia Abalenikhina ◽  
◽  
Elena A. Sudakova ◽  
Pelageya Erokhina ◽  
Aleksey Shchulkin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Nitrosative Stress ◽  
Pregnane X Receptor ◽  
Cell Resistance ◽  
Oxidative And Nitrosative Stress ◽  
High Concentrations ◽  
And Oxidative Stress

The article discusses the new role of pregnane X receptor (PXR) under conditions of oxidative and nitrosative stress. The results showed that the effect of hydrogen peroxide and S-nitrosoglu-tathione in high concentrations on Caco-2 cells leads to a decrease in cell viability, which is accompanied by an increase in the amount of PXR. These changes are offset by the addition of ketoconazole (inhibitor of PXR) to the medium.

scholarly journals TEP production under oxidative stress of the picocyanobacterium Synechococcus

2019 ◽  
Vol 78 (3) ◽  
Author(s):  
Cristiana Callieri ◽  
María B. Sathicq ◽  
Pedro J. Cabello-Yeves ◽  
Ester M. Eckert ◽  
Justo Salvador Hernández-Avilés
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Potential Role ◽  
Hot Spot ◽  
Active Radiation ◽  
C Cell ◽  
Limiting Nutrients ◽  
Acidic Polysaccharides ◽  
A Cell

Transparent exopolymer particles (TEP) are mainly acidic polysaccharides directly or indirectly formed by phytoplankton and bacteria. These particles are often colonized by picoplankton and considered a hot spot for microbial activity. Recent studies suggested an important role of Synechococcus in TEP production found in lakes and prompted us to further investigate this issue using monoclonal xenic cultures of Synechococcus. We tested TEP production under oxidative stress in two treatments, one with hydrogen peroxide and another treated with ultraviolet radiation (UVR) and high photosynthetic active radiation (PAR), compared with an unstressed control. Our results showed a cell-normalized TEP production, ranging from 12 to 238 ng C cell-1 among strains, not only under stress but also in the control with non-limiting nutrients. Our data prove that freshwater communities of Synechococcus and their associated heterotrophic microflora, are capable of producing TEP even during growth phase. The oxidative stress induced extra production of TEP up to 400 ng C cell-1 in one of our phycocyanin-type (PC) strain. The phycoerythrin-type (PE) strains increased TEP production, particularly under UV-PAR stress, whereas the PC strains did it under H2O2 stress. This study provides new perspectives on the potential role of freshwater Synechococcus in TEP production.

scholarly journals The Role of theExo-XisRegion in Oxidative Stress-Mediated Induction of Shiga Toxin-Converting Prophages

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Katarzyna Licznerska ◽  
Aleksandra Dydecka ◽  
Sylwia Bloch ◽  
Gracja Topka ◽  
Bożena Nejman-Faleńczyk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Shiga Toxin ◽  
Regulatory Genes ◽  
Prophage Induction ◽  
Dramatic Decrease ◽  
E Coli ◽  
Genetic Elements ◽  
Efficient Expression

Previous studies indicated that these genetic elements could be involved in the regulation of lysogenization and prophage induction processes. The effects were dramatic in Shiga toxin-converting phageΦ24Bafter treatment with oxidative stress-inducing agent, hydrogen peroxide, while they were less pronounced in bacteriophageλand in both phages irradiated with UV. The hydrogen peroxide-caused prophage induction was found to be RecA-dependent. Importantly, in hydrogen peroxide-treatedE. colicells lysogenic for eitherλorΦ24B, deletion of theexo-xisregion resulted in a significant decrease in the levels of expression of the S.O.S. regulon genes. Moreover, under these conditions, a dramatic decrease in the levels of expression of phage genes crucial for lytic development (particularlyxis, exo, N, cro, O, Q, andR) could be observed inΦ24B-, but not inλ-bearing cells. We conclude that genes located in theexo-xisregion are necessary for efficient expression of both host S.O.S regulon in lysogenic bacteria and regulatory genes of Shiga toxin-converting bacteriophageΦ24B.

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