scholarly journals Reactive Oxygen Species and Thiol Redox Signaling in the Macrophage Biology of Atherosclerosis

2012 ◽  
Vol 17 (12) ◽  
pp. 1785-1795 ◽  
Author(s):  
Sina Tavakoli ◽  
Reto Asmis
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Redox Signaling ◽  
Oxygen Species ◽  
Thiol Redox

scholarly journals Computational simulation of the reactive oxygen species and redox network in the regulation of chloroplast metabolism

2019 ◽  
Author(s):  
Melanie Gerken ◽  
Sergej Kakorin ◽  
Kamel Chibani ◽  
Karl-Josef Dietz
Keyword(s):  
Reactive Oxygen Species ◽  
Regulatory Network ◽  
Electron Flow ◽  
Computational Simulation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Animal Cells ◽  
Unknown Parameters ◽  
Target Proteins ◽  
Thiol Redox

AbstractCells contain a thiol redox regulatory network to coordinate metabolic and developmental activities with exogenous and endogenous cues. This network controls the redox state and activity of many target proteins. Electrons are fed into the network from metabolism and reach the target proteins via redox transmitters such as thioredoxin (TRX) and NADPH-dependent thioredoxin reductases (NTR). Electrons are drained from the network by reactive oxygen species (ROS) through thiol peroxidases, e.g., peroxiredoxins (PRX). Mathematical modeling promises access to quantitative understanding of the network function and was implemented for the photosynthesizing chloroplast by using published kinetic parameters combined with fitting to known biochemical data. Two networks were assembled, namely the ferredoxin (FDX), FDX-dependent TRX reductase (FTR), TRX, fructose-1,6-bisphosphatase pathway with 2-cysteine PRX/ROS as oxidant, and separately the FDX, FDX-dependent NADP reductase (FNR), NADPH, NTRC-pathway for 2-CysPRX reduction. Combining both modules allowed drawing several important conclusions of network performance. The resting H2O2 concentration was estimated to be about 30 nM in the chloroplast stroma. The electron flow to metabolism exceeds that into thiol regulation of FBPase more than 7000-fold under physiological conditions. The electron flow from NTRC to 2-CysPRX is about 5.46-times more efficient than that from TRX-f1 to 2-CysPRX. Under severe stress (30 μM H2O2) the ratio of electron flow to the thiol network relative to metabolism sinks to 1:251 whereas the ratio of electron flow from NTRC to 2-CysPRX and TRX-f1 to 2-CysPRX rises up to 1:80. Thus, the simulation provides clues on experimentally inaccessible parameters and describes the functional state of the chloroplast thiol regulatory network.Authors summaryThe state of the thiol redox regulatory network is a fundamental feature of all cells and determines metabolic and developmental processes. However, only some parameters are quantifiable in experiments. This paper establishes partial mathematical models which enable simulation of electron flows through the regulatory system. This in turn allows for estimating rates and states of components of the network and to tentatively address previously unknown parameters such as the resting hydrogen peroxide levels or the expenditure of reductive power for regulation relative to metabolism. The establishment of such models for simulating the performance and dynamics of the redox regulatory network is of significance not only for photosynthesis but also, e.g., in bacterial and animal cells exposed to environmental stress or pathological disorders.

Effects of acetaminophen on reactive oxygen species and nitric oxide redox signaling in kidney of arsenic-exposed rats

2011 ◽  
Vol 49 (4) ◽  
pp. 974-982 ◽  
Author(s):  
Chhaya Rani Majhi ◽  
Saleem Khan ◽  
Marie Dennis Marcus Leo ◽  
Ayyasamy Manimaran ◽  
Palanisamy Sankar ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Redox Signaling ◽  
Oxygen Species

scholarly journals Ebsulfur Is a Benzisothiazolone Cytocidal Inhibitor Targeting the Trypanothione Reductase of Trypanosoma brucei

2013 ◽  
Vol 288 (38) ◽  
pp. 27456-27468 ◽  
Author(s):  
Jun Lu ◽  
Suman K. Vodnala ◽  
Anna-Lena Gustavsson ◽  
Tomas N. Gustafsson ◽  
Birger Sjöberg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Trypanosoma Brucei ◽  
Mammalian Cells ◽  
Reactive Oxygen ◽  
Redox System ◽  
Trypanothione Reductase ◽  
Oxygen Species ◽  
African Trypanosomiasis ◽  
Thiol Redox

Trypanosoma brucei is the causing agent of African trypanosomiasis. These parasites possess a unique thiol redox system required for DNA synthesis and defense against oxidative stress. It includes trypanothione and trypanothione reductase (TryR) instead of the thioredoxin and glutaredoxin systems of mammalian hosts. Here, we show that the benzisothiazolone compound ebsulfur (EbS), a sulfur analogue of ebselen, is a potent inhibitor of T. brucei growth with a favorable selectivity index over mammalian cells. EbS inhibited the TryR activity and decreased non-protein thiol levels in cultured parasites. The inhibition of TryR by EbS was irreversible and NADPH-dependent. EbS formed a complex with TryR and caused oxidation and inactivation of the enzyme. EbS was more toxic for T. brucei than for Trypanosoma cruzi, probably due to lower levels of TryR and trypanothione in T. brucei. Furthermore, inhibition of TryR produced high intracellular reactive oxygen species. Hydrogen peroxide, known to be constitutively high in T. brucei, enhanced the EbS inhibition of TryR. The elevation of reactive oxygen species production in parasites caused by EbS induced a programmed cell death. Soluble EbS analogues were synthesized and cured T. brucei brucei infection in mice when used together with nifurtimox. Altogether, EbS and EbS analogues disrupt the trypanothione system, hampering the defense against oxidative stress. Thus, EbS is a promising lead for development of drugs against African trypanosomiasis.

scholarly journals The role of reactive oxygen species in myocardial redox signaling and regulation

2017 ◽  
Vol 5 (16) ◽  
pp. 324-324 ◽  
Author(s):  
Demetrios Moris ◽  
Michael Spartalis ◽  
Eleni Tzatzaki ◽  
Eleftherios Spartalis ◽  
Georgia-Sofia Karachaliou ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Redox Signaling ◽  
Oxygen Species

scholarly journals Reactive Oxygen Species and Redox Signaling in Chronic Kidney Disease

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1342 ◽  
Author(s):  
Maria V. Irazabal ◽  
Vicente E. Torres
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Reactive Oxygen ◽  
Public Health Problem ◽  
Redox Signaling ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Related Factor ◽  
Oxygen Species

Chronic kidney disease (CKD) remains a worldwide public health problem associated with serious complications and increased mortality rates. Accumulating evidence indicates that elevated intracellular levels of reactive oxygen species (ROS) play a major role in the pathogenesis of CKD. Increased intracellular levels of ROS can lead to oxidation of lipids, DNA, and proteins, contributing to cellular damage. On the other hand, ROS are also important secondary messengers in cellular signaling. Consequently, normal kidney cell function relies on the “right” amount of ROS. Mitochondria and NADPH oxidases represent major sources of ROS in the kidney, but renal antioxidant systems, such as superoxide dismutase, catalase, or glutathione peroxidase counterbalance ROS-mediated injury. This review discusses the main sources of ROS and antioxidant systems in the kidney, and redox signaling pathways leading to inflammation and fibrosis, which result in abnormal kidney function and CKD progression. We further discuss the important role of the nuclear factor erythroid 2-related factor 2 (Nrf2) in regulating antioxidant responses, and other mechanisms of redox signaling.

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