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Antioxidants
Special Issues
NO and ROS in Redox Signalling
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NO and ROS in Redox Signalling

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 5210

Special Issue Editors

Prof. Dr. Bulent Mutus

E-Mail Website
Guest Editor
Department of Chemistry and Biochemistry, University of Windsor, Windsor, ON N9B 3P4, Canada
Interests: enzymology; protein structure-function; redox signalling; dynamic microscopy; cell biology; intravital fluorescent probes; nanosensors for nitric oxide; thiols and NOx; platelet biochemistry; flow devices; environmental sensor development; the use of biopolymers for the mitigation of environmental phosphate
Special Issues, Collections and Topics in MDPI journals
Dr. Anny Slama-Schwok

E-Mail Website
Guest Editor
Sorbonne Université, INSERM U938, Centre de Recherche Saint Antoine, Biology and Cancer Therapeutics, Saint Antoine Hospital, 75231 Paris, France
Interests: structure-based drug design; NADPH oxidase inhibitors; tumor-associated macrophages; photoactivatable NADPH analogs; antiviral drugs

Special Issue Information

Dear Colleagues,

Nitric oxide (NO) and reactive oxygen species (ROS) superoxide, hydrogen peroxide, and to a lesser extent hydroxyl radical and singlet oxygen regulate a myriad of physiological processes required for the health of organisms.  Our goal in this Special Issue is to present the state of the art on pathways, either physio-pathological or alternative ones, regulating oxidative stress.

NO and ROS can be generated by a variety of oxydoreductases or hemoglobins that, depending on levels of NO or molecular oxygen, can produce either protective or pathological levels of NO or ROS.  Moreover, alternative pathways for producing NO from nitrite or nitrate via various hemoproteins can increase the levels of NO whenever needed under hypoxic conditions. Activators of soluble guanylate cyclase can also improve normal signaling. Additional activities of some hemoproteins to generate ROS by enzymatic decoupling (mitochondrial enzymes, NOS enzymes) or decrease ROS through an increased SOD activity, as recently shown for cytoglobin, will also enhance pathological conditions or reduce oxidative stress.

The goal in redox signaling research is to gain an understanding of the molecular events that underlie the critical point at which the interplay between NO and ROS levels leads to either a physiological or pathological response.  Such studies require the precise and direct measurement of very low levels of NO and ROS during their transient fluxes in vivo.

This Special Issue of Antioxidants invites researchers who are at the forefront of utilizing chemical tools coupled to physical techniques for the intravital determination of NO and/or ROS levels for the elucidation of redox signaling pathways.

Prof. Dr. Bulent Mutus
Dr. Anny Slama-Schwok
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chemical sensors for nitric oxide, peroxide, superoxide and their respective enzymatic sources
  • ROS signaling, nanomaterials, in vivo sensing
  • Redox signaling

Published Papers (4 papers)

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Research

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20 pages, 6996 KiB  
Article
CASK Mediates Oxidative Stress-Induced Microglial Apoptosis-Inducing Factor-Independent Parthanatos Cell Death via Promoting PARP-1 Hyperactivation and Mitochondrial Dysfunction
by Keith Jun Hao Cheong, Duen-Yi Huang, Ponarulselvam Sekar, Rou Jhen Chen, Irene Han-Juo Cheng, Chi-Ming Chan, Yuan-Shen Chen and Wan-Wan Lin
Antioxidants 2024, 13(3), 343; https://doi.org/10.3390/antiox13030343 - 13 Mar 2024
Viewed by 1232
Abstract
Calcium/calmodulin-dependent serine protein kinase (CASK) is a scaffold protein and plays critical roles in neuronal synaptic formation and brain development. Previously, CASK was shown to associate with EGFR to maintain the vulval cell differentiation in C. elegans. In this study, we explored [...] Read more.
Calcium/calmodulin-dependent serine protein kinase (CASK) is a scaffold protein and plays critical roles in neuronal synaptic formation and brain development. Previously, CASK was shown to associate with EGFR to maintain the vulval cell differentiation in C. elegans. In this study, we explored the role of CASK in CHME3 microglial cells. We found that CASK silencing protects cells from H2O2-induced cell death by attenuating PARP-1 activation, mitochondrial membrane potential loss, reactive oxygen species production, and mitochondrial fission, but it increases oxidative phosphorylation. The PARP-1 inhibitor olaparib blocks H2O2-induced cell death, suggesting the death mode of parthanatos. CASK silencing also increases AKT activation but decreases AMPK activation under H2O2 treatment. Pharmacological data further indicate that both signaling changes contribute to cell protection. Different from the canonical parthanatos pathway, we did not observe the AIF translocation from mitochondria into the nucleus, suggesting a non-canonical AIF-independent parthanatos in H2O2-treated CHME3 cells. Moreover, we found that CASK silencing upregulates the EGFR gene and protein expression and increases H2O2-induced EGFR phosphorylation in CHME3 microglia. However, EGFR activation does not contribute to cell protection caused by CASK silencing. In conclusion, CASK plays a crucial role in microglial parthanatos upon H2O2 treatment via stimulation of PARP-1 and AMPK but the inhibition of AKT. These findings suggest that CASK might be an ideal therapeutic target for CNS disorders. Full article
(This article belongs to the Special Issue NO and ROS in Redox Signalling)
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8 pages, 681 KiB  
Communication
In Vivo Analysis of Tissue S-Nitrosothiols in Pediatric Sepsis
by Daniel T. Cater, Charles Clem, Nadzeya Marozkina and Benjamin Gaston
Antioxidants 2024, 13(3), 263; https://doi.org/10.3390/antiox13030263 - 21 Feb 2024
Viewed by 696
Abstract
S-nitrosothiols are endogenous, bioactive molecules. S-nitrosothiols are implicated in many diseases, including sepsis. It is currently cumbersome to measure S-nitrosothiols clinically. We have previously developed an instrument to measure tissue S-nitrosothiols non-invasively using ultraviolet light. We have performed a prospective case control study [...] Read more.
S-nitrosothiols are endogenous, bioactive molecules. S-nitrosothiols are implicated in many diseases, including sepsis. It is currently cumbersome to measure S-nitrosothiols clinically. We have previously developed an instrument to measure tissue S-nitrosothiols non-invasively using ultraviolet light. We have performed a prospective case control study of controls and children with sepsis admitted to the PICU. We hypothesized that tissue S-nitrosothiols would be higher in septic patients than controls. Controls were patients with no cardiopulmonary instability. Cases were patients with septic shock. We measured S-nitrosothiols, both at diagnosis and after resolution of shock. A total of 44 patients were enrolled: 21 controls and 23 with sepsis. At baseline, the controls were younger [median age 5 years (IQR 0, 9) versus 11 years (IQR: 6, 16), p-value = 0.012], had fewer comorbidities [7 (33.3%) vs. 20 (87.0%), p-value < 0.001], and had lower PELOD scores [0 (IQR: 0, 0) vs. 12 (IQR: 11, 21), p-value < 0.001]. S-nitrosothiol levels were higher in sepsis cohort (1.1 ppb vs. 0.8 ppb, p = 0.004). Five patients with sepsis had longitudinal measures and had a downtrend after resolution of shock (1.3 ppb vs. 0.9 ppb, p = 0.04). We dichotomized patients based on S-nitrosothiol levels and found an association with worse clinical outcomes, but further work will be needed to validate these findings. Full article
(This article belongs to the Special Issue NO and ROS in Redox Signalling)
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16 pages, 5634 KiB  
Article
Targeting M2 Macrophages with a Novel NADPH Oxidase Inhibitor
by Sébastien Dilly, Miguel Romero, Stéphanie Solier, Olivier Feron, Chantal Dessy and Anny Slama Schwok
Antioxidants 2023, 12(2), 440; https://doi.org/10.3390/antiox12020440 - 10 Feb 2023
Cited by 4 | Viewed by 1742
Abstract
ROS in cancer cells play a key role in pathways regulating cell death, stemness maintenance, and metabolic reprogramming, all of which have been implicated in resistance to chemo/ immunotherapy. Adjusting ROS levels to reverse the resistance of cancer cells without impairing normal cell [...] Read more.
ROS in cancer cells play a key role in pathways regulating cell death, stemness maintenance, and metabolic reprogramming, all of which have been implicated in resistance to chemo/ immunotherapy. Adjusting ROS levels to reverse the resistance of cancer cells without impairing normal cell functions is a new therapeutic avenue. In this paper, we describe new inhibitors of NADPH oxidase (NOX), a key enzyme in many cells of the tumor microenvironment. The first inhibitor, called Nanoshutter-1, NS1, decreased the level of tumor-promoting “M2” macrophages differentiated from human blood monocytes. NS1 disrupted the active NADPH oxidase-2 (NOX2) complex at the membrane and in the mitochondria of the macrophages, as shown by confocal microscopy. As one of the characteristics of tumor invasion is hypoxia, we tested whether NS1 would affect vascular reactivity by reducing ROS or NO levels in wire and pressure myograph experiments on isolated blood vessels. The results show that NS1 vasodilated blood vessels and would likely reduce hypoxia. Finally, as both NOX2 and NOX4 are key proteins in tumors and their microenvironment, we investigated whether NS1 would probe these proteins differently. Models of NOX2 and NOX4 were generated by homology modeling, showing structural differences at their C-terminal NADPH site, in particular in their last Phe. Thus, the NADPH site presents an unexploited chemical space for addressing ligand specificity, which we exploited to design a novel NOX2-specific inhibitor targeting variable NOX2 residues. With the proper smart vehicle to target specific cells of the microenvironment as TAMs, NOX2-specific inhibitors could open the way to new precision therapies. Full article
(This article belongs to the Special Issue NO and ROS in Redox Signalling)
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Review

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22 pages, 2515 KiB  
Review
Determination of Nitric Oxide and Its Metabolites in Biological Tissues Using Ozone-Based Chemiluminescence Detection: A State-of-the-Art Review
by Junjie Li, Anthea LoBue, Sophia K. Heuser and Miriam M. Cortese-Krott
Antioxidants 2024, 13(2), 179; https://doi.org/10.3390/antiox13020179 - 31 Jan 2024
Viewed by 899
Abstract
Ozone-based chemiluminescence detection (CLD) has been widely applied for determining nitric oxide (•NO) and its derived species in many different fields, such as environmental monitoring and biomedical research. In humans and animals, CLD has been applied to determine exhaled •NO [...] Read more.
Ozone-based chemiluminescence detection (CLD) has been widely applied for determining nitric oxide (•NO) and its derived species in many different fields, such as environmental monitoring and biomedical research. In humans and animals, CLD has been applied to determine exhaled •NO and •NO metabolites in plasma and tissues. The main advantages of CLD are high sensitivity and selectivity for quantitative analysis in a wide dynamic range. Combining CLD with analytical separation techniques like chromatography allows for the analytes to be quantified with less disturbance from matrix components or impurities. Sampling techniques like microdialysis and flow injection analysis may be coupled to CLD with the possibility of real-time monitoring of •NO. However, details and precautions in experimental practice need to be addressed and clarified to avoid wrong estimations. Therefore, using CLD as a detection tool requires a deep understanding of the sample preparation procedure and chemical reactions used for liberating •NO from its derived species. In this review, we discuss the advantages and pitfalls of CLD for determining •NO species, list the different applications and combinations with other analytical techniques, and provide general practical notes for sample preparation. These guidelines are designed to assist researchers in comprehending CLD data and in selecting the most appropriate method for measuring •NO species. Full article
(This article belongs to the Special Issue NO and ROS in Redox Signalling)
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