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Antioxidants
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Nitric Oxide (NO) and Hydrogen Sulfide (H2S) in...
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Nitric Oxide (NO) and Hydrogen Sulfide (H2S) in Biology, Illness, and Therapies—3rd Edition

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

Deadline for manuscript submissions: 31 October 2026 | Viewed by 2203

Special Issue Editor

Dr. Eizo Marutani

E-Mail Website
Guest Editor
Anesthesia Center for Critical Care Research, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
Interests: nitric oxide; hydrogen sulfide; persulfide/polysulfide; sulfur metabolism; redox reaction; interaction/crosstalk; antioxidants; disease; therapy; detection methods
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Gaseous signaling molecules, including nitric oxide (NO), carbon dioxide (CO), and hydrogen sulfide (H2S), have emerged as physiologically and pathophysiologically important mediators in mammals. Manipulating these mediators as a therapeutic measure appears promising in various diseases, and the inhalation of NO has, at least partly, enhanced their clinical application. The manipulation of H2S or persulfide/polysulfide, which are oxidative products of H2S, is being explored in clinical trials. However, these therapies still face challenges regarding broader clinical applications due to their toxicity, rapid diffusion, short half-life, and narrow therapeutic window. Innovative methods or strategies are required to enable more successful clinical applications for these gaseous mediators. These mediators or their metabolites also crosstalk/interact with each other and have the potential to undergo nonspecific diverse reactions, which complicate our understanding of gaseous mediator biology; this remains to be elucidated in future studies.

In this Special Issue, we welcome the submission of original research articles or review articles that focus on physiology/pathophysiology, therapies, detection methods, and redox reactions related to NO, H2S, and their metabolites, facilitating the establishment of novel therapies to overcome illnesses.

Dr. Eizo Marutani
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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

  • nitric oxide
  • hydrogen sulfide
  • persulfide/polysulfide
  • sulfur metabolism
  • redox reaction
  • interaction/crosstalk
  • antioxidants
  • disease
  • therapy
  • detection methods

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Published Papers (3 papers)

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25 pages, 36877 KB  
Article
Endothelial Nitric Oxide Synthase-Dependent Mechanism of Hydroxyurea-Induced S-Phase Arrest in Erythroid Cells
by Teodora Dragojević, Dragoslava Đikić, Slavko Mojsilović, Miloš Lazarević, Dejan Milenković, Olivera Mitrović Ajtić, Emilija Živković, Miloš Diklić, Tijana Subotički, Juan F. Santibanez, Vladan P. Čokić and Milica Vukotić
Antioxidants 2026, 15(4), 435; https://doi.org/10.3390/antiox15040435 - 31 Mar 2026
Viewed by 444
Abstract
Hydroxyurea (HU) is a ribonucleotide reductase inhibitor widely used for the treatment of sickle cell disease and myeloproliferative disorders, yet a precise nitric oxide (NO) synthase (NOS)-dependent mechanism remains incompletely defined. The role of NOS3 in HU-mediated proliferation, cell cycle, and apoptosis was [...] Read more.
Hydroxyurea (HU) is a ribonucleotide reductase inhibitor widely used for the treatment of sickle cell disease and myeloproliferative disorders, yet a precise nitric oxide (NO) synthase (NOS)-dependent mechanism remains incompletely defined. The role of NOS3 in HU-mediated proliferation, cell cycle, and apoptosis was analyzed in HEL92.1.7 erythroleukemic cells and primary mouse erythroid progenitors upon genetic knockdown/knockout and pharmacological NOS2/NOS3 inhibition. NOS3 expression, phosphorylation, NO and citrulline production, and protein nitrosylation were assessed via immunoblotting and biochemical assays. Computational docking and molecular dynamics simulations were performed to examine the interaction between HU and NOS3. HU enhanced NOS3 expression and phosphorylation, leading to increased NO and citrulline production. Computational analysis predicted HU binding within the NOS3 active site, whereas functional activation was AKT1-dependent. A biotin switch assay revealed cooperative NOS2-/NOS3-mediated protein nitrosylation under HU treatment. NOS3 depletion or inhibition abrogated HU-induced S-phase accumulation and restored cell proliferation. NOS3 protein depletion increased late apoptosis in erythroleukemic cells, while in murine erythroid cells, both Nos3 deficiency and inhibition decreased early and increased late apoptosis. NOS2 and NOS3 act as complementary mediators of proliferation and apoptosis, with NOS3 playing a distinct role in HU-induced proliferation arrest in erythroid cells. These findings highlight the therapeutic potential of NOS targeting to enhance the efficacy of HU and overcome resistance in hematologic malignancies. Full article
(This article belongs to the Special Issue Nitric Oxide (NO) and Hydrogen Sulfide (H2S) in Biology, Illness, and Therapies—3rd Edition)
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19 pages, 4901 KB  
Article
Maternal Exposure to Microplastics and High-Fructose Diet Induces Offspring Hypertension via Disruption of H2S Signaling, Gut Microbiota, and Metabolic Networks
by Chien-Ning Hsu, Chih-Yao Hou, Yu-Wei Chen, Guo-Ping Chang-Chien, Shu-Fen Lin and You-Lin Tain
Antioxidants 2026, 15(2), 179; https://doi.org/10.3390/antiox15020179 - 30 Jan 2026
Viewed by 647
Abstract
Maternal consumption of a high-fructose (HF) diet or exposure to microplastics (MPs) can each independently affect kidney development and increase the risk of hypertension in adult offspring, yet their combined impact remains poorly understood. Dysregulation of hydrogen sulfide (H2S) signaling and [...] Read more.
Maternal consumption of a high-fructose (HF) diet or exposure to microplastics (MPs) can each independently affect kidney development and increase the risk of hypertension in adult offspring, yet their combined impact remains poorly understood. Dysregulation of hydrogen sulfide (H2S) signaling and alterations in gut microbiota are potential mediators of this programming. Pregnant rats received either standard chow or a 60% HF diet, with half of each group additionally exposed to sulfate-modified MPs (1 mg/L) with a 5 μm diameter throughout pregnancy and lactation. Male offspring were divided into four groups (n = 7–8 per group): control, HF, MP, and HF+MP. Maternal HF or MP exposure raised offspring blood pressure (BP), with additive effects when combined, and MP exposure caused renal injury. MP treatment also suppressed renal H2S-generating enzymes and reduced H2S production. Both HF and MP exposures altered gut microbial composition linked to BP regulation and induced metabolic changes in taurine/hypotaurine and sulfur pathways, suggesting impaired H2S production. These results indicate that maternal HF and MP exposures interfere with H2S signaling, gut microbiota, and metabolic programming, highlighting the H2S signaling as a potential target to reduce long-term kidney and cardiometabolic risks. Full article
(This article belongs to the Special Issue Nitric Oxide (NO) and Hydrogen Sulfide (H2S) in Biology, Illness, and Therapies—3rd Edition)
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17 pages, 2332 KB  
Article
Role of Sulfide Quinone Oxidoreductase and Supersulfides in Hepatic Ischemia–Reperfusion Injury in Mice
by Shinnosuke Takamori, Kazuhiro Shirozu, Eizo Marutani, Tsuyoshi Takata, Yukie Mizuta, Takahito Kawano, Masaharu Murata, Tomoaki Ida, Tetsuro Matsunaga, Takaaki Akaike, Ken Yamaura and Tomohiko Akahoshi
Antioxidants 2026, 15(1), 94; https://doi.org/10.3390/antiox15010094 - 12 Jan 2026
Viewed by 688
Abstract
Hepatic ischemia–reperfusion injury (IRI) is a critical clinical condition associated with liver transplantation and acute liver injury. This study investigated the role of sulfide quinone oxidoreductase (SQOR) and its downstream product, supersulfides, in hepatic IRI. C57BL/6NJ mice were subjected to 45 min of [...] Read more.
Hepatic ischemia–reperfusion injury (IRI) is a critical clinical condition associated with liver transplantation and acute liver injury. This study investigated the role of sulfide quinone oxidoreductase (SQOR) and its downstream product, supersulfides, in hepatic IRI. C57BL/6NJ mice were subjected to 45 min of partial hepatic ischemia, followed by reperfusion lasting 4 h. Control of shRNA mediated knockdown of SQOR expressing adeno-associated viral vectors were administered 3 weeks prior to liver ischemia. In the shRNA-mediated knockdown of SQOR group, the hydro-trisulfide donor sodium trisulfide was administered daily for 1 week prior to the induction of liver ischemia. SQOR played a crucial protective role during hepatic IRI by facilitating electron transport to the mitochondrial respiratory chain and maintaining the oxidized and reduced nicotinamide adenine dinucleotide ratio. Administration of sodium trisulfide, exhibited protective effects against hepatic IRI. Sodium trisulfide restored the oxidized and reduced nicotinamide adenine dinucleotide ratio, reduced oxidative stress, and preserved the expression of key enzymes involved in the sulfide oxidation pathway. SQOR and supersulfides contribute to hepatic protection against IRI, likely through their potent antioxidative and redox-regulating functions, and highlight sodium trisulfide as a potential therapeutic agent. Full article
(This article belongs to the Special Issue Nitric Oxide (NO) and Hydrogen Sulfide (H2S) in Biology, Illness, and Therapies—3rd Edition)
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