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Keywords = supersulfides

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17 pages, 5547 KiB  
Article
The Selective 3-MST Inhibitor I3MT-3 Works as a Potent Caspase-1 Inhibitor
by Kohei Otani, Ryuto Komatsu, Takuya Noguchi, Wakana Suzuki, Yusuke Hirata and Atsushi Matsuzawa
Int. J. Mol. Sci. 2025, 26(5), 2237; https://doi.org/10.3390/ijms26052237 - 2 Mar 2025
Viewed by 1115
Abstract
I3MT-3 (HMPSNE) has been identified as a selective inhibitor of the supersulfide-producing enzyme 3-MST. In this study, we found that I3MT-3 inhibits inflammatory responses, including the secretion of the pro-inflammatory cytokine interleukin-1β (IL-1β) and inflammatory cell death pyroptosis, induced by the activation of [...] Read more.
I3MT-3 (HMPSNE) has been identified as a selective inhibitor of the supersulfide-producing enzyme 3-MST. In this study, we found that I3MT-3 inhibits inflammatory responses, including the secretion of the pro-inflammatory cytokine interleukin-1β (IL-1β) and inflammatory cell death pyroptosis, induced by the activation of the inflammasomes composed of NLRP1, NLRP3, or AIM2. However, interestingly, the knockdown of 3-MST did not affect the activation of the inflammasomes, suggesting that the inhibitory effect of I3MT-3 on inflammasome activation is mediated by alternative ways rather than the inhibition of 3-MST. Interestingly, an in vitro caspase assay revealed that I3MT-3 directly inhibits caspase-1 activation, and molecular docking simulations raised the possibility that the pyrimidone ring in I3MT-3 stabilizes direct interaction of I3MT-3 with caspase-1. Taken together, our data suggest that I3MT-3 inhibits inflammasome activation by targeting caspase-1, and show I3MT-3 as a potent inhibitor of caspase-1. Full article
(This article belongs to the Special Issue Programmed Cell Death and Oxidative Stress: 3rd Edition)
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13 pages, 6282 KiB  
Brief Report
Sulfide-Responsive Transcription Control in Escherichia coli
by Koichi Hori, Rajalakshmi Balasubramanian and Shinji Masuda
Microorganisms 2025, 13(2), 344; https://doi.org/10.3390/microorganisms13020344 - 5 Feb 2025
Cited by 2 | Viewed by 855
Abstract
To elucidate the mechanism of large-scale transcriptional changes dependent on sulfide in Escherichia coli, a large-scale RNA-sequencing analysis was performed on wild-type and sulfide-responsive transcription factor YgaV deletion mutants grown under three conditions: aerobic, semi-aerobic, and semi-aerobic with sulfide. The resulting dataset [...] Read more.
To elucidate the mechanism of large-scale transcriptional changes dependent on sulfide in Escherichia coli, a large-scale RNA-sequencing analysis was performed on wild-type and sulfide-responsive transcription factor YgaV deletion mutants grown under three conditions: aerobic, semi-aerobic, and semi-aerobic with sulfide. The resulting dataset from these six conditions was subjected to principal component analysis, which categorized the data into five principal components. Estimation of the typical gene expression regulatory mechanisms in each category suggested the presence of mechanisms that are dependent on sulfide but independent of YgaV, as well as those that depend on YgaV but not on sulfide. In YgaV-dependent transcriptional regulation, YgaV was found to function as both a repressor and an activator. These results support the previous hypothesis that YgaV acts as a global regulator responsible for redox homeostasis. Full article
(This article belongs to the Section Molecular Microbiology and Immunology)
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22 pages, 5176 KiB  
Review
The Therapeutic Potential of Supersulfides in Oxidative Stress-Related Diseases
by Yuexuan Pan, Tetsuro Matsunaga, Tianli Zhang and Takaaki Akaike
Biomolecules 2025, 15(2), 172; https://doi.org/10.3390/biom15020172 - 23 Jan 2025
Cited by 1 | Viewed by 1783
Abstract
Oxidation-reduction (redox) reactions are fundamental to sustaining life, with reactive oxygen and nitrogen species playing pivotal roles in cellular signaling and homeostasis. However, excessive oxidative stress disrupts redox balance, contributing to a wide range of diseases, including inflammatory and pulmonary disorders, neurodegeneration, and [...] Read more.
Oxidation-reduction (redox) reactions are fundamental to sustaining life, with reactive oxygen and nitrogen species playing pivotal roles in cellular signaling and homeostasis. However, excessive oxidative stress disrupts redox balance, contributing to a wide range of diseases, including inflammatory and pulmonary disorders, neurodegeneration, and cancer. Although numerous antioxidant therapies have been developed and tested for oxidative stress-related diseases, their clinical efficacy remains limited. Here, we introduce the emerging concept of ‘supersulfides’, a class of redox molecule species with unique antioxidant and nucleophilic properties, which have recently been recognized as crucial regulators of cellular redox homeostasis. Unlike traditional antioxidants, supersulfides offer novel mechanisms of action that directly target the underlying processes of oxidative stress. This review summarizes current knowledge on supersulfides, highlighting their roles in oxidative stress and associated diseases, as well as the mechanisms underlying oxidative stress-related pathology. The therapeutic potential of synthetic supersulfides for treating oxidative stress-related diseases is also discussed. A comprehensive understanding of the molecular and cellular basis of redox biology can help to guide the development of innovative redox-based therapeutic strategies aimed at preventing and treating diseases associated with disturbed redox regulation. Full article
(This article belongs to the Special Issue Bioactive Molecules in the Control of Oxidative Stress and Oxidative Stress-Related Diseases)
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14 pages, 2686 KiB  
Article
Acute Kidney Injury Caused by Rhabdomyolysis Is Ameliorated by Serum Albumin-Based Supersulfide Donors through Antioxidative Pathways
by Mayumi Ikeda-Imafuku, Tatsuya Fukuta, Victor Tuan Giam Chuang, Tomohiro Sawa, Toru Maruyama, Masaki Otagiri, Tatsuhiro Ishida and Yu Ishima
Pharmaceuticals 2024, 17(1), 128; https://doi.org/10.3390/ph17010128 - 18 Jan 2024
Cited by 3 | Viewed by 2581
Abstract
Oxidative stress is responsible for the onset and progression of various kinds of diseases including rhabdomyolysis-induced acute kidney injury (AKI). Antioxidants are, therefore, thought to aid in the recovery of illnesses linked to oxidative stress. Supersulfide species have been shown to have substantial [...] Read more.
Oxidative stress is responsible for the onset and progression of various kinds of diseases including rhabdomyolysis-induced acute kidney injury (AKI). Antioxidants are, therefore, thought to aid in the recovery of illnesses linked to oxidative stress. Supersulfide species have been shown to have substantial antioxidative activity; however, due to their limited bioavailability, few supersulfide donors have had their actions evaluated in vivo. In this study, human serum albumin (HSA) and N-acetyl-L-cysteine polysulfides (NACSn), which have polysulfides in an oxidized form, were conjugated to create a supersulfide donor. HSA is chosen to be a carrier of NACSn because of its extended blood circulation and high level of biocompatibility. In contrast to a supersulfide donor containing reduced polysulfide in HSA, the NACSn-conjugated HSAs exhibited stronger antioxidant activity than HSA and free NACSn without being uptaken by the cells in vitro. The supersulfide donor reduced the levels of blood urea nitrogen and serum creatinine significantly in a mouse model of rhabdomyolysis-induced AKI. Supersulfide donors significantly reduced the expression of oxidative stress markers in the kidney. These results indicate that the developed supersulfide donor has the therapeutic effect on rhabdomyolysis-induced AKI. Full article
(This article belongs to the Special Issue Molecular Modification in Designing Next Generation Drug Delivery Systems)
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