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9 recordsLinked to original sources
PubMed2026

Cystathionine γ-Lyase-Dependent S-Sulfhydration of Smad3: A Novel Target to Alleviate Fibrosis in Systemic Sclerosis.

OBJECTIVE: The cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) axis has emerged as a key regulator in tissue fibrogenesis. This study aimed to explore the role of the CSE/H2S axis in systemic sclerosis (SSc) and to investigate its underlying mechanisms to identify promising therapeutic targets. METHODS: CSE/H2S levels were assessed in serum samples from 25 patients with SSc and 28 healthy controls. Human dermal fibroblasts from patients with SSc and healthy controls were used for functional studies, including propargylglycine (CSE inhibitor) treatment, Gyy4137, a slow-releasing hydrogen sulfide donor, CSE silencing, and CSE overexpression, combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based S-sulfhydration proteomics. Molecular dynamics simulations were performed to study the effects of S-sulfhydration on protein structure, and an Smad3 C121S (cysteine [Cys] 121 mutated to Ser) mutant was generated to verify the function targets of S-sulfhydration. In vivo, bleomycin-induced mouse models of skin and lung fibrosis were constructed to evaluate the effects of CSE overexpression. RESULTS: In human samples, CSE/H2S levels were reduced in SSc. CSE inhibition promoted extracellular matrix deposition. S-sulfhydration proteomics showed that S-sulfhydration levels were globally reduced in SSc compared to controls. CSE overexpression increased S-sulfhydration on Smad3, suppressed transforming growth factor β 1 (TGFβ1)/Smad3 signaling, mitigating skin fibrosis. Notably, Cys121 on Smad3, identified as a pivotal target for S-sulfhydration by proteomics, was shown to fine-tune its MH1 domain, with its mutation impairing the antifibrotic effects. In mice, CSE overexpression attenuated bleomycin-induced skin and lung fibrosis. CONCLUSION: Smad3 S-sulfhydration mediates the antifibrotic effect of CSE in SSc, highlighting it as a critical mechanism and promising therapeutic target.

Humans↗
PubMed2026

Prophage Activation as an Overlooked Mechanism Underlying the Biocidal Effect of Free Nitrous Acid in Sewers.

Biogenic hydrogen sulfide produced in sewer systems causes odor nuisance and concrete corrosion, necessitating effective biocidal control. Free nitrous acid (FNA) has emerged as a promising biocide, but its unclear mechanisms complicate dosage optimization and risk assessment. Here, using Desulfovibrio vulgaris as a model lysogenic bacterium, we demonstrate that low-dose FNA (0.2-4.0 mg N/L) induces bacterial inactivation via prophage activation-associated lysis in addition to chemical oxidation. Reactive nitrogen species (RNS) scavenging tests revealed that RNS-mediated oxidative stress was closely associated with prophage activation. Activated phages further infected new hosts, reducing the viability of freshly cultured D. vulgaris cells by 25.7% and increasing total phage production 15.2-fold. The phenomenon was further validated in real sewage biofilms, where increased phage production and decreased bacterial viability were observed at a low FNA dose of 0.2 mg N/L, below the dose required for cell destruction by chemical oxidation. Furthermore, metagenomic analysis of 896 sewage samples worldwide revealed that 71.9% of recovered sewage-derived microbial genomes harbor prophages, indicating a widespread genomic basis for prophage activation-mediated bacterial inactivation. Overall, this study expands current understanding of the biocidal mechanisms of FNA and contributes to the development of environmentally sustainable biocidal strategies.

Nitrous Acid↗
PubMed2025

Comparative Embryology and Transcriptomics of Asellus infernus, an Isopod Crustacean From Sulfidic Groundwater.

Sulfidic caves are harsh and extreme environments characterized by limited oxygen, low pH, and the presence of hydrogen sulfide. Amazingly, animals can live in sulfidic caves, one such animal being Asellus infernus, a representative of the Asellus aquaticus species complex, originating from Movile Cave and from old wells that represent windows of access to a sulfidic groundwater ecosystem located in southeast Romania. Little previous work has been done on lab-reared populations of A. infernus as they have been historically difficult to raise in the lab. Here, we develop resources for A. infernus, examining questions of timing of morphological differences in cave versus surface individuals, whether the environment (lab-bred vs. wild-caught) influenced size characteristics, and the genes and pathways showing differential expression between cave and surface samples. We found that A. infernus did not develop pigmentation embryonically, and juveniles had increased body length and longer antenna II as compared to surface individuals. Furthermore, we found that some of these measures differed between wild-caught and lab-reared juveniles for a given population, indicating that environmental differences can also influence these size characteristics. In addition, differential expression between cave and surface samples and allele-specific expression studies within F1 hybrids identified multiple genes, including those involved in sulfide metabolism and phototransduction. Strikingly, molecular convergence of genes involved in sulfide detoxification was observed between A. infernus and previous work on a fish that lives in both cave and sulfidic environments, Poecilia mexicana. In sum, we were able to develop embryonic and genomic tools for A. infernus, a model for understanding cave adaptation and adaptation to sulfidic environments.

Animals↗
PubMed2026

Protein persulfidation emerges as a conserved component of the redox response to DNA damage.

Genotoxic stress is frequently accompanied by alterations in cellular redox homeostasis; however, the mechanisms linking redox regulation to the DNA damage response (DDR) remain incompletely understood. Here, we investigated the early redox response to DNA damage induced by methyl methanesulfonate (MMS) in Saccharomyces cerevisiae, focusing on cysteine oxidative post-translational modifications (PTM). We show that activation of the DNA damage response is accompanied by rapid redox changes that occur in the absence of a generalized oxidative stress response. MMS exposure promotes selective remodeling of cysteine oxidative modifications, characterized by decreased free thiols, robust induction of protein persulfidation, and comparatively modest changes in sulfenylation. These alterations are accompanied by increased intracellular hydrogen sulfide levels, supporting the involvement of reactive sulfur species in the cellular response to DNA damage. Proteome-wide analyses revealed that cysteine oxidative modifications preferentially target proteins involved in central metabolism, nucleotide biosynthesis, and genome maintenance. Consistent with these observations, MMS-induced genotoxic stress promotes metabolic adaptation characterized by increased mitochondrial respiration, elevated ATP production, and mitochondrial morphological remodeling, linking bioenergetic adaptation to redox regulation. Importantly, perturbation of intracellular redox balance using N-acetylcysteine compromises survival under DNA-damaging conditions, supporting a functional role for redox signaling during the DDR. Finally, MMS treatment also induces protein persulfidation in mammalian cells. Moreover, exposure to etoposide, a mechanistically distinct genotoxic agent that induces DNA double-strand breaks through topoisomerase II inhibition, showed a similar trend, suggesting that protein persulfidation may not be restricted to alkylation-induced DNA damage. Together our findings identify protein persulfidation as a prominent component of the redox response to DNA damage and provide new insight into the functional interplay between mitochondrial metabolism, cysteine-based redox regulation, and genome maintenance.

Oxidation-Reduction↗
PubMed2025

Interaction and regulation of the mitochondrial proteome - in health and disease.

INTRODUCTION: Mitochondria contain multiple pathways including energy metabolism and several signaling and synthetic pathways. Mitochondrial proteomics is highly valuable for studying diseases including inherited metabolic disorders, complex and common disorders like neurodegeneration, diabetes, and cancer, since they all to some degree have mitochondrial underpinnings. AREAS COVERED: The main mitochondrial functions and pathways are outlined, and systematic protein lists are presented. The main energy metabolic pathways are as follows: iron-sulfur cluster synthesis, one carbon metabolism, catabolism of hydrogen sulfide, kynurenines and reactive oxygen species (ROS), and others, described with the aim of laying a foundation for systematic mitochondrial pathway analysis based on proteomics data. The links of the proteins and pathways to functional effects and diseases are discussed. The disease examples are focussed on inherited metabolic disorders, cancer, neurological, and cardiovascular disorders. EXPERT OPINION: To elucidate the role of mitochondria in health and disease, there is a need for comprehensive proteomics analyses with stringent, systematic data treatment for proper interpretation of mitochondrial pathway data. In that way, comprehensive hypothesis-based research can be performed based on proteomics data.

Humans↗
PubMed2026

Do Multi-Omics Approaches Improve the Diagnosis of Microbial Overgrowth Syndromes?

PURPOSE OF REVIEW: This review investigates how advances in breath testing (BT), small bowel (SB) culture, metagenomics, metatranscriptomics, transcriptomics and proteomics are reshaping the definition and diagnosis of small intestinal bacterial overgrowth (SIBO). It also discusses whether SIBO should be redefined as part of a larger group of microbial overgrowth syndromes. RECENT FINDINGS: Recent studies identify distinct hydrogen-, methane-, and hydrogen sulfide-associated overgrowth phenotypes, termed SIBO, intestinal methanogen overgrowth (IMO), and intestinal sulfide overproduction (ISO). SB sampling shows that these conditions involve different microbial patterns and functional activity, symptoms, and host responses. Quantitative shotgun metagenomics provides greater taxonomic and functional resolution than culture, while metatranscriptomics reveals active microbial pathways. On top of that, host transcriptomics and proteomics contribute to the better understanding of the predominant microbial effects in host cellular mechanisms in each of the distinct small bowel overgrowth types. SIBO has been increasingly identified as a disorder of microbial ecology and function rather than bacterial quantity alone. Integrating BT with SB sampling and multi-omics approaches may improve classification, clarify symptom mechanisms, and support a more individualized treatment, although standardized methods and further clinical validation remain necessary.

Humans↗
PubMed2025

A deep-sea hydrothermal vent worm detoxifies arsenic and sulfur by intracellular biomineralization of orpiment (As2S3).

The alvinellid worm Paralvinella hessleri is the only animal that colonizes the hottest part of deep-sea hydrothermal vents in the west pacific. We found P. hessleri accumulates exceptionally high level of toxic element arsenic (>1% of wet weight) and tolerated elevated concentrations hydrogen sulphide. Using advanced microscopy, elementary analysis, and genomics and proteomics approaches, we identified a previously unrecognized arsenic-sulfide biomineralization process in P. hessleri. Our data suggest that arsenic accumulates within epithelial cell granules, where it likely reacts with sulphide diffused inward from the hydrothermal vent fluid, resulting in the intracellular formation of orpiment (As₂S₃) minerals. In this "fighting poison with poison" manner, the highly toxic arsenic and sulphide were simultaneously detoxified in the form of orpiment minerals within the intracellular granules of the single layer of epithelial cells. This process represents a remarkable adaptation to extreme chemical environments. Our study provides new insights into understanding animals' environment adaptation mechanisms and the diversity and plasticity of biomineralization.

Animals↗
PubMed2026

Low-pH sulfate reduction in acid mine drainage treatment systems: implications for acidophilic and acid-tolerant sulfate-reducing bacteria - a systematic review.

Acid mine drainage (AMD) is characterized by persistent acidity, high sulfate and dissolved metal concentrations. Sulfate-reducing bacteria (SRB) are attractive candidates for AMD remediation because dissimilatory sulfate reduction generates alkalinity while producing sulfide that can facilitate metal removal through precipitation. Extending these processes to acidic conditions has increased interest in acidophilic and acid-tolerant SRB (aSRB and atSRB), yet evidence from cultivation, molecular surveys and treatment systems has often been interpreted separately. This systematic review synthesized 53 culture-dependent, culture-independent, and treatment system studies from 2014 to 2024 to examine relationships among taxonomic occurrence, physiological capability, demonstrated low-pH sulfate reduction and treatment performance. Phylogenetic analysis showed that low-pH sulfate-reducing phenotypes were distributed across multiple lineages and 16S rRNA relatedness alone did not predict acid tolerance. Desulfosporosinus was the most consistently represented genus across studies, although its recurrence was influenced by cultivation strategies. Sulfate reduction was demonstrated below pH 3, with sustained low-pH activity most strongly supported by controlled reactor studies; approximately pH 4.0-5.5 emerged as a comparatively well-supported range, while activity at lower pH was more dependent on microbial physiology and experimental conditions. Low-pH sulfate reduction also emerged as a community-level process shaped by electron-donor use, metabolite turnover and complementary microbial functions, while treatment performance additionally depended on biomass retention, hydraulic conditions and sulfide management. The reviewed studies support a distinction between taxonomic presence, demonstrated activity and treatment contribution. Future work should prioritize standardized reporting of active sulfate-reduction conditions, stronger taxon-function validation and long-term field testing of low-pH sulfidogenic systems.

Sulfates↗
PubMed2026

Sulfonic Ion-Exchange Resins as Versatile Tools for the Oxidative Degradation of Chemical and Biological Hazardous Agents.

Commercial sulfonic styrene-divinylbenzene ion-exchange resins are activated with aqueous H2O2 to generate metal-free decontamination systems that combine strong Brønsted acidity with immobilized oxidizing capability. Among five tested materials, Amberlyst 15 dry showed the best performance in terms of oxidant immobilization capacity and promoting the oxidative degradation of the sulfur mustard simulant (2-chloroethyl)ethyl sulfide, CEES, and the organophosphorus pesticide malathion under very mild conditions. Control experiments with K2CO3-exchanged resin demonstrate that efficient decontamination requires the synergy between surface acidity and peroxide functionality. The activated resins also display rapid biocidal activity, strongly reducing viable Escherichia coli and Staphylococcus aureus and completely suppressing the infectivity of HSV-1 and SARS-CoV-2 within min. These findings identify peroxide-activated sulfonic resins as simple, sustainable, regenerable, and versatile tools for efficient combined hazardous chemical and biological decontamination.

Oxidation-Reduction↗