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Hydrogen sulfide (H2S), mainly produced from L-cysteine (Cys), renders bacteria highly resistant to oxidative stress and potentially increases antimicrobial resistance (AMR). CyuR is a Cys-dependent transcription regulator, responsible for the activation of the cyuPA operon and generation of H2S. Despite its potential importance, its regulatory network remains poorly understood. In this study, we investigate the roles of the CyuR regulon in a Cys-dependent AMR mechanism in E. coli strains. We show: (1) Generation of H2S from Cys affects the sensitivities to growth inhibitors; (2) Cys supplementation decreases stress responses; (3) CyuR negatively controls the expression of mdlAB encoding a potential transporter for antibiotics; (4) CyuR binds to a DNA sequence motif GAAwAAATTGTxGxxATTTsyCC in the absence of Cys; and (5) CyuR may regulate 25 additional genes which were not reported previously. Collectively, our findings expand the understanding of the biological roles of CyuR relevant to antibiotic resistance associated with Cys.

Gestational hypertension, often associated with elevated soluble Fms-related receptor tyrosine kinase 1 (sFlt-1), poses significant risks to both maternal and fetal health. Hydrogen sulfide (H2S), a gasotransmitter, has demonstrated blood pressure-lowering effects in hypertensive animals and humans. However, its role in pregnancy-induced hypertension remains unclear. This study investigated the impact of GYY4137, a slow-release H2S donor, on sFlt-1-induced hypertension in pregnant rats . Pregnant rats were administered sFlt-1 (6 μg/kg/day, intravenously) or vehicle from gestation day (GD) 12-20. A subset of these groups received GYY4137 ( 50 mg/kg/day, intraperitoneal) from GD 16-20. Serum H2S levels, mean arterial blood pressure, uterine artery blood flow, and vascular reactivity were assessed. Elevated sFlt-1 reduced both maternal weight gain and serum H2S levels. GYY4137 treatment restored both weight gain and H2S levels in sFlt-1 dams. sFlt-1 increased mean arterial pressure and decreased uterine artery blood flow in pregnant rats. However, treatment with GYY4137 normalized blood pressure and restored uterine blood flow in sFlt-1 dams. sFlt-1 dams exhibited heightened vasoconstriction to phenylephrine and GYY4137 significantly mitigated the exaggerated vascular contraction. Notably, sFlt-1 impaired endothelium-dependent relaxation, while GYY4137 attenuated this impairment by upregulating eNOS protein levels and enhancing vasorelaxation in uterine arteries. GYY4137 mitigated sFlt-1-induced fetal growth restriction. In conclusion, sFlt-1 mediated hypertension is associated with decreased H2S levels. Replenishing H2S with the donor GYY4137 mitigates hypertension and improves vascular function and fetal growth outcomes. This suggests modulation of H2S could offer a novel therapeutic strategy for managing gestational hypertension and adverse fetal effects.

Adaptation to extreme environments often involves the evolution of dramatic physiological changes. To better understand how organisms evolve these complex phenotypic changes, the repeatability and predictability of evolution, and possible constraints on adapting to an extreme environment, it is important to understand how adaptive variation has evolved. Poeciliid fishes represent a particularly fruitful study system for investigations of adaptation to extreme environments due to their repeated colonization of toxic hydrogen sulfide-rich springs across multiple species within the clade. Previous investigations have highlighted changes in the physiology and gene expression in specific species that are thought to facilitate adaptation to hydrogen sulfide-rich springs. However, the presence of adaptive nucleotide variation in coding and regulatory regions and the degree to which convergent evolution has shaped the genomic regions underpinning sulfide tolerance across taxa are unknown. By sampling across seven independent lineages in which nonsulfidic lineages have colonized and adapted to sulfide springs, we reveal signatures of shared evolutionary rate shifts across the genome. We found evidence of genes, promoters, and putative enhancer regions associated with both increased and decreased convergent evolutionary rate shifts in hydrogen sulfide-adapted lineages. Our analysis highlights convergent evolutionary rate shifts in sulfidic lineages associated with the modulation of endogenous hydrogen sulfide production and hydrogen sulfide detoxification. We also found that regions with shifted evolutionary rates in sulfide spring fishes more often exhibited convergent shifts in either the coding region or the regulatory sequence of a given gene, rather than both.

BackgroundHydrogen sulfide is a highly toxic, flammable, and colorless gas. Hydrogen sulfide has been identified as a potential terrorist chemical threat agent in mass-casualty events. Our previous studies showed that cobinamide, a vitamin B12 analog, effectively reverses the toxicity from hydrogen sulfide poisoning. In this study, we investigate the effectiveness of intratracheally administered cobinamide in treating a lethal dose hydrogen sulfide gas inhalation and compare its performance to saline control administration.MethodsA total of 53 pathogen-free New Zealand White rabbits were used for this study. Four groups were compared: (i) received no saline solution or drug intratracheally (n = 15), (ii) slow drip saline intratracheally (n = 15), (iii) fast drip saline intratracheally (n = 15), and (iv) slow drip cobinamide intratracheally (n = 8). Blood pressure was continuously monitored, and deoxy- and oxyhemoglobin concentration changes were monitored in real-time in vivo using continuous wave near-infrared spectroscopy.ResultsThe mean (± standard deviation) weight for all animals (n = 53) was 3.87 ± 0.10 kg. The survival rates of the slow cobinamide and the fast saline groups were 75 percent and 60 percent, respectively, while the survival rates in the slow saline and control groups were 26.7 percent and 20 percent, respectively. A log-rank (Mantel-Cox) test showed that survival in fast saline and slow cobinamide groups were significantly greater than those of no saline control and slow saline groups (P

In genetically heterogeneous (UM-HET3) mice produced by the CByB6F1 × C3D2F1 cross, the Nrf2 activator astaxanthin (Asta) extended the median male lifespan by 12% (p = 0.003, log-rank test), while meclizine (Mec), an mTORC1 inhibitor, extended the male lifespan by 8% (p = 0.03). Asta was fed at 1840 ± 520 (9) ppm and Mec at 544 ± 48 (9) ppm, stated as mean ± SE (n) of independent diet preparations. Both were started at 12 months of age. The 90th percentile lifespan for both treatments was extended in absolute value by 6% in males, but neither was significant by the Wang-Allison test. Five other new agents were also tested as follows: fisetin, SG1002 (hydrogen sulfide donor), dimethyl fumarate, mycophenolic acid, and 4-phenylbutyrate. None of these increased lifespan significantly at the dose and method of administration tested in either sex. Amounts of dimethyl fumarate in the diet averaged 35% of the target dose, which may explain the absence of lifespan effects. Body weight was not significantly affected in males by any of the test agents. Late life weights were lower in females fed Asta and Mec, but lifespan was not significantly affected in these females. The male-specific lifespan benefits from Asta and Mec may provide insights into sex-specific aspects of aging.

This paper illuminates the significant question of how the oral commensal Fusobacterium nucleatum adapts to the metabolically changing environments of several extra-oral sites such as placenta and colon to promote various diseases as an opportunistic pathogen. We demonstrate here that the highly conserved Rhodobacter nitrogen-fixation complex, commonly known as Rnf complex, is key to fusobacterial metabolic adaptation and virulence. Genetic disruption of this Rnf complex causes global defects in polymicrobial interaction, biofilm formation, cell growth and morphology, hydrogen sulfide production, and ATP synthesis. Targeted metabolomic profiling demonstrates that the loss of this respiratory enzyme significantly diminishes catabolism of numerous amino acids, which negatively impacts fusobacterial virulence as tested in a preterm birth model in mice.

Metal doping is an efficient approach to improve H 2 S gas sensing performances, but the metal-doped NiO is still faced poor recovery capability at low working temperature. Herein, Co-doped NiO@g-C 3 N 4 heterocomposites were constructed firstly via a simple solid phase reaction. Texture characterizations indicate that Co-doped NiO@g-C 3 N 4 heterocomposites with the architecture of hierarchical microspheres show high specific surface areas and rich surface oxygen vacancies. The gas-sensitive measurements exhibit that the response value of the heterocomposites with g-C 3 N 4 content of 30 wt% (Co-NiO@g-C 3 N 4 -3) increases to 45 toward 20 ppm H 2 S gas at 172 °C, which is about 1.8 times of Co-NiO (23), as well as response/recovery times decreased to ca. 100/130 s. Besides, excellent repeatability, stability and selectivity of Co-NiO@g-C 3 N 4 -3 sensors are obtained. The improved H 2 S gas sensing performances of Co-NiO@g-C 3 N 4 heterocomposites is mainly contributed to the formation of nano-heterojunctions, which promotes electron accumulation at nano-heterojunctions near Co-NiO, facilitates O 2 molecules adsorption on the material surface and accelerates the resistance change of the sensors, resulting the enhanced gas sensing performances. [Display omitted] [ABSTRACT FROM AUTHOR]

To prevent the residual sulfur dioxide in Chinese herbal medicines (CHM) caused by sulfur fumigation, which may lead to severe health issues, there is an urgent need for a rapid and quantitative detection technique. Sodium borohydride was used as a reducing agent to convert sulfur dioxide into hydrogen sulfide, which was then detected using lead acetate test strip. An accurate testing apparatus was designed, consisting of reaction bottle cap, reaction bottle, lead acetate test strip, and sulfur dioxide detector. The effect of different reaction variables on detection, including reductant quality, pH of initial media, reaction time, lead acetate concentration, and membrane type was investigated. The optimal conditions were determined by orthogonal experiments. The reaction membrane type and lead acetate concentration on the membrane were optimized to enhance detection accuracy. Standardized gray cards were fabricated and used to calibrate the detector. The detection system demonstrated an exceptional linear correlation (r2 = 0.9992), with a linear detection range of 0–750 mg·kg−1. The colored substances and sulfur-containing substances within the matrix of CHM did not affect the detection results. Therefore, the detection method exhibited superior accuracy and stability. The proposed technique proved to be swift, reliable, and provides a straightforward and convenient approach for the quantitative determination of sulfur dioxide in CHMs. The results of this work may provide insights into the development of test strips for quantitative detection. [ABSTRACT FROM AUTHOR]

The sulfane sulfur pool, comprised of persulfide (RS‐SH) and polysulfide (RS‐SnH) derived from hydrogen sulfide (H2S), has emerged as a major player in redox biochemistry. Mitochondria, besides energy generation, serve as significant cellular redox hubs, mediate stress response and cellular health. However, the effects of endogenous mitochondrial sulfane sulfur (MSS) remain largely uncharacterized as compared with their cytosolic counterparts, cytosolic sulfane sulfur (CSS). To investigate this, we designed a novel artificial substrate for mitochondrial 3‐mercaptopyruvate sulfurtransferase (3‐MST), a key enzyme involved in MSS biosynthesis. Using cells expressing a mitochondrion‐localized persulfide biosensor, we demonstrate this tool's ability to selectively enhance MSS. While H2S was previously known to suppress human immunodeficiency virus (HIV‐1), we found that MSS profoundly affected the HIV‐1 life cycle, mediating viral reactivation from latency. Additionally, we provide evidence for the role of the host's mitochondrial redox state, membrane potential, apoptosis, and respiration rates in managing HIV‐1 latency and reactivation. Together, dynamic fluctuations in the MSS pool have a significant and possibly conflicting effect on HIV‐1 viral latency. The precision tools developed herein allow for orthogonal generation of persulfide within both mitochondria and the cytosol and will be useful in interrogating disease biology. [ABSTRACT FROM AUTHOR]

We present a redox-mediated photocatalysis for separate hydrogen production and sulfide oxidation. The process involves photocatalytic hydrogen production and Fe(CN)64− oxidation, followed by spontaneous Fe(CN)63− reduction and sulfide oxidation to valued sulfur. In this approach, Fe(CN)64−/3− redox mediators were recycled, and the produced sulfur wouldn't interfere with the photocatalytic performance. [ABSTRACT FROM AUTHOR]

Elevated blood pressure is the leading metabolic risk factor in attributable deaths, and hydrogen sulfide (H2S) regulates vascular tone and blood pressure. Thus, this study aims to evaluate the mechanism by which NaHS (H2S donor) produces inhibition of the vasopressor sympathetic outflow in obese rats. For that purpose, animals were fed a high‐fat diet (HFD) (60% calories from fat) for 12 weeks. They were anesthetized, pithed, and cannulated to evaluate the role of the potassium channel on NaHS‐induced sympathoinhibition. Animals received selective electrical stimulation of the vasopressor sympathetic outflow, an intravenous (i.v.) administration of (1) tetraethylammonium (TEA, non‐selective K+ channel blocker, 16.5 mg/kg), (2) 4‐aminopyridine (4‐AP, KV channel blocker, 5 mg/kg), (3) barium chloride (BaCl2, KIR channel blocker, 65 μg/kg), (4) saline solution (vehicle of TEA, 4‐AP, and BaCl2, 1 mL/kg), (5) glibenclamide (KATP channel blocker, 10 mg/kg), and (6) glibenclamide vehicle (DMSO + glucose 10% + NaOH, 1 mL/kg), and then a 310 μg/kg·min NaHS i.v. continuous infusion. We observed that (1) NaHS produced inhibition of the vasopressor sympathetic outflow and (2) the sympathoinhibitory effect by NaHS was reversed by the KIR channel blocker, BaCl2, in obese rats. The above data suggest that the potassium channel could be involved in the sympathoinhibition induced by NaHS. [ABSTRACT FROM AUTHOR]

The evolution of independent lineages along replicated environmental transitions frequently results in convergent adaptation, yet the degree to which convergence is present across multiple levels of biological organization is often unclear. Additionally, inherent biases associated with shared ancestry and variation in selective regimes across geographic replicates often pose challenges for confidently identifying patterns of convergence. We investigated a system in which three species of poeciliid fishes sympatrically occur in a toxic spring rich in hydrogen sulfide (H 2 S) and an adjacent nonsulfidic stream to examine patterns of adaptive evolution across levels of biological organization. We found convergence in morphological and physiological traits and genome-wide patterns of gene expression among all three species. In addition, there were shared signatures of selection on genes encoding H 2 S toxicity targets in the mitochondrial genomes of each species. However, analyses of nuclear genomes revealed neither evidence for substantial genomic islands of divergence around genes involved in H 2 S toxicity and detoxification nor substantial congruence of strongly differentiated regions across population pairs. These non-convergent, heterogeneous patterns of genomic divergence may indicate that sulfide tolerance is highly polygenic, with shared allele frequency shifts present at many loci with small effects along the genome. Alternatively, H 2 S tolerance may involve substantial genetic redundancy, with non-convergent, lineage-specific variation at multiple loci along the genome underpinning similar changes in phenotypes and gene expression. Overall, we demonstrate variability in the extent of convergence across organizational levels and highlight the challenges of linking patterns of convergence across scales. [Display omitted] • A novel system with three lineages evolving along the same ecological gradient • Selection from toxic hydrogen sulfide drives trait divergence at small spatial scales • Convergence is evident in morphology, physiology, and the mitochondrial genome • Genomic divergence is characterized by non-convergent, lineage-specific changes Convergent evolution is rarely studied in disparate but sympatric lineages. Greenway et al. study extremophile fishes and find that exposure to the same source of divergent selection results in variable degrees of convergence across different levels of biological organization. [ABSTRACT FROM AUTHOR]

As a gasotransmitter, the role of hydrogen sulfide (H₂S) in preventing and treating osteoporosis has been confirmed in recent years, and its pathophysiological mechanism is gradually elucidated. H₂S counteracts oxidative stress and inflammatory reactions, promotes angiogenesis, regulates intestinal flora and calcium-phosphorus metabolism, thus enhancing bone formation and inhibiting bone resorption, further preventing and treating various types of osteoporosis, such as postmenopausal osteoporosis and, glucocorticoid, or homocysteine-induced osteoporosis. This article summarizes the existing research to provide new insights for further understanding the pathogenesis and treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

In yeast, control of sulfur amino acid metabolism relies upon Met4 , a transcription factor that activates the expression of a network of enzymes responsible for the biosynthesis of cysteine and methionine. In times of sulfur abundance, the activity of Met4 is repressed via ubiquitination by the SCF Met30 E3 ubiquitin ligase, but the mechanism by which the F-box protein Met30 senses sulfur status to tune its E3 ligase activity remains unresolved. Herein, we show that Met30 responds to flux through the trans-sulfuration pathway to regulate the MET gene transcriptional program. In particular, Met30 is responsive to the biological gas hydrogen sulfide, which is sufficient to induce ubiquitination of Met4 in vivo. Additionally, we identify important cysteine residues in Met30 's WD-40 repeat region that sense the availability of sulfur in the cell. Our findings reveal how SCF Met30 dynamically senses the flow of sulfur metabolites through the trans-sulfuration pathway to regulate the synthesis of these special amino acids. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) is a highly toxic and corrosive gas commonly found in industrial emissions and natural gas processing, posing serious risks to human health and environmental safety even at low concentrations. The early detection of H2S is therefore critical for preventing accidents and ensuring compliance with safety regulations. This study presents the development of porous ZnO/SnO2-nanocomposite gas sensors tailored for the ultrasensitive detection of H2S at sub-ppb levels. Utilizing a screen-printing method, we fabricated five different sensor compositions—ranging from pure SnO2 to pure ZnO—and characterized their structural and morphological properties through X-ray diffraction (XRD) and scanning electron microscopy (SEM). Among these, the SnO2/ZnO sensor with a composition-weight ratio of 3:4 demonstrated the highest response at 325 °C, achieving a low detection limit of 0.14 ppb. The sensor was evaluated for detecting H2S concentrations ranging from 5 ppb to 500 ppb under dry, humid air and N2 conditions. The relative concentration error was carefully calculated based on analytical sensitivity, confirming the sensor's precision in measuring gas concentrations. Our findings underscore the significant advantages of mixture nanocomposites in enhancing gas sensitivity, offering promising applications in environmental monitoring and industrial safety. This research paves the way for the advancement of highly effective gas sensors capable of operating under diverse conditions with high accuracy. [ABSTRACT FROM AUTHOR]

The corrosion behavior and electrochemical damage mechanisms induced by sulfate‐reducing bacteria (SRB) on copper (Cu) were investigated in this study. Electrochemical impedance spectroscopy revealed that SRB accelerated the corrosion of Cu, albeit with a mitigating effect observed due to the formation of a protective and dense biofilm. However, upon the rupture of this protective film, the corrosion tendency of Cu significantly increased. Surface analysis corroborated these findings, with the predominant corrosion product identified as Cu2S, a result further supported by thermodynamic calculations. The accelerated corrosion of Cu was primarily attributed to the physiological metabolism of SRB, which generates hydrogen sulfide as the principal agent driving corrosion processes. [ABSTRACT FROM AUTHOR]

Our previous studies have reported that hydrogen sulfide (H 2 S) has ability to improve diabetes-associated cognitive dysfunction (DACD), but the exact mechanisms remain unknown. Recent research reveals that Warburg effect is associated with synaptic plasticity which plays a key role in cognition promotion. Herein, the present study was aimed to demonstrate whether hippocampal Warburg effect contributes to H 2 S-ameliorated DACD and further explore its potential mechanism. We found that H 2 S promoted the hippocampal Warburg effect and inhibited the OxPhos in the hippocampus of STZ-induced diabetic rats. It also improved the hippocampal synaptic plasticity in STZ-induced diabetic rats, as evidenced by the change of microstructures and the expression of different key-enzymes. Furthermore, inhibited hippocampal Warburg effect induced by DCA markedly abolished the improvement of H 2 S on synaptic plasticity in the hippocampus of STZ-induced diabetic rats. DCA blocked H 2 S-attenuated the cognitive dysfunction in STZ-induced diabetic rats, according to the Y-maze, Novel Objective Recognition, and Morris Water Maze tests. Collectively, these findings indicated that the hippocampal Warburg effect mediates H 2 S-ameliorated DACD by improving hippocampal synaptic plasticity. [Display omitted] • H 2 S enhances the hippocampal Warburg effect and inhibited the OxPhos in diabetic rats. • H 2 S promotes the hippocampal synaptic plasticity in diabetic rats. • Inhibition of hippocampal Warburg effect reverses H 2 S-improved synaptic plasticity in diabetic rats. • Inhibition of hippocampal Warburg effect blocks H 2 S-attenuated cognitive dysfunction in diabetic rats. [ABSTRACT FROM AUTHOR]

Glutathione persulfide (GSSH) is an important cellular metabolite involved in redox regulation and a potential therapeutic agent. Due to its instability and the lack of commercial GSSH standards, the development of procedures for its generation in situ and quantitative determination in various test systems is a problem of considerable current interest. In this work, conditions for the generation of GSSH in a reaction of oxidized glutathione with sodium sulfide with the fluorescent monitoring of released hydrogen sulfide were optimized. To derivatize the generated GSSH and reduced glutathione (GSH) with the formation of both derivatives in similar amounts, the reaction was carried out in the presence of an excess of N-ethylmaleimide. A procedure for the determination of GSSH based on the level of GSH in a model reaction using HPLC–mass spectrometry in the multiple reaction monitoring mode was described. The contribution of the GSH impurity in a solution of oxidized glutathione to the determined amount of GSSH and the detection limit of GSSH in the reaction mixture were found. The results are of interest for the preparation and mass spectrometric analysis of biologically relevant persulfides using various derivatizing agents. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H 2 S) is a toxic gas emitted through natural and anthropogenic activities. Chronic exposure to inhaled H 2 S at low sub-toxic levels is common among workers in oil refineries and may have important health implications. Inhaled H 2 S can be oxidized to thiosulfate or methylated to dimethylsulfide (DMS) which can be methylated to the novel human metabolite trimethylsulfonium (TMS) or oxidized to dimethylsulfoxide (DMSO) but the extent of methylation of inhaled H 2 S is currently unknown in humans. A total of 80 participants were recruited of which 40 were workers in an oil refinery in Kurdistan region, Iraq including those working in close contact with the facility area where H 2 S was measured at 1.5–5.0 mg m−3, and 40 controls living in a nearby city with no detectable H 2 S or perceptible odor (<0.1 mg m−3). A total of 240 urine samples were measured for multiple H 2 S-related metabolites. DMSO was consistently found in all urine samples with concentrations generally within the range of 1.0–10 µM. Although these concentrations were 10–100-fold higher than TMS urinary levels, clear correlation between DMSO and TMS was observed (r s 0.55, P < 0.0001), which supports DMS as common precursor. DMSO urinary levels were elevated in the oil refinery workers in close contact with the facilities (5.0 vs. 3.3 µM, P 0.03), but TMS was unaltered (0.13 vs. 0.14 µM, P 0.68). Overall, the results suggest that the investigated methylation metabolites are not sufficiently sensitive to low occupational exposure levels of inhaled H 2 S. • First investigation of the response of H 2 S-methylation metabolites to inhaled H 2 S in humans. • Total 240 urine samples were collected (120 from oil refinery workers and 120 from controls). • Dimethylsulfoxide (DMSO) was slightly elevated in oil refinery workers (3.3 vs. 5.0 µM), P 0.03. • Trimethylsulfonium (TMS) did not show a response to occupational H 2 S exposure. • H 2 S detoxification via methylation is limited at occupational exposure levels in humans. [ABSTRACT FROM AUTHOR]

Under normal circumstances, high-density lipoprotein (HDL) is considered to have cardiovascular protective effects, but the impact of oxidized HDL (ox-HDL) on vascular endothelial function remains poorly understood. Mitochondrial function is closely related to endothelial function, and hydrogen sulfide (H₂S) is a gas with endothelial protective properties. The novel hydrogen sulfide donor AP39 can target mitochondria to release H₂S, but the combined effects of ox-HDL and AP39 on vascular endothelium are not well studied. We established a cell model of ox-HDL-induced endothelial cell damage and mitochondrial dysfunction using human umbilical vein endothelial cells (HUVECs) and conducted AP39 pretreatment. The experiments confirmed the functional damage and mitochondrial dysfunction in HUVECs caused by ox-HDL. Additionally, to further explore the role of SIRT1 in AS, we analyzed SIRT1 expression in AS carotid artery tissue. This included the analysis of differentially expressed genes from AS-related datasets, presented through volcano plots and heatmaps, with enrichment analysis of downregulated genes in KEGG pathways and GO functions. Furthermore, we evaluated the differences in SIRT1 expression in coronary arteries with varying degrees of stenosis and in early and late-stage AS carotid artery tissues, and analyzed data from SIRT1 knockout mouse models. The experimental results indicate that AP39 effectively alleviated ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1 expression. MTT and CCK-8 assays showed that ox-HDL treatment led to decreased cell viability and proliferation in HUVECs, reduced eNOS expression, and significantly increased levels of ICAM-1, IL-6, and TNF-α, along with enhanced monocyte adhesion. These findings reveal the damaging effects of ox-HDL on HUVECs. Transcriptomic data indicated that while SIRT1 expression did not significantly differ in coronary arteries with varying degrees of stenosis, it was notably downregulated in AS carotid artery tissues, especially in late-stage AS tissues. KEGG pathway enrichment analysis revealed that SIRT1 downregulated genes were associated with processes such as vascular smooth muscle contraction, while GO analysis showed that these downregulated genes were involved in muscle system processes and muscle contraction functions, further confirming SIRT1's critical role in AS pathology. In transcriptomic data from the SIRT1 knockout mouse model, elevated levels of inflammation-related proteins IL-6 and TNF-α were observed after SIRT1 knockout, along with decreased expression of the chaperone protein PGC-1α. The expression of mitochondrial-related functional proteins Nrf2 and PGC-1α was positively correlated with SIRT1 expression, while inflammation-related proteins ICAM-1, IL-6, IL-20, and TNF-α were negatively correlated with SIRT1 expression. We further discovered that ox-HDL triggered mitochondrial dysfunction, as evidenced by reduced expression of Mfn2, Nrf2, PGC1-α, UCP-1, and SIRT1, corroborating the results from the previous database analysis. Additionally, mitochondrial dysfunction was characterized by decreased mitochondrial membrane potential (MMP), increased mitochondrial ROS levels, and reduced ATP content, further impacting cellular energy metabolism and respiratory function. Subsequent experimental results showed that the addition of AP39 mitigated these adverse effects, as evidenced by decreased levels of ICAM-1, IL-6, and TNF-α, increased eNOS expression, reduced monocyte adhesion, increased mitochondrial H₂S content, and upregulated expression of SIRT1 protein associated with mitochondrial function, reduced ROS levels, and increased ATP content. Furthermore, validation experiments using the SIRT1 inhibitor EX527 confirmed that AP39 alleviated ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1 expression. Ox-HDL can induce damage and mitochondrial dysfunction in HUVECs, while AP39 inhibits ox-HDL-induced endothelial cell damage and mitochondrial dysfunction by upregulating SIRT1. • Mechanism Insight: Elucidates ox-HDL's harmful effects on endothelial cells, focusing on SIRT1 downregulation and mitochondrial dysfunction. • Mitochondrial Targeting : AP39, a mitochondria-targeted hydrogen sulfide donor, mitigates ox-HDL-induced damage by upregulating SIRT1. • Cellular and Molecular Impact: AP39 improves cell survival, reduces pro-inflammatory markers, and decreases monocyte adhesion in endothelial cells. • Mitochondrial Function Preservation: AP39 enhances mitochondrial membrane potential, reduces ROS, and increases ATP content, maintaining mitochondrial function. • Therapeutic Potential : Suggests AP39 as a therapy for atherosclerosis by targeting mitochondrial dysfunction and endothelial injury caused by ox-HDL. [ABSTRACT FROM AUTHOR]

To investigate the protective mechanisms of hydrogen sulfide (H 2 S) in sepsis-induced acute kidney injury (SAKI), we conducted an in vivo study using a SAKI mouse model induced by intraperitoneal lipopolysaccharide (LPS) injection. Following 6 h of LPS injection, levels of tumor necrosis factor-alpha (TNF-α) and blood urea nitrogen (Bun) were significantly elevated in mouse plasma. In the kidneys of SAKI mice, expression of H 2 S-generating enzymes cysteinyl-tRNA synthetase (CARS), cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) was markedly downregulated, while glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), phosphorylated protein kinase R-like endoplasmic reticulum kinase/protein kinase R-like endoplasmic reticulum kinase (p-PERK/PERK), and B-cell lymphoma-2 recombinant protein X/B-cell lymphoma-2 (Bax/Bcl2) expression was significantly upregulated. H 2 S improved renal function and attenuated renal histopathological changes in SAKI mice, thereby alleviating LPS-induced endoplasmic reticulum stress (ERS). Additionally, it inhibited the expression of p-PERK/PERK and Bax/Bcl2. After inhibiting CSE activity with dl -propargylglycine (PPG i. p.), the renal tissue pathology in LPS-induced AKI mice was further exacerbated, leading to enhanced activation of the PERK/Bax-Bcl2 pathway. Our findings suggest that endogenous H 2 S influences the pathogenesis of SAKI, while exogenous H 2 S protects against LPS-induced AKI by inhibiting the PERK/Bax-Bcl2 pathway involved in ERS. • The lack of endogenous hydrogen sulfide generation is the cause of SAKI in sepsis. • Exogenous hydrogen sulfide treatment inhibits ER stress and improves SAKI. • Exogenous hydrogen sulfide improves SAKI by suppressing ER stress through inhibition of the PERK/Bax-Bcl2 pathway. [ABSTRACT FROM AUTHOR]

The mutual regulation between hydrogen sulfide (H 2 S) and microRNA (miRNA) is involved in the development of many diseases, including cancer, cardiovascular disease, inflammatory disease, and high-risk pregnancy. Abnormal expressions of endogenous H 2 S-producing enzyme and miRNA in tissues and cells often indicate the occurrence of diseases, so the maintenance of their normal levels in the body can mitigate damages caused by various factors. Many studies have found that H 2 S can promote the migration, invasion, and proliferation of cancer cells by regulating the expression of miRNA, while many H 2 S donors can inhibit cancer progression by interfering with the proliferation, apoptosis, cell cycle, metastasis, and angiogenesis of cancer cells. Furthermore, the mutual regulation between H 2 S and miRNA can also prevent cell injury in cardiovascular disease and inflammatory disease through anti-inflammation, anti-oxidation, anti-apoptosis, and pro-autophagy. In addition, H 2 S can promote angiogenesis and relieve vasoconstriction by regulating the expression of miRNA, thereby improving fetal growth in high-risk pregnancy. In this review, we discuss the mechanism of mutual regulation between H 2 S and miRNA in various diseases, which may provide reliable therapeutic targets for these diseases. • H 2 S promotes the progression of cancer cells by regulating the miRNA expression. • H 2 S donors inhibit cancer growth via the mutual regulation between H 2 S and miRNA. • The mutual regulation between H 2 S and miRNA plays a protective role in diseases. • H 2 S plays a double-edged sword role in inflammation via interaction with miRNA. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) has emerged as a potent therapeutic agent with diverse physiological functions, including vasodilation, anti-inflammation, and cytoprotection. However, its clinical application is limited due to its volatility and potential toxicity at high concentrations. To address these challenges, researchers have developed various H2S prodrugs that release H2S in a controlled and targeted manner. The review underscores the importance of targeting and delivery strategies in maximizing the therapeutic potential of H2S, a gasotransmitter with diverse physiological functions and therapeutic effects. By summarizing recent advancements, the review provides valuable insights for researchers and clinicians interested in harnessing the therapeutic benefits of H2S while minimizing off-target effects and toxicity. The integration of novel targeting and delivery approaches not only enhances the efficacy of H2S-based therapeutics but also expands the scope of potential applications, offering promising avenues for the development of new treatments for a variety of diseases and disorders. • Provide a comprehensive overview of the diverse physiological functions and therapeutic effects of hydrogen sulfide (H2S). • Discuss the limitations of H2S clinical application, highlighting its volatility and potential toxicity at high concentrations. • Summarize recent advancements in the development of H2S prodrugs. • Emphasize the importance of targeting and delivery strategies in maximizing the therapeutic potential. • Discuss future directions in H2S-based therapeutics, including the integration of novel targeting and delivery approaches. [ABSTRACT FROM AUTHOR]

Vegetation has been found to improve the hydrological performance of landfill cover. However, existing studies ignore the effects of hydrogen sulfide (H2S), which forms the toxic odour generated from municipal solid wastes. Hydrogen sulfide is a potential signalling molecule in regulating plant-stomata aperture, but how the plant–hydrogen sulfide interaction affects the water–gas transport in soil remains unknown. This aim of this study was to investigate the effects of hydrogen sulfide on Bermuda grass growth and its influence on water–gas transport in unsaturated soils. Soil columns, with and without vegetation, were prepared and fumigated with different hydrogen sulfide concentrations. These columns were subjected to controlled drought and rainfall sequentially. The results showed that grass leaves almost wilted without hydrogen sulfide fumigation due to the Pythium diseases caused by the antecedent waterlogged conditions. In contrast, hydrogen sulfide fumigation promoted grass growth because of the fungicidal effects of hydrogen sulfide. In drought, hydrogen sulfide fumigation caused stomata closure, which resulted in a lower matric suction in the vegetated soil than that without hydrogen sulfide fumigation. Accordingly, hydrogen sulfide concentration reduced because of oxidation by metal oxides in soil. Upon subsequent rainfall, more infiltration but lower matric suction was observed in vegetated soils than was found in the bare case, whereas hydrogen sulfide concentration decreased continuously due to gas dissolution in the pore water. Direct application of laboratory findings herein to field cases should be used with caution, because the applied continuous lighting and low evapotranspiration rate of the soil column tests may not be representative of field conditions. [ABSTRACT FROM AUTHOR]

Summary: Plant survival to a potential plethora of diverse environmental insults is underpinned by coordinated communication amongst organs to help shape effective responses to these environmental challenges at the whole plant level. This interorgan communication is supported by a complex signal network that regulates growth, development and environmental responses. Nitric oxide (NO) has emerged as a key signalling molecule in plants. However, its potential role in interorgan communication has only recently started to come into view. Direct and indirect evidence has emerged supporting that NO and related species (S‐nitrosoglutathione, nitro‐linolenic acid) are mobile interorgan signals transmitting responses to stresses such as hypoxia and heat. Beyond their role as mobile signals, NO and related species are involved in mediating xylem development, thus contributing to efficient root–shoot communication. Moreover, NO and related species are regulators in intraorgan systemic defence responses aiming an effective, coordinated defence against pathogens. Beyond its in planta signalling role, NO and related species may act as ex planta signals coordinating external leaf‐to‐leaf, root‐to‐leaf but also plant‐to‐plant communication. Here, we discuss these exciting developments and emphasise how their manipulation may provide novel strategies for crop improvement. [ABSTRACT FROM AUTHOR]

Background and Purpose: Sodium glucose cotransporter 2 inhibitors (SGLT2i) have emerged as a potent therapy for heart failure with preserved ejection fraction (HFpEF). Hydrogen sulphide (H2S), a well‐studied cardioprotective agent, could be beneficial in HFpEF. SGLT2i monotherapy and combination therapy involving an SGLT2i and H2S donor in two preclinical models of cardiometabolic HFpEF was investigated. Experimental Approach: Nine‐week‐old C57BL/6N mice received L‐NAME and a 60% high fat diet for five weeks. Mice were then randomized to either control, SGLT2i monotherapy or SGLT2i and H2S donor, SG1002, for five additional weeks. Ten‐week‐old ZSF1 obese rats were randomized to control, SGLT2i or SGLT2i and SG1002 for 8 weeks. SG1002 monotherapy was investigated in additional animals. Cardiac function (echocardiography and haemodynamics), exercise capacity, glucose handling and multiorgan pathology were monitored during experimental protocols. Key Results: SGLT2i treatment improved E/e′ ratio and treadmill exercise in both models. Combination therapy afforded increases in cardiovascular sulphur bioavailability that coincided with improved left end‐diastolic function (E/e′ ratio), exercise capacity, metabolic state, cardiorenal fibrosis, and hepatic steatosis. Follow‐up studies with SG1002 monotherapy revealed improvements in diastolic function, exercise capacity and multiorgan histopathology. Conclusions and Implications: SGLT2i monotherapy remediated pathological complications exhibited by two well‐established HFpEF models. Adjunctive H2S therapy resulted in further improvements of cardiometabolic perturbations beyond SGLT2i monotherapy. Follow‐up SG1002 monotherapy studies inferred an improved phenotype with combination therapy beyond either monotherapy. These data demonstrate the differing effects of SGLT2i and H2S therapy while also revealing the superior efficacy of the combination therapy in cardiometabolic HFpEF. [ABSTRACT FROM AUTHOR]

Fieldwork was carried out in the western area of Edmonton, Alberta, Canada to assess the H2S contribution of a long force main and to investigate the source of H2S generation in a complex sewer network. The study sewer trunk has a length of 10 km, a diameter of up to 1.95 m, and flow rate of up to 0.6 m3/s. In the upstream, there is a 5.6 km forcemain, and the pump station operation can cause a sudden increase of H2S in the sewer air of the discharge manholes to reach 500 ppm. Wastewater samples were collected in 14 manholes in the sewer network and analyzed for sulfide and other relevant parameters. The maximum values of sulfide were 9.7 mg S/L and pH remained mostly neutral. For predicting the sulfide generation rate, an empirical model was applied with readily biodegradable organic matter. Then the emission of H2S in gravity pipes was investigated, and it was found over 90% of H2S stayed in the liquid phase when wastewater flowed in gravity sewer pipes. Finally, the mass transfer in a drop structure of 8 m was investigated. The liquid phase H2S concentration in the upstream was 2.6 times that of the downstream, and about 62% of the H2S was released in this drop structure indicating the significant emission of H2S in drop structures. [ABSTRACT FROM AUTHOR]

We investigated the potential role of hydrogen sulfide (H2S) as a novel therapy for diabetic peripheral neuropathy in diabetic rats. A single dose of streptozotocin (60 mg/kg) was applied to the rats for the diabetic rat models. Sodium bisulfide (50 μmol/kg/d) was injected intraperitoneally daily for 2 weeks as H2S treatment. Electromyogram, haematoxylin eosin staining, transmission electron microscopy, western blotting and enzyme‐linked immunosorbent assay were then performed. H2S treatment did not affect body weights, blood glucose levels or liver function of diabetic rats, while the creatine levels of the H2S‐treated diabetic rats decreased compared with the diabetic control rats. H2S treatment for 2 weeks did not affect the sciatic nerve conduction velocity of the diabetic rats. However, H2S treatment relieved neurons loss and cell atrophy of dorsal root ganglion, and axon degeneration of sciatic nerve in diabetic rats. Serum super oxide dismutase (SOD) levels and SOD2 levels in the sciatic nerve of diabetic rats were lower than the non‐diabetic rats but were restored after H2S treatment. Serum and sciatic nerve homogenate malondialdehyde and aldose reductase expression were higher in diabetic rats but decreased significantly after H2S treatment. Our study revealed that H2S alleviates neural degeneration in diabetic rats probably by reducing oxidative stress and downregulating aldose reductase expression. [ABSTRACT FROM AUTHOR]

Biogas desulphurisation plants aim to remove hydrogen sulphide and other gaseous compounds that occur in the gas mixture. This mainly concerns the reduction of H2S which reacts with most metals such as iron or copper, which leads to the corrosion of pipelines and equipment. The aim of this research was to use two materials to adsorb hydrogen sulphide from biogas and to compare the efficiency of these two processes. Biogas was passed through both adsorbents. The concentration of hydrogen sulphide was measured upstream and downstream of the adsorbent bed. The results are summarised in diagrams. The first material used in the biogas desulphurisation plant at the wastewater treatment plant was bog iron ore. The bed was replaced several times during the year to maintain the efficiency of hydrogen sulphide removal from the biogas. After a year, a new adsorbent called "SulfurE" was used in place of the bog iron ore. The new bed operated with higher efficiency than the bog iron ore. The operating period between bed replacements was also extended. The bog iron ore bed in the desulphurisation plant was replaced on average 3 to 4 times a year, depending on the amount of hydrogen sulphide flowing into the desulphurisation plant (the more H2S, the higher the frequency of bed replacement). The bed in the desulphurisation plant filled with the "SulfurE" product operated for about 9 months with 90% hydrogen sulphide absorption efficiency (depending on the quality of biogas produced). [ABSTRACT FROM AUTHOR]

Biogas, one of potential renewable energies, could play an effective role in fulfilling the world's energy demand. The presence of elevated concentrations of H2S in biogas is problematic because of its highly corrosiveness and toxicity. Recently, there has been interest in utilizing biochar as alternative adsorbent to remove H2S from biogas. In this study, the adsorption capacity of banana peel biochar (BPB) and banana empty fruit bunch biochar (BEFBB) wastes for removing H2S from biogas was investigated. Biochar was produced through the pyrolysis process. Firstly, physical and chemical properties of biochar (moisture content, volatile compound content, ash content, fixed carbon, iodine number, pH, and BET surface) were determined. BEFBB possessed higher fixed carbon content (38.05%), iodine number (146.98 ± 2.29 mg g−1), pH value (8.7 ± 0.3), and larger BET surface (3.18 m2 g−1) than BPB. Secondly, the effect of biochar types and biochar pellet sizes on the adsorption capacity was investigated. The adsorption experiment was carried out, using anaerobically digested biogas, in a packed column containing 10 g of biochar with the pallet size of 1.0 cm of diameter, the initial H2S concentration of 500 ppm at the flowrate of 500 mL min−1. Adsorption efficiency curves showed that the two types of biochar presented high removal capacity for H2S but very low removal capacity for CH4 and CO2. The breakthrough adsorption capacity of BPB and BEFBB was found to be 5.85 mg g−1 and 7.65 mg g−1, respectively, consisting well with their physiochemical characterizations. Then, the effect of biochar pellet sizes on the removal efficiency was studied at three different pallet sizes (0.50 cm, 1.00 cm, and 1.50 cm of diameter). Smaller pellet size adsorbent showed higher removal efficiency than larger pellet size owning to its larger surface area. The FTIR analysis result of BEFBB shown that carboxylic and hydroxide radical groups were most likely responsible for H2S adsorption. Finally, the SEM/EDX results showed significant changes in morphological and chemical properties after the adsorption process. Therefore, BPB and BEFBB could be used as an alternative adsorbent for removing H2S from biogas. [ABSTRACT FROM AUTHOR]

In this paper, we study the effects of spinning speed on the electrical, optical, structural, morphological, and gas sensing properties of thin films deposited on glass substrates by sol–gel spin coating, using copper acetate dihydrate as the precursor. The deposition of the films was carried out at varying spinning speeds from 1500 rpm to 2500 rpm to achieve different thicknesses ranging from 157 nm to 470 nm, respectively. The results revealed that the resistivity of the films decreased from 75.5 Ω·m to 42.5 Ω·m with the decrease in spinning speed. X-ray diffraction (XRD) studies demonstrated that the crystallite size varied in the range of 18.14–27.48 nm. The band gap of the samples was found to vary from 2 eV to 1.69 eV, revealing that these samples were suitable for gas sensing applications. Field-emission scanning microscopy (FESEM) studies showed that the prepared samples were porous in nature and were suitable for H2S gas detection. The films were examined at different operating temperatures with different concentrations of H2S gas. The results showed that the response toward hydrogen sulfide gas varied with varying thickness of the samples. The CuO thin films showed the highest response toward hydrogen sulfide gas at a temperature of 25°C. [ABSTRACT FROM AUTHOR]

Spherical shaped Barium titanate (BaTiO3) nanospheres was synthesized, using co‐precipitate technique. The as‐synthesized nanospheres was discovered to be discriminatory in terms of sensing carbon dioxide (CO2) gas. The structural parameters like, shape, optical properties, morphology, and thermal stability were explored using XRD, FT‐IR, UV‐Visible, EDS and FE‐SEM. Spherical shaped BaTiO3 nanospheres material have the highest response (63 %) for CO2 gas. CO2 gas reaction and recovery times were 23.5 and 20.3 seconds, respectively. The CO2 gas concentration climbs from 1 to 50 ppm, reaction to gas sensors increases. CO2 gas has higher selectivity for BaTiO3 nanospheres as compared to other gases like carbon dioxide (CO2), methane (CH4), carbon monoxide (CO), nitric oxide (NO), hydrogen sulphide (H2S) and hydrogen (H2). The repeatability of BaTiO3 nanospheres was researched for 42 days and discovered to be impressive. [ABSTRACT FROM AUTHOR]

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Excessive oxidative response, unbalanced immunomodulation, and impaired mesenchymal stem cell function in periodontitis in diabetes makes it a great challenge to achieve integrated periodontal tissue regeneration. Here, a polyphenol-mediated redox-active algin/gelatin hydrogel encapsulating a conductive poly(3,4-ethylenedioxythiopene)-assembled polydopamine-mediated silk microfiber network and a hydrogen sulfide sustained-release system utilizing bovine serum albumin nanoparticles is developed. This hydrogel is found to reverse the hyperglycemic inflammatory microenvironment and enhance functional tissue regeneration in diabetic periodontitis. Polydopamine confers the hydrogel with anti-oxidative and anti-inflammatory activity. The slow, sustained release of hydrogen sulfide from the bovine serum albumin nanoparticles recruits mesenchymal stem cells and promotes subsequent angiogenesis and osteogenesis. Moreover, poly(3,4-ethylenedioxythiopene)-assembled polydopamine-mediated silk microfiber confers the hydrogel with good conductivity, which enables it to transmit endogenous bioelectricity, promote cell arrangement, and increase the inflow of calcium ion. In addition, the synergistic effects of hydrogen sulfide gaseous-bioelectric coupling promotes bone formation by amplifying autophagy in periodontal ligament stem cells and modulating macrophage polarization via lipid metabolism regulation. This study provides innovative insights into the synergistic effects of conductivity, reactive oxygen species scavenging, and hydrogen sulfide on the periodontium in a hyperglycemic inflammatory microenvironment, offering a strategy for the design of gaseous-bioelectric biomaterials to promote functional tissue regeneration in immune-related diseases. Biomaterials have potential in treating periodontitis in diabetes, but addressing the range of issues with one material is challenging. Here, the authors report the development of a redox-active hydrogel for reducing inflammation and promoting tissue regeneration in diabetic periodontitis. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H₂S), a metabolite of the transsulfuration pathway, has been implicated in ferroptosis, a unique form of cell death caused by lipid peroxidation. While the exact mechanisms controlling ferroptosis remain unclear, our study reveals that H₂S sensitizes human non-small cell lung cancer (NSCLC) cells to this process, particularly when cysteine levels are low. Combining H₂S with cystine depletion significantly enhances the effectiveness of ferroptosis-based cancer therapy. Mechanistically, H₂S persulfidates the 195th cysteine on S-adenosyl homocysteine hydrolase (SAHH), reducing its enzymatic activity. This leads to decreased homocysteine levels, subsequently lowering cysteine and glutathione concentrations under cystine depletion conditions. These changes ultimately increase the vulnerability of NSCLC cells to ferroptosis. Our findings establish H₂S as a key regulator of homocysteine metabolism and a critical factor in determining NSCLC cell susceptibility to ferroptosis. These results highlight the potential of H₂S-based therapies to improve the efficacy of ferroptosis-targeted cancer treatments for NSCLC. [Display omitted] • H 2 S promotes ferroptosis induced by cystine depletion in non-small cell lung cancer • H 2 S inhibits the transsulfuration pathway by decreasing homocysteine levels • H 2 S inhibits S-adenosyl homocysteine hydrolase activity through cysteine persulfidation • H 2 S enhances ferroptosis-based cancer therapies for NSCLC Zheng et al. show that H₂S sensitizes NSCLC cells to ferroptosis through cysteine persulfidation of S-adenosyl homocysteine hydrolase, reducing its activity. This leads to decreased levels of homocysteine, cysteine, and glutathione, promoting ferroptosis, particularly in low-cystine conditions. These results suggest H₂S enhances ferroptosis-based treatments for NSCLC. [ABSTRACT FROM AUTHOR]

The Aeolian archipelago is known worldwide for its volcanic activity and hydrothermal emissions, of mainly carbon dioxide and hydrogen sulfide. Hydrogen, methane, and carbon monoxide are minor components of these emissions which together can feed large quantities of bacteria and archaea that do contribute to the removal of these notorious greenhouse gases. Here we analyzed the metagenome of samples taken from the Levante bay on Vulcano Island, Italy. Using a gene-centric approach, the hydrothermal vent community appeared to be dominated by Proteobacteria, and Sulfurimonas was the most abundant genus. Metabolic reconstructions highlight a prominent role of formaldehyde oxidation and the reverse TCA cycle in carbon fixation. [NiFe]-hydrogenases seemed to constitute the preferred strategy to oxidize H2, indicating that besides H2S, H2 could be an essential electron donor in this system. Moreover, the sulfur cycle analysis showed a high abundance and diversity of sulfate reduction genes underpinning the H2S production. This study covers the diversity and metabolic potential of the microbial soil community in Levante bay and adds to our understanding of the biogeochemistry of volcanic ecosystems. [ABSTRACT FROM AUTHOR]

Developing activatable photodynamic agents is becoming a promising mode for realizing selective photodynamic therapy (PDT) in cancer treatment. However, till now only a few H2S‐activatable photodynamic agents have been involved in this field. Here, we fabricated H2S‐activatable nano‐assemblies (P@TPPCY) for the treatment of colon cancer containing high concentration H2S. The H2S‐activatable photosensitizer (TPPCY) was synthesized by covalent conjugation between tetraphenylporphyrin (TPP) and heptamethine cyanine (Cy7), and then TPPCY was encapsulated by an amphiphilic polymer DSPE‐mPEG to form P@TPPCY nano‐assemblies. We demonstrated that the photosensitizing effect of TPP was efficiently quenched by Cy7 with strong absorption in the NIR region via fluorescence resonance energy transfer (FRET) effect. Interestingly, the FRET effect between Cy7 and TPP was attenuated by the decrease of absorption of Cy7 in the NIR region after the Cy7 reacted with H2S, and then the photosensitizing effect of TPP in P@TPPCY was activated. Strikingly, the P@TPPCY showed efficient H2S‐activatable photodynamic therapy (PDT) in vitro against HCT116 cells (human colon carcinoma cell line), thus this work provides a new method for realizing accurate treatment of colon cancer in virtue of high H2S concentration microenvironment. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) and nitric oxide (NO) are important gaseous biological signaling molecules that are involved in complex cellular pathways. A number of physiological processes require both H2S and NO, which has led to the proposal that different H2S/NO⋅ crosstalk species, including thionitrite (SNO−) and perthionitrite (SSNO−), are responsible for this observed codependence. Despite the importance of these S/N hybrid species, the reported properties and characterization, as well as the fundamental pathways of formation and subsequent reactivity, remain poorly understood. Herein we report new experimental insights into the fundamental reaction chemistry of pathways to form SNO− and SSNO−, including mechanisms for proton‐mediated interconversion. In addition, we demonstrate new modes of reactivity with other sulfur‐containing potential crosstalk species, including carbonyl sulfide (COS). [ABSTRACT FROM AUTHOR]

The coexistence of numerous Mississippi-Valley-type (MVT) Zn–Pb deposits and (paleo) oil/gas reservoirs in the world suggests a close genetic relationship between mineralization and hydrocarbon accumulation. Xuequ–Shandouya middle MVT Zn–Pb deposits are mainly hosted in the Lower Cambrian Maidiping Member siliceous dolostone on the southwestern margin of the Yangtze Block, accompanied by large amount of bitumen in the orebodies. Therefore, this type of Zn–Pb deposit is a natural laboratory for studying the relationship between the mineralization and the accumulation of paleo-oil/gas reservoirs. The deposit is characterized by spheroidal and concentric banded sphalerite. In situ sulfur isotope studies are carried out to determine the sulfur sources, sulfate reduction mechanisms, and role of hydrocarbons in the zinc–lead mineralization process. According to the mineral paragenesis and relative temporal relationship, two mineralization stages (1 and 2) are identified. An in situ sulfur isotope analysis of spheroidal and concentric banded sphalerite particles from Stage 2 shows that there are the two following types of sulfur isotopes in the sphalerite: one with relatively invariable δ34S values in the core (+8.31 to +9.30‰), and the other with a gradual increase from the core margin (core) to the rim (+0.39 to +16.18‰). These two types reflect that they may have formed in different times, with first type forming in the early period of Stage 2, while the second type was formed in the late period of Stage 2. The sulfur isotopic data suggest the sulfur source of evaporated sulfate minerals and multiple formation mechanisms for reduced sulfur (H2S). In the early period of Stage 2 mineralization, the sulfate reduction mechanism is mainly a mixture of bacterial sulfate reduction (BSR) and/or thermochemical sulfate reduction (TSR), while a very small amount may come from the thermal decomposition of organic compounds (DOCs). In the late period of Stage 2, TSR is dominant, and the gradual increase in the δ34S value may be related to Rayleigh fractionation. The oil/gasreservoir not only acts as a reducing agent to provide the required hydrogen sulfide for zinc–lead mineralization through TSR or BSR, but also provides reduced sulfur for mineralization through the thermal decomposition of organic compounds directly. [ABSTRACT FROM AUTHOR]

Isorhamnetin (ISO) is an active flavonoid compound mainly isolated from the fruits of Hippophae rhamnoides L. and the leaves of Ginkgo biloba L. Previous studies have revealed the antifibrotic action of ISO in the liver and lungs, although its potential protective effects against renal fibrosis and the underlying mechanisms are still poorly understood. Given that many actions of ISO could be similarly attained by hydrogen sulfide (H2S), we speculated that ISO may work through the induction of endogenous H2S. To test the hypothesis, we established the unilateral ureteral obstruction (UUO) renal fibrosis rat model and transforming growth factor-β1(TGF-β1)-induced fibrosis in cultured renal tubular cells. ISO treatment inhibited epithelial–mesenchymal transition (EMT) formation, decreased extracellular matrix (ECM) deposition, and relieved renal fibrosis. Further analysis revealed that ISO stimulated the expression of the H2S-synthesizing enzyme cystathionine lyase (CSE) and cystathionine beta-synthase (CBS), and promoted H2S production in vivo and in vitro. The elevated H2S attenuated oxidative stress and elevated the thiol level. It induced Keap1 sulfhydration, disrupted Keap1-Nrf2 interaction, and promoted the entry of Nrf2 into the nucleus. Finally, we found that circulating H2S mainly derived from the liver, and not the kidney. Collectively, our study revealed that ISO alleviated renal fibrosis by inducing endogenous H2S and regulating Keap1-Nrf2 interaction through sulfhydration of Keap1. Endogenous H2S could be an important mediator underlying the pharmacological actions of ISO. Due to the multifunctional properties of H2S, the H2S-inducing nature of ISO could be exploited to treat various diseases. [ABSTRACT FROM AUTHOR]

Background: Hydrogen sulfide (H2S) is an endogenous transmitter with the potential to regulate aqueous humor dynamics and protect retinal neurons from degeneration. The aim of the present study was two-fold: (a) to evaluate the release of H2S from two polysulfides, diallyl disulfide (DADS), and diallyl trisulfide (DATS); and (b) to investigate their ocular hypotensive actions in normotensive male and female rabbits in the presence and absence of GSH. Materials and Methods: H2S was quantified hourly for up to 6 h using a H2S-Biosensor (World Precision Instruments, Sarasota, Fl). Intraocular pressure (IOP) was assessed in normotensive New Zealand Albino rabbits using a pneumotonometer (model 30 classic; Reichert Ophthalmic Instruments, Depew, NY, USA). Results: In the presence of GSH, there was an increase in the in vitro release of H2S produced by DADS and DATS. Both DADS and DATS also caused a dose-dependent reduction in IOP in male and female rabbits, in both treated and untreated eyes. For instance, in male animals, the presence of GSH (3% and 5%) significantly (p < 0.05, n = 5) enhanced the ocular hypotensive action of DADS (2%) and DATS (2%) from 14.02 ± 2.89% to 18.67 ± 5.6% and from 16.22 ± 3.48 to 23.62 ± 5.79%, respectively. Conclusions: GSH enhanced both H2S release and ocular hypotensive action of the polysulfides in a manner that was dependent on the number of sulfur atoms present in each polysulfide. Furthermore, female animals were less sensitive to the IOP-lowering action of the polysulfides, when compared to their male counterparts. [ABSTRACT FROM AUTHOR]

Background: We have evidence that hydrogen sulfide (H2S)-releasing compounds can reduce intraocular pressure in normotensive and glaucomatous rabbits by increasing the aqueous humor (AH) outflow through the trabecular meshwork. Since H2S has been reported to possess neuroprotective actions, the prevention of retinal ganglion cell loss is an important strategy in the pharmacotherapy of glaucoma. Consequently, the present study aimed to investigate the neuroprotective actions of H2S-releasing compounds against hydrogen peroxide (H2O2)-induced oxidative stress in an isolated bovine retina. Materials and Methods: The isolated neural retinae were pretreated with a substrate for H2S biosynthesis called L-cysteine, with the fast H2S-releasing compound sodium hydrosulfide, and with a mitochondrial-targeting H2S-releasing compound, AP123, for thirty minutes before a 30-min oxidative insult with H2O2 (100 µM). Lipid peroxidation was assessed via an enzyme immunoassay by measuring the stable oxidative stress marker, 8-epi PGF2α (8-isoprostane), levels in the retinal tissues. To determine the role of endogenous H2S, studies were performed using the following biosynthesis enzyme inhibitors: aminooxyacetic acid (AOAA, 30 µM); a cystathione-β-synthase/cystathionine-γ-lyase (CBS/CSE) inhibitor, α–ketobutyric acid (KBA, 1 mM); and a 3-mercaptopyruvate-s-sulfurtransferase (3-MST) inhibitor, in the absence and presence of H2S-releasing compounds. Results: Exposure of the isolated retinas to H2O2 produced a time-dependent (10–40 min) and concentration-dependent (30–300 µM) increase in the 8-isoprostane levels when compared to the untreated tissues. L-cysteine (10 nM–1 µM) and NaHS (30 –100 µM) significantly (p < 0.001; n = 12) prevented H2O2-induced oxidative damage in a concentration-dependent manner. Furthermore, AP123 (100 nM–1 µM) attenuated oxidative H2O2 damage resulted in an approximated 60% reduction in 8-isoprostane levels compared to the tissues treated with H2O2 alone. While AOAA (30 µM) and KBA (1 mM) did not affect the L-cysteine evoked attenuation of H2O2-induced oxidative stress, KBA reversed the antioxidant responses caused by AP123. Conclusions: In conclusion, various forms of H2S-releasing compounds and the substrate, L-cysteine, can prevent H2O2-induced lipid peroxidation in an isolated bovine retina. [ABSTRACT FROM AUTHOR]

Background: Hydrogen sulfide (H2S)-releasing compounds can reduce intraocular pressure in normotensive rabbits by increasing aqueous humor (AH) outflow through the trabecular meshwork. In the present study, we investigated the contribution of endogenous H2S and the role of intramurally generated prostaglandins in the observed increase in AH outflow facility in an ex vivo porcine ocular anterior segment model. Material and Methods: Porcine ocular anterior segment explants were perfused with Dulbecco's Modified Eagle's Medium maintained at 37 °C and gassed with 5% CO2 and 95% air under an elevated pressure of 15 mmHg for four hours. Perfusates from the anterior segment explants were collected and immediately assayed for their H2S and prostaglandin E2 content. Results: Elevating perfusion pressure from 7.35 to 15 mm Hg significantly (p < 0.001) increased H2S concentration in the perfusate from 0.4 ± 0.1 to 67.6 ± 3.6 nM/µg protein. In the presence of an inhibitor of cystathionine ß-synthase/cystathionine γ-lyase, aminooxyacetic acid (AOAA, 30 µM), or an inhibitor of 3-mercaptopyruvate sulfurtransferase, α-ketobutyric acid (KBA, 1 mM), the effects of elevated pressure on H2S levels in the perfusate was significant (p < 0.001). Furthermore, flurbiprofen (30 µM) and indomethacin (10 µM) attenuated the elevated pressure-induced increase in H2S levels in the perfusate. Interestingly, elevating perfusion pressure had no significant effect on PGE2 concentrations in the perfusate. While the inhibition of H2S biosynthesis by AOAA or KBA did not affect PGE2 levels in perfusate, flurbiprofen (30 µM) caused a significant (p < 0.05) decrease in the concentration of PGE2 under conditions of elevated perfusion pressure. Conclusions: We conclude that the elevated perfusion pressure-induced increase in H2S concentrations depends upon the endogenous biosynthesis of H2S and intramurally produced prostaglandins in the porcine anterior segment explants. While the concentration of PGE2 in the perfusate under elevated perfusion pressure was unaffected by pretreatment with inhibitors of H2S biosynthesis, it was reduced in the presence of an inhibitor of cyclooxygenase. [ABSTRACT FROM AUTHOR]

Aging is an inevitable and irreversible biological process that gradually heightens the risks of various diseases and death. As a newly discovered endogenous gasotransmitter, hydrogen sulfide (H2S) has been identified to exert multiple beneficial impacts on the regulation of aging and age-related pathologies. This study was aimed at systematically exploring the relationship between asynchronous aging processes and H2S concentrations in various tissues of aging mice. Samples of plasma and 13 tissues were collected from four cross-sectional age groups (3, 6, 12 and 18 months of age) covering the lifespan of male C57BL/6J mice. The H2S concentration was quantified by a reported liquid chromatography-tandem mass spectrometry (LC-MS/MS) method with monobromobimane derivatization. Additionally, the expressions of cystathionine γ-lyase (CSE), cystathionine β-synthase and 3-mercaptopyruvate sulfurtransferase, in those tissues were analyzed by Western blotting. We discovered that the H2S concentrations decreased asynchronously with the aging process in plasma, heart, liver, kidney, spleen, subcutaneous fat and brown fat and increased in brain and lung. At least one of the three H2S-generating enzymes expressions was compensatorily up-regulated with the aging process in most tissues, among which the up-regulation of CSE was the most prominent. [ABSTRACT FROM AUTHOR]

Posttranslational modifications (PTMs) can modulate the activity, localization and interactions of proteins and (re)define their biological function. Understanding how changing environments can alter cellular processes thus requires detailed knowledge about the dynamics of PTMs in time and space. A PTM that gained increasing attention in the last decades is protein persulfidation, where a cysteine thiol (-SH) is covalently bound to sulfane sulfur to form a persulfide (-SSH). The precise cellular mechanisms underlying the presumed persulfide signaling in plants are, however, only beginning to emerge. In the mitochondrial matrix, strict regulation of persulfidation and H2S homeostasis is of prime importance for maintaining mitochondrial bioenergetic processes because H2S is a highly potent poison for cytochrome c oxidase. This review summarizes the current knowledge about protein persulfidation and corresponding processes in mitochondria of the model plant Arabidopsis. These processes will be compared to the respective processes in non-plant models to underpin similarities or highlight apparent differences. We provide an overview of mitochondrial pathways that contribute to H2S and protein persulfide generation and mechanisms for H2S fixation and de-persulfidation. Based on current proteomic data, we compile a plant mitochondrial persulfidome and discuss how persulfidation may regulate protein function. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S), as a key gas signaling molecule, plays an important role in regulating various diseases, with appropriate concentrations providing antioxidative, anti-inflammatory, and anti-apoptotic effects. The specific role of H2S in acute hypoxic injury remains to be clarified. This study focuses on the H2S donor sodium hydrosulfide (NaHS) and explores its protective effects and mechanisms against acute hypoxic lung injury. First, various mouse hypoxia models were established to evaluate H2S's protection in hypoxia tolerance. Next, a rat model of acute lung injury (ALI) induced by hypoxia at 6500 m above sea level for 72 h was created to assess H2S's protective effects and mechanisms. Evaluation metrics included blood gas analysis, blood routine indicators, lung water content, and lung tissue pathology. Additionally, LC-MS/MS and bioinformatic analyses were combined in performing quantitative proteomics on lung tissues from the normoxic control group, the hypoxia model group, and the hypoxia model group with NaHS treatment to preliminarily explore the protective mechanisms of H2S. Further, enzyme-linked immunosorbent assays (ELISA) were used to measure oxidative stress markers and inflammatory factors in rat lung tissues. Lastly, Western blot analysis was performed to detect Nrf2, HO-1, P-NF-κB, NF-κB, HIF-1α, Bcl-2, and Bax proteins in lung tissues. Results showed that H2S exhibited significant anti-hypoxic effects in various hypoxia models, effectively modulating blood gas and blood routine indicators in ALI rats, reducing pulmonary edema, improving lung tissue pathology, and alleviating oxidative stress, inflammatory responses, and apoptosis levels. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is the main cause of mortality in industrialized countries, with over 500 million people affected worldwide. In this work, the roles of low-molecular-weight metabolites originating from the gut microbiome, such as short-chain fatty acids, hydrogen sulfide, trimethylamine, phenylacetic acid, secondary bile acids, indoles, different gases, neurotransmitters, vitamins, and complex lipids, are discussed in relation to their CVD-promoting or preventing activities. Molecules of mixed microbial and human hepatic origin, such as trimethylamine N-oxide and phenylacetylglutamine, are also presented. Finally, dietary agents with cardioprotective effects, such as probiotics, prebiotics, mono- and poly-unsaturated fatty acids, carotenoids, and polyphenols, are also discussed. A special emphasis is given to their gut microbiota-modulating properties. [ABSTRACT FROM AUTHOR]

Oxidative stress caused by pregnancy‐induced hypertension syndrome significantly affects the health of pregnant women. Hydrogen sulfide is a typical gaseous signal molecule against oxidative stress, and it is of profound significance to develop a detection method. In this study, a stimuli‐responsive hydrogel was constructed based on the coordination and bonding principle of metal ions and chitosan (CS) to realize the quantitative detection of hydrogen sulfide (H2S). The chain of CS contains a large number of amino groups and hydroxyl groups, which can form the coordination structure with Cu2+, triggering CS to form a stable hydrogel. The hydrogel can be formed within about 5 s, which has the characteristics of rapid preparation. In the presence of target H2S, the cross‐linking agent Cu2+ in the hydrogel can compete out, resulting in the collapse of the hydrogel and the release of the electrochemical probe. By detecting the concentration of the released electrochemical probe, the quantitative detection of H2S can be achieved. The prepared hydrogel has a good linear relationship with the concentration of H2S from 1 μM to 60 μm. At the same time, the hydrogel has good specificity and stability, and it can be applied to the detection of H2S in serum samples. [ABSTRACT FROM AUTHOR]

Background: Impairment of synaptic plasticity along with the formation of amyloid-β (Aβ) plaques and tau-protein neurofibrillary tangles have been associated with Alzheimer's disease (AD). Earlier studies with rat and mouse hippocampal slices have revealed the association of AD with the absence of synthesis of memory related proteins leading to impairment in cognitive functions. The role of hydrogen sulfide (H2S), a gaseous neurotransmitter, has been gaining attention as a neuroprotective agent. However, its role in AD-like conditions has not been studied so far. Objective: To study the neuroprotective role of H2S in AD conditions using rat hippocampal slices and the organic molecule GYY4137, a slow releasing H2S donor. Methods: Electrophysiological recordings were carried out in rat hippocampal slices to look into the impairment of LTP, a cellular correlate of memory. The Aβ42 peptide was bath-applied to mimic AD-like conditions and checked for both late-LTP and synaptic tagging and capture (STC) mechanisms of the synapses. GYY4137 was applied to look into its neuroprotective role at different stages during the recording of fEPSP. Results: There has been a steady decline in the plasticity properties of the synapses, in the form of late-LTP and STC, after the application of Aβ42 peptide in the hippocampal slices. However, application of GYY4137 rescued these conditions in vitro. Conclusions: GYY4137, with its slow release of H2S, could possibly act as a therapeutic agent in cognitive dysfunctions of the brain, mainly AD. [ABSTRACT FROM AUTHOR]

Aim: Renal ischemia‐reperfusion injury (IRI) is a major cause of acute kidney injury. Hydrogen sulphide (H2S) exerts a protective effect in renal IRI. The present study was carried out to investigate the effects of exogenous H2S on renal IRI by regulating autophagy in mice. Methods: Mice were randomly assigned to control, IRI and NaHS (an H2S donor, 28, 56 and 100 μmol/kg) groups. Renal IRI was induced by clamping the bilateral renal pedicles with non‐traumatic arterial clamp for 45 min and then reperfused for 24 h. Mice were administered intraperitoneally with NaHS 20 min prior to renal ischemia. Sham group mice underwent the same procedures without clamping. Serum and kidney tissues were harvested 24 h after reperfusion for functional, histological, oxidative stress, and autophagic determination. Results: Compared with the control group, the concentrations of serum creatinine (Scr), blood urea nitrogen (BUN), and malondialdehyde (MDA), the protein levels of LC3II/I, Beclin‐1 and P62, as well as the number of autophagosomes were significantly increased, but the activity of superoxide dismutase (SOD) was decreased after renal IRI. NaHS pre‐treatment dramatically attenuated renal IRI‐induced renal dysfunction, histological changes, MDA concentration and p62 expression in a dose‐dependent manner. However, NaHS increased the SOD activity and the protein levels of LC3II/I and Beclin‐1. Conclusion: These results indicate that exogenous H2S protects the kidney from IRI through enhancement of autophagy and reduction of oxidative stress. Novel H2S donors could be developed in the treatment of renal IRI. [ABSTRACT FROM AUTHOR]