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Diaryldithiocarbamate complexes, [Fe(S[sub.2]CNAr[sub.2])[sub.3]], have been prepared and their structure, reactivity, and thermal degradation to afford iron sulfide nanomaterials have been investigated. The addition of three equivalents of LiS[sub.2]CNAr[sub.2] to FeCl[sub.2]·4H[sub.2]O in water-air affords dark red [Fe(S[sub.2]CNAr[sub.2])[sub.3]] in high yields. All show magnetic measurements consistent with a predominantly high-spin electronic arrangement at room temperature. The molecular structure of [FeS[sub.2]C(N-p-MeOC[sub.6]H[sub.4])[sub.2][sub.3]] reveals the expected distorted octahedral geometry, but Fe-S distances are more consistent with a low-spin electronic configuration, likely a result of the low temperature (120 K) of the data collection. The thermal stability of [FeS[sub.2]C(N-p-MeC[sub.6]H[sub.4])[sub.2][sub.3]] has been investigated. TGA shows that it begins to decompose at a significantly lower temperature (ca. 160 °C) than previously observed for [Fe(S[sub.2]CNEt[sub.2])[sub.3]], and this is further lowered (to ca. 100 °C) in oleylamine. The decomposition of [FeS[sub.2]C(N-p-MeC[sub.6]H[sub.4])[sub.2][sub.3]] in oleylamine, via either a heat-up or hot injection process, affords nanoparticles of Fe[sub.3]S[sub.4] (greigite), while in contrast, dry heating at 450 °C affords FeS (troilite) as large agglomerates.

The extent to which sulfur dissolves in silicate melts saturated in an immiscible sulfide phase is a fundamental question in igneous petrology and plays a primary role in the generation of magmatic ore deposits, volcanic degassing, and planetary differentiation. In igneous systems, sulfide melts can be described as FeS-NiS-CuS0.5 solutions with Fe/(Fe+Ni+Cu) significantly less than 1. Despite the presence of Ni and Cu in the sulfide, however, most experimental studies to date have concentrated on the effects of silicate melt composition on sulfur solubility and have used essentially pure FeS as the sulfide liquid. We have carried out 49 new experiments at pressures of 1.5-24 GPa and temperatures of 1400 to 2160 °C to investigate the effects of sulfide composition on sulfur solubility as well as extending the pressure and temperature ranges of the available data on sulfide saturation. We find that in the compositional range of most igneous sulfide melts [Fe/(Fe+Ni+Cu) > 0.6] sulfur solubility decreases linearly with Fe content such that at Fe/(Fe+Ni+Cu) of 0.6 the sulfur content at saturation is 0.6 times the value at pure FeS saturation. At lower values of Fe/(Fe+Ni+Cu), however, deviations from this ideal solution relationship need to be taken into consideration. We have treated these non-idealities by assuming that FeS-NiS-CuS0.5 liquids approximate ternary regular solutions.We have fitted our data, together with data from the literature (392 in total), to equations incorporating the effects of silicate melt composition, sulfide liquid composition, and pressure on the solubility of sulfur at sulfide saturation ([S]SCSS). The temperature dependence of [S]SCSS was assumed either to be an unknown or was taken from 1 bar thermodynamic data. The most important best-fit silicate melt compositional term reflects the strongly positive dependence of [S]SCSS on the FeO content of the silicate melt. The best-fit value of this parameter is essentially independent of our assumptions about temperature dependence of [S]SCSS or the solution properties of the sulfide. All natural compositions considered here exhibit positive dependences of [S]SCSS on temperature and negative dependences on pressure, in accord with previous studies using smaller data sets.

Hydrogen sulfide is a highly toxic gas—second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known and no specific therapy exists for sulfide poisoning. We show in several cell types, including human inducible pluripotent stem cell (hiPSC)-derived neurons, that sulfide inhibited complex IV of the mitochondrial respiratory chain and induced apoptosis. Sulfide increased hydroxyl radical production in isolated mouse heart mitochondria and F 2 -isoprostanes in brains and hearts of mice. The vitamin B 12 analog cobinamide reversed the cellular toxicity of sulfide and rescued Drosophila melanogaster and mice from lethal exposures of hydrogen sulfide gas. Cobinamide worked through two distinct mechanisms: direct reversal of complex IV inhibition and neutralization of sulfide-generated reactive oxygen species. We conclude that sulfide produces a high degree of oxidative stress in cells and tissues and that cobinamide has promise as a first specific treatment for sulfide poisoning.

Microbial inoculation is a commonly applied approach in composting to enhance organic matter biodegradation and reduce odor emissions. However, the different characteristics of bacteria in terms of temperature can be considered to optimize their effect during different phases of composting. A mesophilic bacterium, namely Aquamicrobium lusatiense NLF 2–7, was evaluated to mitigate odor emissions and enhance the bacterial community under mesophilic composting. Two different treatments were designed: treatment 1 with a single inoculation on the initial day and treatment 2 with split inoculation at the initial and after 2 weeks. Results show that the treatments improve organic matter decomposition by 17.7–28.6% and significantly reduce volatile sulfur compound emissions, especially dimethyl sulfide (DMS) and hydrogen sulfide (H 2 S) during the initial phase of composting. DMS emissions were mostly emitted in the first week, with reduction rates of 60.3% and 61.5% in both treatments, respectively. Additionally, mean phenol emissions were reduced by 7.9% in treatment 1 and 11.7% in treatment 2. The dominant bacterial phyla during composting were Bacillota , Pseudomonadota , Bacteroidota , and Actinomycetota , comprising 74 to 95% of the total population. This experiment suggests that A. lusatiense NLF 2–7, which is known for reducing sulfur emissions, can also enhance organic matter decomposition. Split inoculation appears more beneficial, with an initial inoculation managing sulfur emissions early on, followed by a second inoculation after the thermophilic phase to control phenol emissions throughout the composting process.

Growth media have been developed to facilitate the enrichment and isolation of acidophilic and acid-tolerant sulfate-reducing bacteria (aSRB) from environmental and industrial samples, and to allow their cultivation in vitro. The main features of the ‘standard’ solid and liquid devised media are as follows: (i) use of glycerol rather than an aliphatic acid as electron donor; (ii) inclusion of stoichiometric concentrations of zinc ions to both buffer pH and to convert potentially harmful hydrogen sulphide produced by the aSRB to insoluble zinc sulphide; (iii) inclusion of Acidocella aromatica (an heterotrophic acidophile that does not metabolize glycerol or yeast extract) in the gel underlayer of double layered (overlay) solid media, to remove acetic acid produced by aSRB that incompletely oxidize glycerol and also aliphatic acids (mostly pyruvic) released by acid hydrolysis of the gelling agent used (agarose). Colonies of aSRB are readily distinguished from those of other anaerobes due to their deposition and accumulation of metal sulphide precipitates. Data presented illustrate the effectiveness of the overlay solid media described for isolating aSRB from acidic anaerobic sediments and low pH sulfidogenic bioreactors. The paper describes how bacteria that live in acidic environments, and that form hydrogen sulphide from sulfate, may be isolated and grown in the laboratory. Graphical Abstract Figure. The paper describes how bacteria that live in acidic environments, and that form hydrogen sulphide from sulfate, may be isolated and grown in the laboratory.

Short-chain fatty acids (SCFAs) are produced by various human gut microbes. SCFAs act as an energy source to the colonic epithelium and are also sensed by host signaling pathways that modulate appetite and inflammation. Deficiency of gut SCFAs is associated with type 2 diabetes. Zhao et al. found that adopting a high-fiber diet promoted the growth of SCFA-producing organisms in diabetic humans. The high-fiber diet induced changes in the entire gut microbe community and correlated with elevated levels of glucagon-like peptide-1, a decline in acetylated hemoglobin levels, and improved blood-glucose regulation. Science , this issue p. 1151 Increasing dietary fiber intake increases the abundance of short-chain fatty acid–producing gut microbes and relieves diabetes. The gut microbiota benefits humans via short-chain fatty acid (SCFA) production from carbohydrate fermentation, and deficiency in SCFA production is associated with type 2 diabetes mellitus (T2DM). We conducted a randomized clinical study of specifically designed isoenergetic diets, together with fecal shotgun metagenomics, to show that a select group of SCFA-producing strains was promoted by dietary fibers and that most other potential producers were either diminished or unchanged in patients with T2DM. When the fiber-promoted SCFA producers were present in greater diversity and abundance, participants had better improvement in hemoglobin A1c levels, partly via increased glucagon-like peptide-1 production. Promotion of these positive responders diminished producers of metabolically detrimental compounds such as indole and hydrogen sulfide. Targeted restoration of these SCFA producers may present a novel ecological approach for managing T2DM.

As the closest transiting hot Jupiter to Earth, HD 189733b has been the benchmark planet for atmospheric characterization 1 – 3 . It has also been the anchor point for much of our theoretical understanding of exoplanet atmospheres from composition 4 , chemistry 5 , 6 , aerosols 7 to atmospheric dynamics 8 , escape 9 and modelling techniques 10 , 11 . Previous studies of HD 189733b have detected carbon and oxygen-bearing molecules H 2 O and CO (refs.  12 , 13 ) in the atmosphere. The presence of CO 2 and CH 4 has been claimed 14 , 15 but later disputed 12 , 16 , 17 . The inferred metallicity based on these measurements, a key parameter in tracing planet formation locations 18 , varies from depletion 19 , 20 to enhancement 21 , 22 , hindered by limited wavelength coverage and precision of the observations. Here we report detections of H 2 O (13.4 σ ), CO 2 (11.2 σ ), CO (5 σ ) and H 2 S (4.5 σ ) in the transmission spectrum (2.4–5.0 μm) of HD 189733b. With an equilibrium temperature of about 1,200 K, H 2 O, CO and H 2 S are the main reservoirs for oxygen, carbon and sulfur. Based on the measured abundances of these three main volatile elements, we infer an atmospheric metallicity of three to five times stellar. The upper limit on the methane abundance at 5 σ is 0.1 ppm, which indicates a low carbon-to-oxygen ratio (<0.2), suggesting formation through the accretion of water-rich icy planetesimals. The low oxygen-to-sulfur and carbon-to-sulfur ratios also support the planetesimal accretion formation pathway 23 . The exoplanet HD 189733b has a metal-enriched atmosphere with the possible presence of H 2 O (13.4 σ ), CO 2 (11.2 σ ), CO (5 σ ) and H 2 S (4.5 σ ).

Diabetic kidney disease develops in approximately 40% of diabetic patients and is a major cause of chronic kidney diseases (CKD) and end stage kidney disease (ESKD) worldwide. Hydrogen sulfide (H2S), the third gasotransmitter after nitric oxide (NO) and carbon monoxide (CO), is synthesized in nearly all organs, including the kidney. Though studies on H2S regulation of renal physiology and pathophysiology are still in its infancy, emerging evidence shows that H2S production by renal cells is reduced under disease states and H2S donors ameliorate kidney injury. Specifically, aberrant H2S level is implicated in various renal pathological conditions including diabetic nephropathy. This review presents the roles of H2S in diabetic renal disease and the underlying mechanisms for the protective effects of H2S against diabetic renal damage. H2S may serve as fundamental strategies to treat diabetic kidney disease. These H2S treatment modalities include precursors for H2S synthesis, H2S donors, and natural plant-derived compounds. Despite accumulating evidence from experimental studies suggests the potential role of the H2S signaling pathway in the treatment of diabetic nephropathy, these results need further clinical translation. Expanding understanding of H2S in the kidney may be vital to translate H2S to be a novel therapy for diabetic renal disease.

Central nervous system (CNS)-related conditions are currently the leading cause of disability worldwide, posing a significant burden to health systems, individuals and their families. Although the molecular mechanisms implicated in these disorders may be varied, neurological conditions have been increasingly associated with inflammation and/or impaired oxidative response leading to further neural cell damages. Therefore, therapeutic approaches targeting these defective molecular mechanisms have been vastly explored. Hydrogen sulphide (H 2 S) has emerged as a modulator of both inflammation and oxidative stress with a neuroprotective role, therefore, has gained interest in the treatment of neurological disorders. H 2 S, produced by endogenous sources, is maintained at low levels in the CNS. However, defects in the biosynthetic and catabolic routes for H 2 S metabolism have been identified in CNS-related disorders. Approaches to restore H 2 S availability using H 2 S-donating compounds have been recently explored in many models of neurological conditions. Nonetheless, we still need to elucidate the potential for these compounds not only to ameliorate defective biological routes, but also to better comprehend the implications on H 2 S delivery, dosage regimes and feasibility to successfully target CNS tissues. Here, we highlight the molecular mechanisms of H 2 S-dependent restoration of neurological functions in different models of CNS disease whilst summarising current administration approaches for these H 2 S-based compounds. We also address existing barriers in H 2 S donor delivery by showcasing current advances in mediating these constrains through novel biomaterial-based carriers for H 2 S donors.

Abnormal sulfide catabolism, especially the accumulation of hydrogen sulfide (H2S) during hypoxic or inflammatory stresses, is a major cause of redox imbalance-associated cardiac dysfunction. Polyhydroxynaphtoquinone echinochrome A (Ech-A), a natural pigment of marine origin found in the shells and needles of many species of sea urchins, is a potent antioxidant and inhibits acute myocardial ferroptosis after ischemia/reperfusion, but the chronic effect of Ech-A on heart failure is unknown. Reactive sulfur species (RSS), which include catenated sulfur atoms, have been revealed as true biomolecules with high redox reactivity required for intracellular energy metabolism and signal transduction. Here, we report that continuous intraperitoneal administration of Ech-A (2.0 mg/kg/day) prevents RSS catabolism-associated chronic heart failure after myocardial infarction (MI) in mice. Ech-A prevented left ventricular (LV) systolic dysfunction and structural remodeling after MI. Fluorescence imaging revealed that intracellular RSS level was reduced after MI, while H2S/HS− level was increased in LV myocardium, which was attenuated by Ech-A. This result indicates that Ech-A suppresses RSS catabolism to H2S/HS− in LV myocardium after MI. In addition, Ech-A reduced oxidative stress formation by MI. Ech-A suppressed RSS catabolism caused by hypoxia in neonatal rat cardiomyocytes and human iPS cell-derived cardiomyocytes. Ech-A also suppressed RSS catabolism caused by lipopolysaccharide stimulation in macrophages. Thus, Ech-A has the potential to improve chronic heart failure after MI, in part by preventing sulfide catabolism.