Cadmium (Cd) is a significant heavy metal contaminant within the environment, carrying a notable level of toxicity that presents a substantial hazard to both plant and human. Carrot (Daucus carota), a significant root vegetable crop globally, have evolved multiple transcriptional regulatory mechanisms to cope with Cd stress, with a crucial involvement of the myeloblastosis (MYB) transcription factor. In this study, the DcMYB62 gene encoding 288 amino acids, localized in the nucleus and demonstrated transcription activation property, was isolated from carrot (cv. \'Kuroda\'). There was a positive relationship observed between the levels of DcMYB62 expression and the accumulation patterns of carotenoids in two distinct carrot cultivars. Further investigation revealed that the expression of DcMYB62 improved Cd tolerance of Arabidopsis by increasing seed germination rate, root length, and overall survival rate. The levels of carotenoids in DcMYB62 transgenic Arabidopsis surpassed those in wild type, accompanied by elevated expression levels of 15-cis-phytoene desaturase, zeta-carotene desaturase, and carotenoid isomerase. Meanwhile, the heterologous expression of DcMYB62 promoted the biosynthesis of abscisic acid (ABA) and hydrogen sulfide (H2S), which in turn suppressed the formation of hydrogen peroxide and superoxide anion, while also stimulating stomatal closure. Furthermore, the heterologous expression of DcMYB62 increased the transcription of genes associated with heavy metal resistance in Arabidopsis, notably nicotianamine synthase. Overall, this study contributes to understanding how DcMYB62 promote Cd stress resistance of plants by regulating the biosynthesis pathways of carotenoids, ABA, and H2S, which offers valuable insights into the regulatory mechanism connecting DcMYBs with Cd stress response of carrot.

Air pollution is a long-standing environmental challenge as well an important economic subject. Hydrogen sulfide is one the major pollutants in the industrial releases. This review focuses on the thermochemical treatment of hydrogen sulfide based on the most recent works to date regarding its removal. By analyzing fundamental steps in chemical reaction engineering, some useful factors are emphasized since they are often neglected in scientific studies, catalysts design and process scale-up. From processing side, the fluid flow conditions including velocity, H2S concentration, relative humidity, temperature and pressure strongly influence the kinetic behavior and so the catalytic performance of the H2S removal reactor. From material side, the catalyst properties including nature, porosity, pore types, size, sites distribution and layer structuration largely influence the removal performance via among others the accessibility to catalytic sites, pores connection and mass transfer resistance. Plasma-assisted catalytic removal of H2S combines many novelties in comparison with a classical thermo-catalytic process. From patents review, we can see that main concerns are about electrodes mounting, reactor lifetime and modular design to solve the problems in the industrial practice. We attempt to provide for scientists, engineers and industrialists a guidance on the design of catalysts and processes for H2S removal which could be applied in laboratorial studies and industrial processes as well.

Hydrogen sulfide (H2S) has a comprehensive contribution to the normal operation and stability of organisms and is also present in environmental water samples and food deterioration. Thus, it is exceedingly promising and significant to develop a highly sensitive detection technique for tracing H2S. Inspired by this, we designed and synthesized a new fluorescent probe 2-[3-[2-[3-bromo-4-(2,4- dinitrobenzenesulfonate)] ethenyl]-5,5-dimethyl-2-cyclohexen-1-ylidene]propanedinitrile (SP-Br) for hydrosulfide ion detection by introducing bromine atom. Compared with reported H2S probes based on the same fluorescent parent, SP-Br has longer fluorescence emission (λem = 670 nm), shorter response time (3 min), lower detection limit (149 nM), and wider detection range (0-30 nM). SP-Br can emit weak yellow fluorescence, and the emission intensity at 670 nm is considerably enhanced in the presence of hydrosulfide ions. The identification mechanism of hydrosulfide ion by SP-Br was verified by high-resolution mass spectrometry, fluorescence, and UV-vis absorption spectroscopy. In addition, SP-Br has been successfully applied to the monitoring of actual water samples and beer samples and has certain development prospects and value in the fields of environmental pollution and food quality analysis.

Cystathionine gamma-lyase (CSE) is a key enzyme in reverse transsulfuration pathway and contributes to the majority of H2S generation in liver tissues via cysteine metabolism. Dysfunction of the CSE/H2S system is linked to both chronic and acute liver damage. This study investigated the regulatory role of CSE deficiency on diethylnitrosamine (DEN)-induced liver damage in mice. A single injection of DEN was administered into 4-week-old male CSE knockout (CSE-KO) mice and wild-type (WT) littermates, and the mice were sacrificed at 28 weeks of age. Compared to age-matched WT mice, CSE-KO mice spontaneously developed steatosis with increased oxidative stress and higher expressions of inflammation and fibrosis-related genes at 28-weeks of age. Following DEN injection, CSE-KO mice experienced more severe liver damage in comparison with the WT group as reflected by elevated levels of lipid accumulation, increased activities of alanine aminotransferase and aspartate aminotransferase, higher oxidative stress and fibrosis development, and increased expressions of inflammation and fibrosis-related genes. No visible tumors were observed in both types of mice with DEN treatment. In addition, the expression levels of the three H2S-generating proteins (CSE, cystathionine beta-synthase, and 3-mercaptopyruvate sulfurtransferase) and the H2S production rate in liver tissues were unaffected by DEN. Taken together, our study demonstrates that CSE provides a significant hepatoprotective effect and deficiency of CSE exaggerates DEN-induced liver damage in mice. Based on these findings, it can be suggested that targeting the CSE/H2S signaling pathway could be a potential therapeutic target for the treatment of liver diseases.

Hexavalent chromium [Cr(VI)] is a highly hazardous heavy metal with multiple toxic effects. Occupational studies indicate that its accumulation in humans can lead to liver damage. However, the exact mechanism underlying Cr(VI)-induced hepatotoxicity remains unknown. In this study, we explored the role of CTH/H2S/Drp1 pathway in Cr(VI)-induced oxidative stress, mitochondrial dysfunction, apoptosis, and liver injury. Our data showed that Cr(VI) triggered apoptosis, accompanied by H2S reduction, reactive oxygen species (ROS) accumulation, and mitochondrial dysfunction in both AML12 cells and mouse livers. Moreover, Cr(VI) reduced cystathionine γ-lyase (CTH) and dynamin related protein 1 (Drp1) S-sulfhydration levels, and elevated Drp1 phosphorylation levels at Serine 616, which promoted Drp1 mitochondrial translocation and Drp1-voltage-dependent anion channel 1 (VDAC1) interactions, ultimately leading to mitochondria-dependent apoptosis. Elevated hydrogen sulfide (H2S) levels eliminated Drp1 phosphorylation at Serine 616 by increasing Drp1 S-sulfhydration, thereby preventing Cr(VI)-induced Drp1-VDAC1 interaction and hepatotoxicity. These findings indicated that Cr(VI) induced mitochondrial apoptosis and hepatotoxicity by inhibiting CTH/H2S/Drp1 pathway and that targeting either CTH/H2S pathway or Drp1 S-sulfhydration could serve as a potential therapy for Cr(VI)-induced liver injury.

Landfill mining (LFM) has gained widespread recognition due to its benefits in terms of resource utilization of landfill waste and reuse of landfill sites. However, it is important to thoroughly assess the associated environmental risks. This study simulated the pressure release induced from LFM in small-scale batch anaerobic reactors subject to different initial pressures (0.2-0.6 MPa). The potential risk of hydrogen sulfide (H2S) pollution resulting from pressure release caused by LFM was investigated. The results demonstrated that the concentration of H2S significantly increased following the simulated pressure treatments. At the low (25 °C) and high (50 °C) temperatures tested, the peak H2S concentration reached 19366 and 24794 mg·m-3, respectively. Both of these concentrations were observed under highest initial pressure condition (0.6 MPa). However, the duration of H2S release was remarkably longer (>90 days) at the low temperature tested. Microbial diversity analysis results revealed that, at tested low temperature, the sulfate-reducing bacteria (SRB) communities of various pressure-bearing environments became phylogenetically similar following the pressure releases. In contrast, at the high temperature tested, specific SRB genera (Desulfitibacter and Candidatus Desulforudis) showed further enrichment. Moreover, the intensified sulfate reduction activity following pressure release was attributed to the enrichment of specific SRBs, including Desulfovibrio (ASV585 and ASV1417), Desulfofarcimen (ASV343), Candidatus Desulforudis (ASV24), and Desulfohalotomaculum (ASV506 and ASV2530). These results indicate that the pressure release associated with LFM significantly increases the amount of H2S released from landfills, and the SRB communities have different response mechanisms to pressure release at different temperature conditions. This study highlights the importance of considering the potential secondary environmental risks associated with LFM.

In this study, non-thermal plasma (NTP) was employed to modify the Cu/TiO2 adsorbent to efficiently purify H2S in low-temperature and micro-oxygen environments. The effects of Cu loading amounts and atmospheres of NTP treatment on the adsorption-oxidation performance of the adsorbents were investigated. The NTP modification successfully boosted the H2S removal capacity to varying degrees, and the optimized adsorbent treated by air plasma (Cu/TiO2-Air) attained the best H2S breakthrough capacity of 113.29 mg H2S/gadsorbent, which was almost 5 times higher than that of the adsorbent without NTP modification. Further studies demonstrated that the superior performance of Cu/TiO2-Air was attributed to increased mesoporous volume, more exposure of active sites (CuO) and functional groups (amino groups and hydroxyl groups), enhanced Ti-O-Cu interaction, and the favorable ratio of active oxygen species. Additionally, the X-ray diffraction (XRD) and X-ray photoelectron spectroscopy (XPS) results indicated the main reason for the deactivation was the consumption of the active components (CuO) and the agglomeration of reaction products (CuS and SO42-) occupying the active sites on the surface and the inner pores of the adsorbents.

With the increasing demand for heavy metals due to the advancement of industrial activities, large proportions of heavy metals have been discharged into aquatic ecosystems, causing serious harm to human health and the environment. Existing physical and chemical methods for recovering heavy metals from wastewater encounter challenges, such as low efficiency, high processing costs, and potential secondary pollution. In this study, we developed a novel approach by engineering the endogenous sulphur metabolic pathway of Yarrowia lipolytica, providing it with the ability to produce approximately 550 ppm of sulphide. Subsequently, sulphide-producing Y. lipolytica was used for the first time in heavy metal remediation. The engineered strain exhibited a high capacity to remove various heavy metals, especially achieving over 90 % for cadmium (Cd), copper (Cu) and lead (Pb). This capacity was consistent when applied to both synthetic and actual wastewater samples. Microscopic analyses revealed that sulphide-mediated biological precipitation of metal sulphides on the cell surface is responsible for their removal. Our findings demonstrate that sulphide-producing yeasts are a robust and effective bioremediation strategy for heavy metals, showing great potential for future heavy metal pollution remediation practices.

Hydrogen sulfide (H2S) is a pungent gas that is one of the key mediators of signal transduction in biological systems, and its presence is related to the freshness of some protein foods. Using phenothiazine derivatives as fluorophores and 2, 4-dinitrobenzene sulfonate (DNBS) fragments as reaction groups, a near-infrared (NIR) probe WX-HS for H2S identification was designed. With the addition of H2S, WX-HS appeared a strong fluorescence signal at 660 nm with short reaction time (90 s) and high sensitivity, and fluorescence state change from non-fluorescent to orange-red. In addition, WX-HS could effectively detect H2S produced during food oxidation. Based on its low cytotoxicity, the WX-HS probe further enabled the detection and imaging of H2S in A549 cells.

A large amount of hydrogen sulfide (H2S) is produced in the process of chicken breeding, which can cause serious inflammation and oxidative damage to the respiratory system of chickens. Tea tree oil (TTO) has antioxidant and anti-inflammatory properties. No studies have been reported on the use of TTO in H2S-induced lung injury in chickens. Therefore, in this study, 240 one-day-old Roman pink laying hens were randomly and equally divided into 3 groups: control group (CON), H2S exposure group (AVG, containing H2S), and TTO treatment group (TTG, containing H2S and 0.02 mL/L TTO) to establish an experimental model of TTO treatment with H2S exposure for a period of 42 d. Hematoxylin and eosin (H&E) staining was used to detect lung histopathology. Gene expression profiles were analyzed using transcriptomics. The underlying mechanism of the amelioration of lung injury by TTO was further revealed by antioxidant enzyme assays and qRT-PCR. The results showed that H2S exposure induced significant gene expression of CYP450s (CYP1B1 and CYP1C1) (P < 0.05), and caused intense oxidative stress, apoptosis and inflammation compared with CON. TTO could reduce ROS production and enhance antioxidant capacity (SOD, CAT, T-AOC, and GSH-PX) by regulating the CYP450s/ROS pathway (P < 0.05). Compared with the control group, the treatment group showed significantly decreased expression of apoptotic (Caspase-8, Caspase-3, Bid and Fas) (P < 0.05) and inflammatory (IL-4, IL-16, NF-κB, TNF-α and IFN-γ) (P < 0.05) factors in the lung. This study revealed that TTO regulated CYP450s/ROS pathway to alleviate H2S-induced lung injury in chickens. These results enrich the theory of the action mechanism of TTO on H2S-exposed chicken lungs and are of great value for the treatment of H2S-exposed animals.