Role of hydrogen sulfide in dermatological diseases.

Hydrogen sulfide (H2S), together with carbon monoxide (CO) and nitric oxide (NO), is recognized as a vital gasotransmitter. H2S is biosynthesized by enzymatic pathways in the skin and exerts significant physiological effects on a variety of biological processes, such as apoptosis, modulation of inflammation, cellular proliferation, and regulation of vasodilation. As a major health problem, dermatological diseases affect a large proportion of the population every day. It is urgent to design and develop effective drugs to deal with dermatological diseases. Dermatological diseases can arise from a multitude of etiologies, including neoplastic growth, infectious agents, and inflammatory processes. The abnormal metabolism of H2S is associated with many dermatological diseases, such as melanoma, fibrotic diseases, and psoriasis, suggesting its therapeutic potential in the treatment of these diseases. In addition, therapies based on H2S donors are being developed to treat some of these conditions. In the review, we discuss recent advances in the function of H2S in normal skin, the role of altering H2S metabolism in dermatological diseases, and the therapeutic potential of diverse H2S donors for the treatment of dermatological diseases.

A meta-analysis of animal studies evaluating the effect of hydrogen sulfide on ischemic stroke: is the preclinical evidence sufficient to move forward?

Hydrogen sulfide (H2S) is a gasotransmitter that has been studied for its potential therapeutic effects, including its role in the pathophysiology and treatment of stroke. This systematic review and meta-analysis aimed to determine the sufficiency of overall preclinical evidence to guide the initiation of clinical stroke trials with H2S and provide tailored recommendations for their design. PubMed, Web of Science, Scopus, EMBASE, and MEDLINE were searched for studies evaluating the effect of any H2S donor on in vivo animal models of regional ischemic stroke, and 34 publications were identified. Pooling of the effect sizes using the random-effect model revealed that H2S decreased the infarct area by 34.5% (95% confidence interval (CI) 28.2-40.8%, p < 0.0001), with substantial variability among the studies (I2 = 89.8%). H2S also caused a 37.9% reduction in the neurological deficit score (95% CI 29.0-46.8%, p < 0.0001, I2 = 63.8%) and in the brain water content (3.2%, 95% CI 1.4-4.9%, p = 0.0014, I2 = 94.6%). Overall, the studies had a high risk of bias and low quality of evidence (median quality score 5/15, interquartile range 4-9). The majority of the included studies had a "high" or "unclear" risk of bias, and none of the studies overall had a "low" risk. In conclusion, H2S significantly improves structural and functional outcomes in in vivo animal models of ischemic stroke. However, the level of evidence from preclinical studies is not sufficient to proceed to clinical trials due to the low external validity, high risk of bias, and variable design of existing animal studies.

Hydrogen sulfide enhances kiwifruit resistance to soft rot by regulating jasmonic acid signaling pathway.

As the third active gas signal molecule in plants, hydrogen sulfide (H2S) plays important roles in physiological metabolisms and biological process of fruits and vegetables during postharvest storage. In the present study, the effects of H2S on enhancing resistance against soft rot caused by Botryosphaeria dothidea and the involvement of jasmonic acid (JA) signaling pathway in kiwifruit during the storage were investigated. The results showed that 20 µL L-1 H2S fumigation restrained the disease incidence of B. dothidea-inoculated kiwifruit during storage, and delayed the decrease of firmness and the increase of soluble solids (SSC) content. H2S treatment increased the transcription levels of genes related to JA biosynthesis (AcLOX3, AcAOS, AcAOC2, and AcOPR) and signaling pathway (AcCOI1, AcJAZ5, AcMYC2, and AcERF1), as well as the JA accumulation. Meanwhile, H2S promoted the expression of defense-related genes (AcPPO, AcSOD, AcGLU, AcCHI, AcAPX, and AcCAT). Correlation analysis revealed that JA content was positively correlated with the expression levels of JA biosynthesis and defense-related genes. Overall, the results indicated that H2S could promote the increase of endogenous JA content and expression of defense-related genes by regulating the transcription levels of JA pathway-related genes, which contributed to the inhibition on the soft rot occurrence of kiwifruit.

Comparison of 3 methods characterizing H2S exposure in water and wastewater management work.

This study evaluates the effectiveness of self-assessed exposure (SAE) data collection for characterization of hydrogen sulfide (H2S) risks in water and wastewater management, challenging the adequacy of traditional random or campaign sampling strategies. We compared 3 datasets derived from distinct strategies: expert data with activity metadata (A), SAE without metadata (B), and SAE with logbook metadata (C). The findings reveal that standard practices of random sampling (dataset A) fail to capture the sporadic nature of H2S exposure. Instead, SAE methods enhanced by logbook metadata and supported by reliable detection and calibration infrastructure (datasets B and C) are more effective. When assessing risk, particularly peak exposure risks, it is crucial to adopt measures that capture exposure variability, such as the range and standard deviations. This finer assessment is vital where high H2S peaks occur in confined spaces. Risk assessment should incorporate indices that account for peak exposure, utilizing variability measures like range and standard or geometric standard deviation to reflect the actual risk more accurately. For large datasets, a histogram is just as useful as statistical measures. This approach has revealed that not only wastewater workers but also water distribution network workers, can face unexpectedly high H2S levels when accessing confined underground spaces. Our research underscores the need for continuous monitoring with personal electrochemical gas detector alarm systems, particularly in environments with variable and potentially hazardous exposure levels.

Multipressure Sampling for Improving the Performance of MOF-based Electronic Noses.

Metal-organic frameworks (MOFs) are a promising class of porous materials for the design of gas sensing arrays, which are often called electronic noses. Due to their chemical and structural tunability, MOFs are a highly diverse class of materials that align well with the similarly diverse class of volatile organic compounds (VOCs) of interest in many gas detection applications. In principle, by choosing the right combination of cross-sensitive MOFs, layered on appropriate signal transducers, one can design an array that yields detailed information about the composition of a complex gas mixture. However, despite the vast number of MOFs from which one can choose, gas sensing arrays that rely too heavily on distinct chemistries can be impractical from the cost and complexity perspective. On the other hand, it is difficult for small arrays to have the desired selectivity and sensitivity for challenging sensing applications, such as detecting weakly adsorbing gases with weak signals, or conversely, strongly adsorbing gases that readily saturate MOF pores. In this work, we employed gas adsorption simulations to explore the use of a variable pressure sensing array as a means of improving both sensitivity and selectivity as well as increasing the information content provided by each array. We studied nine different MOFs (HKUST-1, IRMOF-1, MgMOF-74, MOF-177, MOF-801, NU-100, NU-125, UiO-66, and ZIF-8) and four different gas mixtures, each containing nitrogen, oxygen, carbon dioxide, and exactly one of the hydrogen, methane, hydrogen sulfide, or benzene. We found that by lowering the pressure, we can limit the saturation of MOFs, and by raising the pressure, we can concentrate weakly adsorbing gases, in both cases, improving gas detection with the resulting arrays. In many cases, changing the system pressure yielded a better improvement in performance (as measured by the Kullback-Liebler divergence of gas composition probability distributions) than including additional MOFs. We thus demonstrated and quantified how sensing at multiple pressures can increase information content and cross-sensitivity in MOF-based arrays while limiting the number of unique materials needed in the device.

Hydrogen Sulfide Promotes Platelet Autophagy via PDGFR-α/PI3K/Akt Signaling in Cirrhotic Thrombocytopenia.

Background and Aims: The role of platelet autophagy in cirrhotic thrombocytopenia (CTP) remains unclear. This study aimed to investigate the impact of platelet autophagy in CTP and elucidate the regulatory mechanism of hydrogen sulfide (H2S) on platelet autophagy. Methods: Platelets from 56 cirrhotic patients and 56 healthy individuals were isolated for in vitro analyses. Autophagy markers (ATG7, BECN1, LC3, and SQSTM1) were quantified using enzyme-linked immunosorbent assay, while autophagosomes were visualized through electron microscopy. Western blotting was used to assess the autophagy-related proteins and the PDGFR/PI3K/Akt/mTOR pathway following treatment with NaHS (an H2S donor), hydroxocobalamin (an H2S scavenger), or AG 1295 (a selective PDGFR-α inhibitor). A carbon tetrachloride-induced cirrhotic BALB/c mouse model was established. Cirrhotic mice with thrombocytopenia were randomly treated with normal saline, NaHS, or hydroxocobalamin for 15 days. Changes in platelet count and aggregation rate were observed every three days. Results: Cirrhotic patients with thrombocytopenia exhibited significantly decreased platelet autophagy markers and endogenous H2S levels, alongside increased platelet aggregation, compared to healthy controls. In vitro, NaHS treatment of platelets from severe CTP patients elevated LC3-II levels, reduced SQSTM1 levels, and decreased platelet aggregation in a dose-dependent manner. H2S treatment inhibited PDGFR, PI3K, Akt, and mTOR phosphorylation. In vivo, NaHS significantly increased LC3-II and decreased SQSTM1 expressions in platelets of cirrhotic mice, reducing platelet aggregation without affecting the platelet count. Conclusions: Diminished platelet autophagy potentially contributes to thrombocytopenia in cirrhotic patients. H2S modulates platelet autophagy and functions possibly via the PDGFR-α/PI3K/Akt/mTOR signaling pathway.

Lactoperoxidase catalytically oxidize hydrogen sulfide via intermediate formation of sulfheme derivatives.

The biological chemistry of hydrogen sulfide (H2S) with physiologically important heme proteins is in the focus of redox biology research. In this study, we investigated the interactions of lactoperoxidase (LPO) with H2S in the presence and absence of molecular dioxygen (O2) or hydrogen peroxide (H2O2). Under anaerobic conditions, native LPO forms no heme-H2S complex upon sulfide exposure. However, under aerobic conditions or in the presence of H2O2 the formation of both ferrous and ferric sulfheme (sulfLPO) derivatives was observed based on the appearances of their characteristic optical absorptions at 638 nm and 727 nm, respectively. Interestingly, we demonstrate that LPO can catalytically oxidize H2S by H2O2 via intermediate formation of relatively short-lived ferrous and ferric sulfLPO derivatives. Pilot product analyses suggested that the turnover process generates oxidized sulfide species, which include sulfate S O 4 2 - and inorganic polysulfides ( H S x - ; x = 2-5). These results indicated that H2S can serve as a non-classical LPO substrate by inducing a reversible sulfheme-like modification of the heme porphyrin ring during turnover. Furthermore, electron paramagnetic resonance data suggest that H2S can act as a scavenger of H2O2 in the presence of LPO without detectable formation of any carbon-centered protein radical species, suggesting that H2S might be capable of protecting the enzyme from radical-mediated damage. We propose possible mechanisms, which explain our results as well as contrasting observations with other heme proteins, where either no sulfheme formation was observed or the generation of sulfheme derivatives provided a dead end for enzyme functions.

Endogenous hydrogen sulfide accelerated trauma-induced heterotopic ossification through the Ca2+/ERK pathway-enhanced aberrant osteogenic activity.

Unveiling of the mechanism involved in the occurrence and development of trauma-induced heterotopic ossification (tHO) is highly demanding due to current ineffective clinical treatment for it. Previous studies proposed that hydrogen sulfide (H2S) was vital for fate determination of stem cells, suggesting a potential role in the regulation of tHO development. In the current study, We found that expression of metabolic enzyme within sulfur conversion pathway was enhanced after tendon injury, leading to H2S accumulation within the tHO region. Increased production of endogenous H2S was shown to promote aberrant osteogenic activity of tendon-derived stem cells (TDSCs), which accelerated tHO formation. The inhibition of metabolic enzyme of H2S production or directly absorption of H2S could abolished osteogenic induction of TDSCs and the formation of tHO. Mechanistically, through RNA sequencing combined with rescue experiments, we demonstrated that activation of Ca2+/ERK pathway was the downstream molecular event of H2S-induced osteogenic commitment of TDSCs and tHO. For treatment strategy exploration, zine oxide nanoparticles (ZnO) as an effective H2S elimination material was validated to ideally halt the tHO formation in this study. Furthermore, in terms of chirality of nanoparticles, D-ZnO or L-ZnO nanoparticles showed superiority over R-ZnO nanoparticles in both clearing of H2S and inhibition of tHO. Our study not only revealed the mechanism of tHO through the endogenous gas signaling event from a new perspective, but also presented a applicable platform for elimination of the inordinate gas production, thus aiding the development of clinical treatment for tHO.

Tarnished jewellery and skin - a subtle external marker indicating exposure to hydrogen sulfide.

A 39-year-old woman was found lying in the rear of a car at her home address. A smell of rotten eggs was noted and bottles of brick, tile and paver cleaner and lime sulfur were found in the rear of the vehicle. Suicide notes were found in the house. At autopsy there was no evidence of significant trauma with black tarnishing of a silver-coloured ring and a silver-coloured necklace noted with staining of the underlying skin, in keeping with a chemical reaction between hydrogen sulfide and silver. Internally the most significant finding was unusual greenish discolouration of the gray matter of the external and cut surfaces of the cerebral hemispheres, cerebellum and brain stem. No other organs had this discoloration. Death was attributed to hydrogen sulfide poisoning. Skin discoloration from silver jewellery may represent a subtle external marker for lethal or non-lethal hydrogen sulfide exposure.

Gene-centered metagenome analysis of Vulcano Island soil (Aeolian archipelago, Italy) reveals diverse microbial key players in methane, hydrogen and sulfur cycles.

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.

The role of hydrogen sulfide regulation of ferroptosis in different diseases.

Ferroptosis is a programmed cell death that relies on iron and lipid peroxidation. It differs from other forms of programmed cell death such as necrosis, apoptosis and autophagy. More and more evidence indicates that ferroptosis participates in many types of diseases, such as neurodegenerative diseases, ischemia-reperfusion injury, cardiovascular diseases and so on. Hence, clarifying the role and mechanism of ferroptosis in diseases is of great significance for further understanding the pathogenesis and treatment of some diseases. Hydrogen sulfide (H2S) is a colorless and flammable gas with the smell of rotten eggs. Many years ago, H2S was considered as a toxic gas. however, in recent years, increasing evidence indicates that it is the third important gas signaling molecule after nitric oxide and carbon monoxide. H2S has various physiological and pathological functions such as antioxidant stress, anti-inflammatory, anti-apoptotic and anti-tumor, and can participate in various diseases. It has been reported that H2S regulation of ferroptosis plays an important role in many types of diseases, however, the related mechanisms are not fully clear. In this review, we reviewed the recent literature about the role of H2S regulation of ferroptosis in diseases, and analyzed the relevant mechanisms, hoping to provide references for future in-depth researches.

Pills of Multi-Target H2S Donating Molecules for Complex Diseases.

Among the various drug discovery methods, a very promising modern approach consists in designing multi-target-directed ligands (MTDLs) able to modulate multiple targets of interest, including the pathways where hydrogen sulfide (H2S) is involved. By incorporating an H2S donor moiety into a native drug, researchers have been able to simultaneously target multiple therapeutic pathways, resulting in improved treatment outcomes. This review gives the reader some pills of successful multi-target H2S-donating molecules as worthwhile tools to combat the multifactorial nature of complex disorders, such as inflammatory-based diseases and cancer, as well as cardiovascular, metabolic, and neurodegenerative disorders.

In-situ Generation of Hydrogen Polysulfides (H2Sn) with Thioglucose, Glucose Oxidase, and Chloroperoxidase.

Hydrogen polysulfides (H2Sn) have emerged as critical physiological mediators that are closely associated with hydrogen sulfide (H2S) signaling. H2Sn exhibit greater nucleophilicity than H2S while also having electrophilic characteristics, enabling unique activities such as protein S-persulfidation. Despite their physiological importance, mechanisms and reactivities of H2Sn remain inadequately explored due to their inherent instability in aqueous environments. Consequently, there is a need to develop biocompatible methods for controlled H2Sn generation to elucidate their behaviors in biological contexts. Herein, we present a dual enzyme system (containing glucose oxidase (GOx) and chloroperoxidase (CPO)) with thioglucose as the substrate to facilitate the controlled release of H2Sn. Fluorescence measurements with SSP4 and the trapping studies allowed us to confirm the production of H2Sn. Such a method may be useful in elucidating the reactivity of hydrogen polysulfides in biological systems as well as provide a potential delivery of H2Sn to target sites for biological applications.

Hippocampal Warburg effect Mediates Hydrogen Sulfide-Ameliorated Diabetes-Associated Cognitive Dysfunction: Involving Promotion of Hippocampal Synaptic Plasticity.

Our previous studies have reported that hydrogen sulfide (H2S) 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 H2S-ameliorated DACD and further explore its potential mechanism. We found that H2S 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 H2S on synaptic plasticity in the hippocampus of STZ-induced diabetic rats. DCA blocked H2S-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 H2S-ameliorated DACD by improving hippocampal synaptic plasticity.

One-Step Synthesis of Chitosan Hydrogel as Electrochemical Chemosensor for Hydrogen Sulfide Detection in Pregnancy-Induced Hypertension Syndrome Serum Sample.

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.

Vibrational spectroscopy characterization of impregnated activated carbon adsorption of H2S.

Activated carbon filters are used for the removal of hazardous gases from the air. This research applied vibrational spectroscopy methods, including Fourier-transform infrared spectroscopy and Raman spectroscopy to characterize hydrogen sulfide adsorption on impregnated carbon materials with metals having reactivity toward hydrogen sulfide. The Fourier-transform infrared spectroscopy results demonstrated the formation of a new chemical bond between the impregnating metals and the sulfur, indicated by the appearance of a new band at 618 cm-1. The Raman spectra results showed that for the copper-impregnated activated carbon with the highest hydrogen sulfide adsorption capacity, a new vibrational band at 475 cm-1 evolved, indicating a copper-sulfur bond. In addition, upshifts in the carbon D sub-bands were observed after efficient hydrogen sulfide adsorption, along with a larger area of the approximately 1500 cm-1 band. Therefore, Fourier-transform infrared spectroscopy and Raman spectroscopy combination can potentially indicate H2S adsorption on impregnated activated carbon filters.

Cystathionine γ-lyase-derived H2S negatively regulates thymic egress via allosteric inhibition of sphingosine-1-phosphate lyase.

Thymic egress is a crucial process for thymocyte maturation, strictly regulated by sphingosine-1-phosphate lyase (S1PL). Recently, cystathionine γ-lyase (CSE), one of the enzymes producing hydrogen sulfide (H2S), has emerged as a vital immune process regulator. However, the molecular connection between CSE, H2S and thymic egress remains largely unexplored. In this study, we investigated the regulatory function of CSE in the thymic egress of immune cells. We showed that genetic knockout of CSE or pharmacological inhibition by CSE enzyme inhibitor NSC4056 or D,L-propargylglycine (PAG) significantly enhanced the migration of mature lymphocytes and monocytes from the thymus to the peripheral blood, and this redistribution effect could be reversed by treatment with NaHS, an exogenous donor of H2S. In addition, the CSE-generated H2S significantly increased the levels of S1P in the peripheral blood, thymus and spleen of mice, suppressed the production of proinflammatory cytokines and rescued pathogen-induced sepsis in cells and in vivo. Notably, H2S or polysulfide inhibited S1PL activity in cells and an in vitro purified enzyme assay. We found that this inhibition relied on a newly identified C203XC205 redox motif adjacent to the enzyme's active site, shedding light on the biochemical mechanism of S1PL regulation. In conclusion, this study uncovers a new function and mechanism for CSE-derived H2S in thymic egress and provides a potential drug target for treating S1P-related immune diseases.

Influence of oxidation-reduction potential and pH on polysulfide concentrations and chain lengths in the biological desulfurization process under haloalkaline conditions.

Biological desulfurization under haloalkaline conditions has been applied worldwide to remove hydrogen sulfide (H2S) from sour gas steams. The process relies on sulfide-oxidizing bacteria (SOB) to oxidize H2S to elemental sulfur (S8), which can then be recovered and reused. Recently, a dual-reactor biological desulfurization system was implemented where an anaerobic (sulfidic) bioreactor was incorporated as an addition to a micro-oxic bioreactor, allowing for higher S8 selectivity by limiting by-product formation. The highly sulfidic bioreactor environment enabled the SOB to remove (poly)sulfides (Sx2-) in the absence of oxygen, with Sx2- speculated as a main substrate in the removal pathway, thus making it vital to understand its role in the process. The SOB are influenced by the oxidation-reduction potential (ORP) set-point of the micro-oxic bioreactor as it is used to control the product of oxidation (S8 vs. SO42-), while the uptake of Sx2- by SOB has been qualitatively linked to pH. Therefore, to quantify these effects, this work determined the concentration and speciation of Sx2- in the biological desulfurization process under various pH values and ORP set-points. The total Sx2- concentrations in the sulfidic zone increased at elevated pH (8.9) compared to low pH (< 8.0), with on average 3.3 ± 1.0 mM-S more Sx2-. Chain lengths varied, with S72- only doubling in concentration while S52- increased 9 fold, which is in contrast with observations from abiotic systems. Changes to the ORP set-point of the micro-oxic reactor did not produce substantial changes in Sx2- concentration in the sulfidic zone. This illustrates that the reduction degree of the SOB in the micro-oxic bioreactor does not enhance their ability to interact with Sx2- in the sulfidic bioreactor. This increased understanding of how both pH and ORP affect changes in Sx2- concentration and chain length can lead to improved efficiency and design of the dual-reactor biological desulfurization process.

Expanding roles of cross-talk between hydrogen sulfide and nitric oxide under abiotic stress in plants.

Abiotic stress such as salt, heavy metals, drought, temperature, and others can affect plants from seed germination to seedling growth to reproductive maturity. Abiotic stress increases reactive oxygen species and lowers antioxidant enzymes in plants resulted the plant tolerance ability against stress conditions decrease. Hydrogen sulfide (H2S) and nitric oxide (NO) are important gasotransmitters involved in seed germination, photosynthesis, growth and development, metabolism, different physiological processes and functions in plants. In plants, various enzymes are responsible for the biosynthesis of both H2S and NO via both enzymatic and non-enzymatic pathways. They also mediate post-translation modification, such as persulfidation, and nitrosylation, which are protective mechanisms against oxidative damage. They also regulate some cellular signalling pathways in response to various abiotic stress. H2S and NO also stimulate biochemical reactions in plants, including cytosolic osmoprotectant accumulation, reactive oxygen species regulation, antioxidant system activation, K+ uptake, and Na+ cell extrusion or vacuolar compartmentation. In this review, we summarize how H2S and NO interact with each other, the function of both H2S and NO, the mechanism of biosynthesis, and post-translational modification under different abiotic stress. Our main emphasis was to find the cross-talk between NO and H2S and how they regulate genes in plants under abiotic stress.

Hydrogen sulfide and its role in female reproduction.

Hydrogen sulfide (H2S) is a gaseous signaling molecule produced in the body by three enzymes: cystathionine-ß-synthase (CBS), cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST). H2S is crucial in various physiological processes associated with female mammalian reproduction. These include estrus cycle, oocyte maturation, oocyte aging, ovulation, embryo transport and early embryo development, the development of the placenta and fetal membranes, pregnancy, and the initiation of labor. Despite the confirmed presence of H2S-producing enzymes in all female reproductive tissues, as described in this review, the exact mechanisms of H2S action in these tissues remain in most cases unclear. Therefore, this review aims to summarize the knowledge about the presence and effects of H2S in these tissues and outline possible signaling pathways that mediate these effects. Understanding these pathways may lead to the development of new therapeutic strategies in the field of women's health and perinatal medicine.