NaHS Research Articles

Hydrogen sulfide delays softening of banana fruit by inhibiting cell wall polysaccharides disassembly

SummaryHarvested banana undergoes rapid softening, which limits its shelf life. To delay softening, banana fruit was treated with hydrogen sulfide (H2S) emitted by 0.6 mm sodium hydrosulfide (NaHS) and stored at 15 °C for 16 days. The effects of H2S on cell wall degradation and other physiological characteristics were investigated. In comparison to control fruits, H2S‐treated bananas retained a higher level of fruit firmness, but lower hue values. Ethylene metabolism analysis suggested that H2S inhibited the production of ethylene and the accumulation of 1‐aminocyclopropane‐1‐carboxylic acid (ACC) and decreased the activities of ACC synthase (ACS) and ACC oxidase (ACO). Cell wall polysaccharides determination assays suggested that H2S treatment increased the proportion of HCl‐soluble pectin (HSP), NaOH‐soluble pectin (NSP), cellulose and hemicellulose but decreased water‐soluble pectin (WSP) in fruits. H2S treatment also inhibited the activities of polysaccharide degrading enzymes such as polygalacturonase (PG), pectin methylesterase (PME), pectin lyase (PL), cellulase (CL) and β‐galactosidase (β‐Gal). Transmission electron microscopy analysis suggested that H2S protected cell walls from structural breakdown. These results indicated that H2S is effective in delaying banana softening by regulating cell wall polysaccharide metabolism.

Hydrogen sulfide promoted retinoic acid-related orphan receptor α transcription to alleviate diabetic cardiomyopathy

Diabetic cardiomyopathy (DCM) is one serious and common complication in diabetes without effective treatments. Hydrogen sulfide (H2S) fights against a variety of cardiovascular diseases including DCM. Retinoic acid-related orphan receptor α (RORα) has protective effects on cardiovascular system. However, whether RORα mediates the protective effect of H2S against DCM remains unknown. The present research was to explore the roles and mechanisms of RORα in H2S against DCM. The study demonstrated that H2S donor sodium hydrosulfide (NaHS) alleviated cell injury but enhanced RORα expression in high glucose (HG)-stimulated cardiomyocytes. However, NaHS no longer had the protective effect on attenuating cell damage and oxidative stress, improving mitochondrial membrane potential, inhibiting necroptosis and enhanced signal transducer and activator of transcription 3 (STAT3) Ser727 phosphorylation in HG-stimulated cardiomyocytes after RORα siRNA transfection. Moreover, NaHS improved cardiac function, attenuated myocardial hypertrophy and fibrosis, alleviated oxidative stress, inhibited necroptosis, but increased STAT3 phosphorylation in wild type (WT) mice but not in RORα knockout mice (a spontaneous staggerer mice, sg/sg mice) with diabetes. Additionally, NaHS increased RORα promoter activity in cardiomyocytes with HG stimulation, which was related to the binding sites of E2F transcription factor 1 (E2F1) in the upstream region of RORα promoter. NaHS enhanced E2F1 expression and increased the binding of E2F1 to RORα promoter in cardiomyocytes with HG stimulation. In sum, H2S promoted RORα transcription via E2F1 to alleviate necroptosis and protect against DCM. It is helpful to propose a novel therapeutic implication for DCM.

Inhibition of cystathionine-gamma lyase dampens vasoconstriction in mouse and human intracerebral arterioles.

In extracerebral vascular beds cystathionine-gamma lyase (CSE) activity plays a vasodilatory role but the role of this hydrogen sulfide (H2 S) producing enzyme in the intracerebral arterioles remain poorly understood. We hypothesized a similar function in the intracerebral arterioles. Intracerebral arterioles were isolated from wild type C57BL/6J mouse (9-12 months old) brains and from human brain biopsies. The function (contractility and secondary dilatation) of the intracerebral arterioles was tested ex vivo by pressure myography using a perfusion set-up. Reverse transcription polymerase chain reaction was used for detecting CSE expression. CSE is expressed in human and mouse intracerebral arterioles. CSE inhibition with L-propargylglycine (PAG) significantly dampened the K+ -induced vasoconstriction in intracerebral arterioles of both species (% of maximum contraction: in human control: 45.4 ± 2.7 versus PAG: 27 ± 5.2 and in mouse control: 50 ± 1.5 versus PAG: 33 ± 5.2) but did not affect the secondary dilatation. This effect of PAG was significantly reversed by the H2 S donor sodium hydrosulfide (NaSH) in human (PAG + NaSH: 38.8 ± 7.2) and mouse (PAG + NaSH: 41.7 ± 3.1) arterioles, respectively. The endothelial NO synthase (eNOS) inhibitor, Nω-Nitro-l-arginine methyl ester (L-NAME), and the inhibitor of soluble guanylate cyclase (sGC), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) reversed the effect of PAG on the K+ -induced vasoconstriction in the mouse arterioles and attenuated the K+ -induced secondary dilatation significantly. CSE contributes to the K+ -induced vasoconstriction via a mechanism involving H2 S, eNOS, and sGC whereas the secondary dilatation is regulated by eNOS and sGC but not by CSE.

Effects of sodium hydrosulfide (NaHS) on cisplatin-induced hepatic and cardiac toxicity

In recent years, the cardiotoxicity and hepatotoxicity induced by chemotherapeutic drugs such as cisplatin (CP) have become significant issues. The current research looks into the effects of sodium hydrosulfide (NaHS) on CP-induced hepatotoxicity and cardiotoxicity in rats. A total of 32 male Sprague Dawley rats were separated into four different groups: (1) control group, received only normal saline; (2) NaHS group, was intraperitoneally injected with NaHS (200 µg/kg/d, dissolved in saline) for 15 days; (3) CP group, was intraperitoneally injected only one dose of CP (5 mg/kg) and (4) CP plus NaHS group, received CP along with NaHS. Blood and tissues samples were harvested for biochemical, histopathological, and immunohistochemical investigations. To determine the data’s statistical significance, a one-way analysis of variance was used. CP injection significantly increased alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), Creatine phospho kinase (CK-MB), cholesterol, low-density lipoprotein (LDL), triglyceride (TG), and lipid peroxidation levels, while high-density lipoprotein (HDL), albumin, glutathione peroxidase, superoxide dismutase, and catalase (CAT) levels were significantly reduced with pathological alterations in liver and heart tissues. Co-treatment NaHS with CP ameliorates the biochemical and histological parameters. Also, Treatment solely with CP resulted in increased tissue expression of interleukin-1β (IL-1β) in liver and heart but co-treatment NaHS with CP reduced the expression of this inflammatory factor. We conclude that NaHS operates in the liver and heart as an anti-inflammatory and powerful free radicals’ scavenger to inhibit the toxic effects of CP, both at the biochemical and histopathological levels.

H<sub>2</sub>S-Mediated Dilation of Pial Arteries in Rats of Different Ages: Contribution of K<sub>ATP </sub>and BK<sub>Ca</sub>-Channels

Reactions of pial arteries to exogenous hydrogen sulfide exposure and assessment of the contribution of KATP and BKCa-channels to H2S-mediated dilation was studied in rats of different ages. Intravital microphotography in Sprague-Dawley rats aged 4 and 18 months was used to study the reactions of pial arteries of various diameters to the exposure of exogenous hydrogen sulfide donor solution – sodium hydrosulfide (NaHS, 30 μM), as well as their change with the preliminary use of potassium channel blockers: KATP (glibenclamide, 10 μM) and BKCa (tetraethyl ammonium, 2 mM). It was found that inhibition of H2S-mediated dilation of pial arteries and increase in constrictor responses to exogenous hydrogen sulfide exposure are taking place in rats with age. Age-related changes in H2S-induced dilatory response of the pial arteries in rats depend on the size of the vessels. With age, there is a decrease in the number of dilations of pial arteries with a diameter of more than 20 μm. At the same time, aging does not affect the dilatation of smaller arteries. These disorders are probably associated with changes in the processes caused by the activation of potassium channels. It was found that aging is accompanied by the increasing of KATP-channels contribution to the implementation of H2S-mediated dilation in pial arteries with diameters less than 40 μm. BKCa-channels contribution to the dilatation decreases with age. In 18 months, rats, these channels barely participate in H2S-mediated dilation in arteries with diameters more than 20 μm.

Citric acid and hydrogen sulfide cooperate to mitigate chromium stress in tomato plants by modulating the ascorbate-glutathione cycle, chromium sequestration, and subcellular allocation of chromium

The study aimed to investigate the role of hydrogen sulfide (H2S) in regulating chromium stress (Cr–S) tolerance of tomato plants treated with citric acid (CA). Prior to the Cr treatment, tomato plants were foliar-fed with CA (100 μM) daily for 3 days. Subsequently, the plants were grown for another ten days in a hydroponic system in a 50 μM Cr (VI) solution. Chromium treatment reduced photosynthetic pigments and plant biomass, but boosted the levels of hydrogen peroxide (H2O2) malondialdehyde (MDA), H2S, phytochelatins (PCs), and glutathione (GSH), electrolyte leakage (EL), and antioxidant enzyme activity in tomato plants. However, the foliar spray of CA mitigated the levels of H2O2, MDA, and EL, promoted plant growth and chlorophyll content, enhanced antioxidant enzymes’ activities, and increased H2S production in Cr–S-tomato plants. CA also increased the levels of GSH and PCs, potentially reducing the toxicity of Cr through regulated sequestration. Additionally, the application of sodium hydrogen sulfide (NaHS), a donor of H2S, improved CA-induced Cr stress tolerance. The addition of CA promoted Cr accumulation in root cell wall and leaf vacuoles to suppress its toxicity. To assess the involvement of H2S in CA-mediated Cr–S tolerance, 0.1 mM hypotaurine (HT), an H2S scavenger, was provided to the control and Cr–S-plants along with CA and CA + NaHS. HT reduced the beneficial effects of CA by decreasing H2S production in tomato plants. However, the NaHS addition with CA + HT inverted the adverse impacts of HT, indicating that H2S is required for CA-induced Cr–S tolerance in tomato plants.

Purification of arsenic-containing nitric acid solutions using sodium hydrosulfide in the presence of oxidizing agents

Purification of arsenic-containing nitric acid solutions using sodium hydrosulfide in the presence of oxidizing agents

Sodium hydrosulfide moderately alleviates the hallmark symptoms of Duchenne muscular dystrophy in mdx mice

Duchenne muscular dystrophy (DMD) is an incurable disease caused by mutations in the X-linked DMD gene that encodes a structural muscle protein, dystrophin. This, in turn, leads to progressive degeneration of the skeletal muscles and the heart. Hydrogen sulfide (H2S), the pleiotropic agent with antioxidant, anti-inflammatory, and pro-angiogenic activities, could be considered a promising therapeutic factor for DMD.In this work, we studied the effect of daily intraperitoneal administration of the H2S donor, sodium hydrosulfide (NaHS, 100 μmol/kg/day for 5 weeks) on skeletal muscle (gastrocnemius, diaphragm and tibialis anterior) pathology in dystrophin-deficient mdx mice, characterized by decreased expression of H2S-generating enzymes.NaHS reduced the level of muscle damage markers in plasma (creatine kinase, lactate dehydrogenase and osteopontin). It lowered oxidative stress by affecting the GSH/GSSG ratio, up-regulating the level of cytoprotective heme oxygenase-1 (HO-1) and down-regulating the NF-κB pathway. In the gastrocnemius muscle, it also increased angiogenic vascular endothelial growth factor (Vegf) and its receptor (Kdr) expression, accompanied by the elevated number of α-SMA/CD31/lectin-positive blood vessels. The expression of fibrotic regulators, like Tgfβ, Col1a1 and Fn1 was decreased by NaHS in the tibialis anterior, while the level of autophagy markers (AMPKα signalling and Atg genes), was mostly affected in the gastrocnemius. Histological and molecular analysis showed no effect of H2S donor on regeneration and the muscle fiber type composition.Overall, the H2S donor modified the gene expression and protein level of molecules associated with the pathophysiology of DMD, contributing to the regulation of oxidative stress, inflammation, autophagy, and angiogenesis.

Exogenous application of sodium hydrosulfide and salicylic acid mitigate salinity stress in maize by regulating ionic balance, biochemical attributes, photosynthetic pigments and some key antioxidants

Hydrogen sulfide (H2S) and salicylic acid (SA) have been recently explored as important priming agents for plant growth and development. The effects of NaHS alone and in combination with SA to alleviate salt stress effects on maize plants are not determined yet. Here, we executed an approach to examine the effects of NaHS (H2S donor) and SA treatments to overcome the salt stress in maize plants. In vitro screening exhibited that SA (0.1 mM) and NaHS (0.5 mM) as the most effective concentrations to increase biomass and germination of maize plant under salt stress. Furthermore, data revealed that alone and combined treatments of H2S and SA during salt stress showed improved morphological, biochemical, and physiological attributes compared to non-treated plants. However, combined treated plants exhibited maximum salinity resistance than individual treatments. The combined treatment showed increased chlorophyll a (165%), chlorophyll b (138%) and carotenoid (54.4%) and increased activities of antioxidants enzymes like catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), and polyphenol oxidase (PPO) by 441%, 416.7%, 501.4% and 510%, respectively while reduced Na+accumulation and enhanced K+accumulation. Combined treatment protects the plants by lowering proline and MDA content by 300% and 108% respectively. Our in-silico outcomes of the NaHS-SA pathway verify experimental results regarding modulation of salt stress response mechanisms depicts ideal picture of above-mentioned parameters during stress hence suggesting NaHS-SA mediated biofertilizers could strengthen genomic stability and maintenance capability under stress.

Foliar Spraying of NaHS Alleviates Cucumber Salt Stress by Maintaining N+/K+ Balance and Activating Salt Tolerance Signaling Pathways.

Hydrogen sulfide (H2S) is involved in the regulation of plant salt stress as a potential signaling molecule. This work investigated the effect of H2S on cucumber growth, photosynthesis, antioxidation, ion balance, and other salt tolerance pathways. The plant height, stem diameter, leaf area and photosynthesis of cucumber seedlings were significantly inhibited by 50 mmol·L-1 NaCl. Moreover, NaCl treatment induced superoxide anion (O2·-) and Na+ accumulation and affected the absorption of other mineral ions. On the contrary, exogenous spraying of 200 μmol·L-1 sodium hydrosulfide (NaHS) maintained the growth of cucumber seedlings, increased photosynthesis, enhanced the ascorbate-glutathione cycle (AsA-GSH), and promoted the absorption of mineral ions under salt stress. Meanwhile, NaHS upregulated SOS1, SOS2, SOS3, NHX1, and AKT1 genes to maintain Na+/K+ balance and increased the relative expression of MAPK3, MAPK4, MAPK6, and MAPK9 genes to enhance salt tolerance. These positive effects of H2S could be reversed by 150 mmol·L-1 propargylglycine (PAG, a specific inhibitor of H2S biosynthesis). These results indicated that H2S could mitigate salt damage in cucumber, mainly by improving photosynthesis, enhancing the AsA-GSH cycle, reducing the Na+/K+ ratio, and inducing the SOS pathway and MAPK pathway.

Effect of Ozone on Oxygen Transport and Pro-Oxidant- Antioxidant Balance of Red Blood Cell Suspension

Introduction: Ozone affects blood oxygen transport and the pro-oxidant-antioxidant balance. However, the role of blood formed elements and gas transmitters in these processes still remains unclear. The aim of the present study was to investigate the effect of ozone on oxygen transport and the pro-oxidant-antioxidant balance in a red cell suspension. Methods: The red cell suspension was incubated with ozone at a concentration of 6 mg/l and substances affecting the synthesis of gas transmitters (nitroglycerin, sodium hydrosulfide). Parameters of blood oxygen transport and pro-oxidant-antioxidant balance were determined. Results: The effect of ozone on blood oxygen transport was found which was manifested in an increase in oxygen partial pressure and the degree of oxygenation. The index of hemoglobin –oxygen affinity p50 actual was raised and a shift of the oxyhemoglobin dissociation curve rightwards was noticed. The addition of the gas transmitter donor, nitric oxide, enhanced the effect of this gas on the parameters of oxygen transport in the erythrocyte suspension Conclusion: We found that ozone induced a change in oxygen-binding properties of the erythrocyte suspension which is a mechanism of action of the above gas on the adaptive processes in the body realized directly at the level of erythrocytes.

Structural and Dynamic Behaviour of Heterocycles Derived from Ethylenediamines with Formaldehyde: 1,3,5-Triazinanes and Bis(imidazolidinyl)methanes

Formaldehyde is a simple chemical compound that is used as a building block in obtaining a wide range of products. The versatility of formaldehyde in chemical synthesis becomes evident when it is reacted with N-alkylethylenediamines. Therefore, this paper reports the structure and reactivity of a series of compounds derived from easily accessible molecules, such as formaldehyde, sodium hydrosulphide, and N-alkylethylenediamines. The 1,3,5-triazines (1a-1d) and bis(3-alkyl-imidazolidin-1-yl)methanes (2a-2d) were obtained by simple reaction conditions. Additionally, different proportions of sodium hydrosulphide and formaldehyde were used with N-benzylamine to obtain N-benzyltriazinane (3), N-benzylthiadiazinane (4) and N-benzyldithiazinane (5). All these compounds were characterized by analytical, spectroscopic, and spectrometric techniques, such as melting point, solubility, one-dimensional and two-dimensional nuclear magnetic resonance (13C, 1H, 15N, COSY, HETCOR, NOESY, COLOC), elemental analysis, high- and low-resolution mass spectrometry, among others. The structures of compounds 4 and 5 were obtained by single-crystal X-ray diffraction. The results show that small variations in the stoichiometry and the reaction conditions significantly influence the products obtained.

Dose-Dependent Effect of Hydrogen Sulfide in Cyclophosphamide-Induced Hepatotoxicity in Rats.

Cyclophosphamide is a commonly used anticancer and immunosuppressive agent; however, hepatotoxicity is one of its severe toxicities. Hydrogen sulfide is a gaseous signaling molecule that plays crucial regulatory roles in various physiological functions. This study aimed to evaluate the hepatoprotective effect of hydrogen sulfide against cyclo phosp hamid e-ind uced hepatic damage in rats. Hepatotoxicity was induced by the single intraperitoneal administration of cyclophosphamide (200 mg/kg). Sprague-Dawley rats were treated by hydrogen sulfide donor, sodium hydrosulfide (25, 50, and 100 μmol/kg, intraperitoneal) 7 days before and 7 days after the administration of a single intraperitoneal injection of cyclophosphamide (200 mg/kg). Cyclo phosp hamide-ind uced hepatotoxicity was evaluated by serum and tissue biochemical and histopathological assessments. The levels of hydrogen sulfide, nitric oxide, cyclic guanosine monophosphate, interleukin 6, and interleukin 10 in liver homogenates were also determined by ELISA. One-way analysis of variance and Kruskal-Wallis tests were used as statistical analyses. Cyclophosphamide increased liver function enzymes (alanine aminotransferase and aspartate aminotransferase), immunoreactivity to caspase-3 and Apaf-1, and proinflammatory cytokines. Cyclophosphamide also induced histopathological alterations including pycnotic nucleus with eosinophilic cytoplasm, increased sinusoidal dilatation, congestion, and edema. Hydrogen sulfide cotreatment significantly reduced cyclo phosp hamid e-ind uced inflammation, histological alterations, and apoptosis in the liver. 50 mg/kg sodium hydrosulfide was more effective against cyclo phosp hamid e-ind uced hepatotoxicity. In conclusion, hydrogen sulfide with its anti-inflammatory and anti-apoptotic effects seems to be beneficial as an adjunct to cyclophosphamide treatment to reduce cyclo phosp hamid e-ind uced hepatotoxicity and thereby can be suggested as a promising agent to increase the therapeutic efficacy of cyclophosphamide.

Hydrogen sulfide alleviates chromium toxicity by promoting chromium sequestration and re-establishing redox homeostasis in Zea mays L

Hydrogen sulfide (H2S) is a multifunctional gaseous signaling molecule involved in the regulation of Cr stress responses. In the present study, we combined transcriptomic and physiological analyses to elucidate the mechanism underlying the mitigation of Cr toxicity by H2S in maize (Zea mays L.). We showed that treatment with sodium hydrosulfide (NaHS, a donor of H2S) partially alleviated Cr-induced growth inhibition. However, Cr uptake was not affected. RNA sequencing suggested that H2S regulates the expression of many genes involved in pectin biosynthesis, glutathione metabolism, and redox homeostasis. Under Cr stress, NaHS treatment significantly increased pectin content and pectin methylesterase activity; thus, more Cr was retained in the cell wall. NaHS application also increased the content of glutathione and phytochelatin, which chelate Cr and transport it into vacuoles for sequestration. Furthermore, NaHS treatment mitigated Cr-induced oxidative stress by enhancing the capacity of enzymatic and non-enzymatic antioxidants. Overall, our results strongly support that H2S alleviates Cr toxicity in maize by promoting Cr sequestration and re-establishing redox homeostasis rather than by reducing Cr uptake from the environment.

Impakt of Ozone on the Oxyge Affinity Blood Properties and Prooxidant–Antioxidant Balance under Effect of H<sub>2</sub>S-Generating System

Hydrogen sulfide belongs to the group of signaling agents called gaseous transmitters and plays an important role in many physiological processes, in particular, in the realization of oxygen-dependent mechanisms. The aim of this study was to evaluate the significance of hydrogen sulfide in the effect of ozone on the oxygen affinity blood properties and the prooxidant-antioxidant balance in vitro experiment. Ozone (6 mg/L concentration) and drugs that affect the synthesis of hydrogen sulfide (propargylglycine, sodium hydrosulfide and its combination with nitroglycerin) were used. The use of propargylglycine, an inhibitor of the synthesis of hydrogen sulfide, leads to a decrease in the effect of ozone on the blood oxygen transport function (decrease in PO2, SO2, P50real). When sodium hydrosulfide is added, the effect of this gas on these parameters does not increase, but in its combination with nitroglycerin, the effect of ozone on the blood oxygen transport function increases. Propargylglycine does not affect the prooxidant-antioxidant balance under the conditions of the experiment, and donors of hydrogen sulfide and nitrogen monoxide increase the activity of catalase. Propargylglycine under the action of ozone leads to a decrease in the level of nitrate/nitrite, and sodium hydrosulfide increases their concentration. The combination of sodium hydrosulfide and nitroglycerin leads to the accumulation of hydrogen sulfide in the blood plasma.

Testing chemical priming with sodium hydrosulfide in commercial avocado (Persea americanaMill. ‘Hass’) orchards for improving the response to chilling conditions

Testing chemical priming with sodium hydrosulfide in commercial avocado (<i>Persea americana</i>Mill. ‘Hass’) orchards for improving the response to chilling conditions

Hydrogen sulfide protects Sertoli cells against toxicant Acrolein-induced cell injury.

Acrolein (ACR), a highly toxic α,β-unsaturated aldehyde, is considered to be a common mediator behind the reproductive injury induced by various factors. However, the understanding of its reproductive toxicity and prevention in reproductive system is limited. Given that Sertoli cells provide the first-line defense against various toxicants and that dysfunction of Sertoli cell causes impaired spermatogenesis, we, therefore, examined ACR cytotoxicity in Sertoli cells and tested whether hydrogen sulfide (H2S), a gaseous mediator with potent antioxidative actions, could have a protective effect. Exposure of Sertoli cells to ACR led to cell injury, as indicated by reactive oxygen species (ROS) generation, protein oxidation, P38 activation and ultimately cell death that was prevented by antioxidant N-acetylcysteine (NAC). Further studies revealed that ACR cytotoxicity on Sertoli cells was significantly exacerbated by the inhibition of H2S-synthesizing enzyme cystathionine γ-lyase (CSE), while significantly suppressed by H2S donor Sodium hydrosulfide (NaHS). It was also attenuated by Tanshinone IIA (Tan IIA), an active ingredient of Danshen that stimulated H2S production in Sertoli cells. Apart from Sertoli cells, H2S also protected the cultured germ cells from ACR-initiated cell death. Collectively, our study characterized H2S as endogenous defensive mechanism against ACR in Sertoli cells and germ cells. This property of H2S could be used to prevent and treat ACR-related reproductive injury.

Application of silicon and sodium hydrosulfide alleviates arsenic toxicity by regulating the physio-biochemical and molecular mechanisms of Zea mays.

Soil contamination with toxic heavy metals (such as arsenic (As)) is becoming a serious global problem due to rapid development of social economy, although the use of silicon (Si) and sodium hydrosulfide (NaHS) has been found effective in enhancing plant tolerance against biotic and abiotic stresses including the As toxicity. For this purpose, a pot experiment was conducted using the different levels of As toxicity in the soil, i.e., (0mM (no As), 50, and 100µM) which were also supplied with the different exogenous levels of Si, i.e., (0 (no Si), 1.5, and 3mM) and also with the NaHS, i.e., (0 (no NaHS), 1, and 2mM) on growth, photosynthetic pigments, gas exchange characteristics, oxidative stress biomarkers, antioxidant machinery (enzymatic and non-enzymatic antioxidants), and their gene expression, ion uptake, organic acid exudation, and As uptake of maize (Zea mays L.). Results from the present study showed that the increasing levels of As in the soil significantly (P < 0.05) decreased plant growth and biomass, photosynthetic pigments, gas exchange attributes, sugars, and nutritional contents from the roots and shoots of the plants. In contrast, increasing levels of As in the soil significantly (P < 0.05) increased oxidative stress indicators in terms of malondialdehyde, hydrogen peroxide, and electrolyte leakage and also increased organic acid exudation patter in the roots of Z. mays, although the activities of enzymatic antioxidants and the response of their gene expressions in the roots and shoots of the plants and non-enzymatic such as phenolic, flavonoid, ascorbic acid, and anthocyanin contents were initially increased with the exposure of 50µM As, but decreased by the increasing the As concentration 100µM in the soil. The negative impact of As toxicity can overcome the application of Si and NaHS, which ultimately increased plant growth and biomass by capturing the reactive oxygen species and decreased oxidative stress in Z. mays by decreasing the As contents in the roots and shoots of the plants. Our results also showed that the Si was more sever and showed better results when we compared with NaHS under the same treatment of As in the soil. Research findings, therefore, suggest that the combined application of Si and NaHS can ameliorate As toxicity in Z. mays, resulting in improved plant growth and composition under metal stress, as depicted by balanced exudation of organic acids.

Hydrogen sulfide attenuates TMAO‑induced macrophage inflammation through increased SIRT1 sulfhydration.

Chronic inflammation is a key factor that accelerates the progression of inflammatory vascular disease. Hydrogen sulfide (H2S) has potent anti‑inflammatory effects; however, its underlying mechanism of action has not been fully elucidated. The present study aimed to investigate the potential effect of H2S on sirtuin 1 (SIRT1) sulfhydration in trimethylamine N‑oxide (TMAO)‑induced macrophage inflammation, and its underlying mechanism. Pro‑inflammatory M1 cytokines (MCP‑1, IL‑1β, and IL‑6) and anti‑inflammatory M2 cytokines (IL‑4 and IL‑10) were detected by RT‑qPCR. CSE, p65 NF‑κB, p‑p65 NF‑κB, IL‑1β, IL‑6 and TNF‑α levels were measured by Western blot. The results revealed that cystathionine γ‑lyase protein expression was negatively associated with TMAO‑induced inflammation. Sodium hydrosulfide (a donor of H2S) increased SIRT1 expression and inhibited the expression of inflammatory cytokines in TMAO‑stimulated macrophages. Furthermore, nicotinamide, a SIRT1 inhibitor, antagonized the protective effect of H2S, which contributed to P65 NF‑κB phosphorylation and upregulated the expression of inflammatory factors in macrophages. H2S ameliorated TMAO‑induced activation of the NF‑κB signaling pathway via SIRT1 sulfhydration. Moreover, the antagonistic effect of H2S on inflammatory activation was largely eliminated by the desulfhydration reagent dithiothreitol. These results indicated that H2S may prevent TMAO‑induced macrophage inflammation by reducing P65 NF‑κB phosphorylation via the upregulation and sulfhydration of SIRT1, suggesting that H2S may be used to treat inflammatory vascular diseases.

Fast and slow releasing sulphide donors engender distinct transcriptomic alterations in Atlantic salmon hepatocytes

Hydrogen sulphide (H2S) is a naturally occurring compound generated either endogenously or exogenously and serves both as a gaseous signalling molecule and an environmental toxicant. Though it has been extensively investigated in mammalian systems, the biological function of H2S in teleost fish is poorly identified. Here we demonstrate how exogenous H2S regulates cellular and molecular processes in Atlantic salmon (Salmo salar) using a primary hepatocyte culture as a model. We employed two forms of sulphide donors: the fast-releasing salt form, sodium hydrosulphide (NaHS) and the slow-releasing organic analogue, morpholin-4-ium 4-methoxyphenyl(morpholino) phosphinodithioate (GYY4137). Hepatocytes were exposed to either a low (LD, 20 µg/L) or high (HD, 100 µg/L) dose of the sulphide donors for 24 hrs, and the expression of key sulphide detoxification and antioxidant defence genes were quantified by qPCR. The key sulphide detoxification genes sulfite oxidase 1 (soux) and the sulfide: quinone oxidoreductase 1 and 2 (sqor) paralogs in salmon showed pronounced expression in the liver and likewise responsive to the sulphide donors in the hepatocyte culture. These genes were ubiquitously expressed in different organs of salmon as well. HD-GYY4137 upregulated the expression of antioxidant defence genes, particularly glutathione peroxidase, glutathione reductase and catalase, in the hepatocyte culture. To explore the influence of exposure duration, hepatocytes were exposed to the sulphide donors (i.e., LD versus HD) either transient (1h) or prolonged (24h). Prolonged but not transient exposure significantly reduced hepatocyte viability, and the effects were not dependent on concentration or form. The proliferative potential of the hepatocytes was only affected by prolonged NaHS exposure, and the impact was not concentration dependent. Microarray analysis revealed that GYY4137 caused more substantial transcriptomic changes than NaHS. Moreover, transcriptomic alterations were more marked following prolonged exposure. Genes involved in mitochondrial metabolism were downregulated by the sulphide donors, primarily in NaHS-exposed cells. Both sulphide donors influenced the immune functions of hepatocytes: genes involved in lymphocyte-mediated response were affected by NaHS, whereas inflammatory response was targeted by GYY4137. In summary, the two sulphide donors impacted the cellular and molecular processes of teleost hepatocytes, offering new insights into the mechanisms underlying H2S interactions in fish.