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Abstract Hydrogen sulfide (H2S) has emerged as a novel endogenous gas signaling molecule, joining the ranks of nitric oxide (NO) and carbon monoxide (CO). Recent research has highlighted its involvement in various physiological processes, such as promoting root organogenesis, regulating stomatal movement and photosynthesis, and enhancing plant growth, development, and stress resistance. Tobacco, a significant cash crop crucial for farmers’ economic income, relies heavily on root development to affect leaf growth, disease resistance, chemical composition, and yield. Despite its importance, there remains a scarcity of studies investigating the role of H2S in promoting tobacco growth. This study exposed tobacco seedlings to different concentrations of NaHS (an exogenous H2S donor) − 0, 200, 400, 600, and 800 mg/L. Results indicated a positive correlation between NaHS concentration and root length, wet weight, root activity, and antioxidant enzymatic activities (CAT, SOD, and POD) in tobacco roots. Transcriptomic and metabolomic analyses revealed that treatment with 600 mg/L NaHS significantly effected 162 key genes, 44 key enzymes, and two metabolic pathways (brassinosteroid synthesis and aspartate biosynthesis) in tobacco seedlings. The addition of exogenous NaHS not only promoted tobacco root development but also potentially reduced pesticide usage, contributing to a more sustainable ecological environment. Overall, this study sheds light on the primary metabolic pathways involved in tobacco root response to NaHS, offering new genetic insights for future investigations into plant root development.

Abstract Cryopreservation of sperm can cause oxidative stress and damage, leading to decreased different functional parameters and fertilization potential. In this study, we evaluated two types of H2S donors: NaHS, a fast-releasing donor, and GYY4137, a slow-releasing donor during cryopreservation of goat sperm. Initially, we determined that 1.5 and 3 μM NaHS, and 15 and 30 μM GYY4137 are optimal concentrations that improved different sperm functional parameters including motility, viability, membrane integrity, lipid peroxidation, and ROS production during incubation at 38.5 °C for 90 min. We subsequently evaluated the impact of the optimal concentration of NaHS and GYY4137 supplementation on various functional parameters following thawing during cryopreservation. Our data revealed that supplementation of extender improved different parameters including post-thaw sperm motility, viability, membrane integrity, and reduced DNA damage compared to the frozen-thawed control group. The supplementation also restored the redox state, decreased lipid peroxidation, and improved mitochondrial membrane potential in the thawed sperm. Finally, we found that supplementation of the extender with NaHS and GYY4137 enhanced IVF outcomes in terms of blastocyst rate and quality of blastocysts. Our results suggest that both donors can be applied for cryopreservation as antioxidants to improve sperm quality and IVF outcomes of frozen-thawed goat sperm.

Objective To investigate the effect of sodium hydrosulfide (NaHS) on renal ischemia-reperfusion (I/R) injury in rats, and the relationship between its mechanism and Klotho protein. Methods We selected 18 male SD rats and randomly divided them into the sham group, I/R group, and NaHS intervention group (I/R + NaHS group), with 6 rats in each group. In the I/R group, we removed the right kidney, and then used non-invasive arterial clips to clamp the left renal pedicle to simulate the state of acute renal ischemia, and released the arterial clip after 45 minutes of clamping to simulate the state of renal reperfusion. After the acute renal ischemia model was established in the NaHS intervention group, NaHS was injected into the left renal artery, followed by reperfusion. The sham operation group was not clamped. After 24 h of reperfusion, blood samples were collected from each group, and serum renal function indexes such as urea ni- trogen (BUN) and creatinine (Scr) were detected by colorimetry. Renal tissue samples were taken from each group, and the histopathological changes of kidney were observed by HE staining, the content of SOD and MDA in renal tissues were detected by colorimetry, and the expression levels of Klotho and Nrf2 protein in renal tissues were detected by Western blotting. Results Compared with the sham group, serum creatinine and urea nitrogen increased, renal tubular injury was aggravated, SOD activity decreased, MDA content increased, the expression of Klotho protein in the renal tissues de- creased, and the expression of Nrf2 proteion increased in the I/R group (P<0.05 or P<0.01). Compared with the I/R group, the serum levels of creainine and urea nitrogen decreased, renal tubular injury was alleviated, SOD activity in- creased, MDA content decreased, the Klotho protein expression increased, and the Nrf2 protein expression decreased in the I/R + NaHS group （P<0. 05 or P<0. 01）. Conclusion NaHS can alleviate renal I/R injury in rats with acute renal ischemia， and its mechanism may be related to up-regulating Klotho protein expression and reducing oxidative stress. [ABSTRACT FROM AUTHOR]

Abstract Background Hydrogen sulfide (H2S) is a novel signaling molecule involved in the growth and development of plants and their response to stress. However, the involvement of H2S in promoting the growth and development of tobacco plants is still unclear. Results In this study, we explored the effect of pre-soaking or irrigating the roots of tobacco plants with 0.0, 2.0, 4.0, 6.0, and 8.0 mM of sodium hydrosulfide (NaHS) on endogenous H2S production, antioxidant enzymatic and cysteine desulfhydrase activities, seed germination, agronomic traits, photosynthetic pigments contents, and root vigor. The results revealed that exogenous NaHS treatment could significantly promote endogenous H2S production by inducing gene expression of D/L-CD and the activities of D/L-CD enzymes. Additionally, a significant increase in the agronomic traits and the contents of photosynthetic pigments, and no significant difference in carotenoid content among tobacco plants treated with 0.0 to 8.0 mM of NaHS was observed. Additionally, a significant increase in the germination speed, dry weight, and vigor of tobacco seeds, whereas no significant effect on the percentage of seed germination was observed on NaHS treatment. Furthermore, NaHS treatment could significantly increase the activity of superoxide dismutase (SOD) and peroxidase (POD) enzymes, which reduces damage due to oxidative stress by maintaining reactive oxygen species homeostasis. Conclusions These results would aid in enhancing our understanding of the involvement of H2S, a novel signaling molecule to promote the growth and development of tobacco plants.

Background: Hydrogen sulfide (H2S) is a novel signaling molecule involved in the growth and development of plants and their response to stress. However, the involvement of H2S in promoting the growth and development of tobacco plants is still unclear. Results: In this study, we explored the effect of pre-soaking or irrigating the roots of tobacco plants with 0.0, 2.0, 4.0, 6.0, and 8.0 mM of sodium hydrosulfide (NaHS) on endogenous H2S production, antioxidant enzymatic and cysteine desulfhydrase activities, seed germination, agronomic traits, photosynthetic pigments contents, and root vigor. The results revealed that exogenous NaHS treatment could significantly promote endogenous H2S production by inducing gene expression of D/L-CD and the activities of D/L-CD enzymes. Additionally, a significant increase in the agronomic traits and the contents of photosynthetic pigments, and no significant difference in carotenoid content among tobacco plants treated with 0.0 to 8.0 mM of NaHS was observed. Additionally, a significant increase in the germination speed, dry weight, and vigor of tobacco seeds, whereas no significant effect on the percentage of seed germination was observed on NaHS treatment. Furthermore, NaHS treatment could significantly increase the activity of superoxide dismutase (SOD) and peroxidase (POD) enzymes, which reduces damage due to oxidative stress by maintaining reactive oxygen species homeostasis. Conclusions: These results would aid in enhancing our understanding of the involvement of H2S, a novel signaling molecule to promote the growth and development of tobacco plants. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine if there is a difference in hip survivorship rates and patient-reported outcomes (PROs) at a 5-year follow-up after arthroscopic treatment of femoroacetabular impingement syndrome (FAIS) between patients with versus without systemic inflammatory diseases (SIDs). A retrospective single-surgeon matched cohort study of FAIS patients who underwent hip arthroscopy and had a minimum of a 5-year follow-up was conducted. Subjects with SIDs were matched at a ratio of 2:3 of age and body mass index (BMI) with respect to controls without SIDs. Subjects completed the modified Harris Hip Score (mHHS) and Non-Arthritic Hip Score (NAHS) prior to surgery and at a 2-year and 5-year follow-up. Survival distributions for time to reoperation and to total hip arthroplasty (THA) were compared between groups using the log-rank test. Fifteen subjects with SIDs (mean age 41.5 years) were matched with twenty-five controls (41.8 years). There were no significant differences in reoperation rates (SIDs 27% vs. controls 20%, p = 0.71) or THA conversion rates (SIDs 7% vs. controls 12%, p = 1.00) at the 5-year follow-up, nor were there differences in survival distributions for reoperations (p = 0.72) or THAs (p = 0.55). There were no significant differences in postoperative mHHS (SIDs 79.3 vs. controls 88.5, p = 0.09) or NAHS (SIDs 82.7 vs. controls 89.3, p = 0.77) by the 5-year follow-up. At the 5-year follow-up, FAIS patients with comorbid SIDs experienced a significant clinical improvement from hip arthroscopy that is comparable to that of FAIS patients without SIDs. [ABSTRACT FROM AUTHOR]

An efficient method for the synthesis of thioquinazolinediones from 2-aminobenzonitriles and carbonyl sulfide (COS) catalyzed by NaHS was established. In this synthetic method, NaHS was used to catalyze the reaction of COS with a broad range of 2-aminobenzonitrile to form the corresponding thioquinazolinedione. Moreover, the controlled experiments demonstrated that NaHS not only reacted with 2-aminobenzonitrile to form 2-aminobenzothioamide, but also acted as a strong nucleophile to react with COS to form the active intermediate dithiocarbonate. Subsequently, 2-aminobenzothioamide reacted with dithiocarbonate to form the thioquinazolinedione easily. Meanwhile, the generated H2S was recycled as sulfur source and hydrogen source to produce 2-aminobenzothioamide. [ABSTRACT FROM AUTHOR]

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The goal of this study was to determine the effectiveness of exogenous application of some chemicals [Salicylic acid (SA; 200 and 400 mg/l), Ascorbic acid (AA; 1000 and 2000 mg/l), Proline (Pro; 100 and 200 mg/l), and Sodium hydrosulfide (NaHS; 250 and 500 M)] as well as planting distances (10 and 50 meters off the freeway) in alleviating air pollutants stress on "Le Conte" productivity and fruit quality of pears. During the 2019 & 2020 seasons, a study was accomplished at the 6th of October Agriculture Company. SA, AA, proline, and NaHS had a positive effect on reducing the fruit heavy metal content for the pear trees under stress. Also, SA (400 mg/l), AA, Pro (100 mg/l), and NaHS (500 μM) treatments were very helpful in increasing the tolerance index for air pollution (APTI) in pear leaves. Exogenous application of Pro, SA (200 mg/l), and AA (2000 mg/l) increased Pro in leaves. Pear trees' yield, fruit firmness, TSS, TSS/acid, V.C., total sugars, total phenolics, antioxidants, peroxidase, and superoxide dismutase were increased. Fruit from trees planted at 10 m deferred in ripening and had higher total phenolics, antioxidants, peroxidase, and superoxide dismutase.

Summary. Diabetic nephropathy is a common microvascular complication of diabetes mellitus (DM), which develops in approximately 40 % of patients with type 2 DM. For the treatment of diabetic kidney damage, metformin is widely used – a drug that controls blood glucose levels and has proven nephroprotective properties. In present time, the role of the H2 S system in the mechanisms of the nephroprotective activity of metformin has not been investigated. The aim of the study – to assess the influence of modulators of H2 S exchange on the main mechanisms of nephroprotective action of metformin in experimental diabetes. Materials and Methods. Experimental studies were conducted on 75 white non-linear male rats, which were divided into five groups: group 1 – control; group 2 – animals with experimental diabetes, which was initiated by a single intraperitoneal injection of streptozotocin (40 mg/kg of weight); group 3 – animals with experimental diabetes, which were treated with metformin (500 mg/kg/ day, intragastrically) from the 3rd to the 28th day; group 4 – animals with DM, which were administered metformin together with NaHS (56 μmol/kg/day, intragastrically); group 5 – animals with diabetes, to which metformin was administered together with propargylglycine (PPG, 442 μmol/kg/day, intragastrically). Glucose content was determined in peripheral blood, and the level of H2 S, galectin-3, caspase-3, IL-1β, malondialdehyde (MDA), protein carbonyl groups (PCG), NADPH oxidase and superoxide dismutase (SOD) activity was assessed in the supernatant of the kidney homogenate. Results. It was established that the use of metformin in experimental diabetes showed antioxidant (the level of MDA and PCG decreased by 24.7–27.4%, p˂0.001), anti-inflammatory (the level of IL-1β decreased by 25.3 %, p˂ 0.001), antiapoptotic (the level of caspase-3 decreased by 36.1 %, p˂0.001) and antifibrogenic (the level of galectin decreased by 48.4 %, p˂0.001) activity in the kidneys, which was associated with an increase (by 27.9 % p˂ 0.001) of H2 S level (│rs │ = 0.59–0.75, p˂0.01). The use of H2 S modulators modified the nephroprotective properties of metformin in diabetes condition. Administration of NaHS (the hydrogen sulfide donor) potentiated the protective effect of metformin in the kidneys: the levels of galectin-3, caspase-3, IL-1β, MDA, and PCG in the kidneys were significantly lower, respectively, by 18–37 % (p˂0.001) than in animals that received only metformin. At the same time, the use of the PPG (hydrogen sulfide synthesis inhibitor) probably reduced metformin protective activity in the kidney. Conclusions. The conducted studies proved the important role of the H2 S system in the implementation of anti-inflammatory, anti-fibrogenic, anti-apoptotic and antioxidant effects of metformin in the kidneys in diabetes condition. Along with this, the obtained results pathogenetically substantiate the expediency of H2 S donors using to potentiate the nephroprotective properties of metformin

Triple negative breast cancer (TNBC) is a highly aggressive subtype with a poor prognosis due to its high rates of proliferation and metastasis. Recently, hydrogen sulfide (H2S) has been recognized as a novel gasotransmitter that plays a significant role in various pathological processes, including cancer. Here, we show that exogenous H2S inhibited TNBC cancer cell proliferation, migration and invasion in vitro, and also decreased cancer malignances in the mouse model of TNBC. To investigate the underlying mechanisms of H2S's anti-cancer effects in TNBC, we performed transcriptome sequencing and bioinformatic analyses. 2121 differentially expressed genes (DEGs) were revealed, and mainly enriched in cell cycle and DNA replication pathways. Further analysis revealed changes in alternative splicing after exogenous H2S treatment. Protein-protein interaction (PPI) network analysis was performed, which identified 458 interactions among 276 DEGs enriched in cell cycle and DNA replication pathways.We identified seven hub genes (MCM3, MCM4, MCM5, MCM6, CDC6, CDC45, and GINS2) through PPI network analysis, which were up-regulated in clinical human breast cancer but down-regulated after H2S treatment. Based on the hub genes selected, we developed a model predicting that exogenous H2S mainly exerts its anti-TNBC role by delaying DNA replication. Our findings suggest that exogenous H2S has potential as a therapeutic agent in TNBC and may exert its therapeutic potential through DNA replication and the cell cycle pathway.

Copper sulfide minerals are the major raw materials for copper products. Copper sulfide minerals are mined at copper mines and concentrated by flotation process. In recent years, the mining of refractory copper ores, which is difficult to concentrate by flotation due to their fine grain size, presence of multiple copper mineral species, and fluctuation of the content ratio of these minerals in feed ore. In addition, the hydrophilization of copper mineral surfaces due to oxidation and the mineral content variation of ore result in poor and unpredictable performance of flotation operation. In this study, therefore, we focused on the activation of the copper mineral surfaces using sodium hydrosulfide (NaHS) to render the surfaces hydrophobic and tried to quantify the effect of the fluctuation of mineral content ratio by using a new flotation kinetic model. Two samples showing different content ratios of chalcocite, bornite, and chalcopyrite and having fully oxidized surface were used in the flotation tests. We established a new flotation kinetic model by considering the reaction between the copper mineral surface and NaHS and the depression of floatability by adsorption of hydrogen sulfide ions onto the copper mineral surface. As a result, a good relation was confirmed between the model and the flotation test results for both ore samples. This result showed that our model can accurately predict the flotation results of refractory copper ores and will encourage the further usage of these refractory copper ores in the future.

Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to determine and establish the MCID for the NAHS at 2 years in patients undergoing hip arthroscopy for femoroacetabular impingement syndrome (FAIS). Methods: Patients that underwent primary hip arthroscopy for FAIS between 2010 and 2016 were analyzed for eligibility. Data were collected from a single surgeon's hip arthroscopy database. MCID was calculated for the NAHS utilizing a distribution-based method. Results: The study included 298 patients (184 females) with an average age of 40.4 ± 13.0 years and average body mass index (BMI) of 25.7 ± 4.2 kg/m2. At baseline, the cohort's average NAHS score was 48.7 ± 13.6 and demonstrated an improvement of 36.5 ± 17.0 for NAHS at follow-up. This resulted in MCID values of + 8.5 for NAHS. Conclusion: This is the first study to report the MCID (+ 8.5) for NAHS following primary hip arthroscopy, and as such, is a valuable contribution to future hip arthroscopy research. Level of evidence: IV. [ABSTRACT FROM AUTHOR]

Fe(II)EDTA can remove NO efficiently, but it has not been industrially applied. This is because the oxygen present in the flue gas will oxidize Fe(II)EDTA and Fe(II)EDTA-NO to Fe(III)EDTA and deactivate them. In order to solve this problem, this paper innovatively proposes to use NaHS to reduce Fe(III) EDTA, because NaHS has high reducing ability and low price. Therefore, a series of experimental conditions were explored in order to obtain the best reaction setup. The results indicate that increasing the concentrations of NaHS, temperature, and pH enhances the rate of NaHS reduction. The mechanism of the increase in reduction rate was studied in depth using potentiometric titration. It was found that an increase in OH- concentration will generate S 8 precipitate, which is beneficial to the forward progress of the reaction and promotes the large-scale production of the active component Fe2+. Oxygen is an inevitable factor in actual flue gas, so this study innovatively proposed a kinetic model under aerobic conditions and used this model to predict the trend of Fe(III)EDTA reduction by NaHS. On this basis, NO removal experiments were conducted under high oxygen conditions. After 15 cycles, the reduction performance of NaHS was still very high, and the NO removal rate was higher than 70%. The reason for this phenomenon is that the stabilizer exists in a form that is conducive to the removal of NO by the active component Fe2+. Therefore, this study provides theoretical guidance for promoting the industrial application of Fe(II) EDTA technology for NO removal. [Display omitted] • The mechanism of reduction of Fe (III)EDTA by NaHS was determined. • The reaction order of NaHS reduction reaction for Fe(III)EDTA is 2. • The derived kinetic model in an aerobic environment was utilized to predict the trend of Fe(III)EDTA reduction by NaHS and validated experimentally. • NaHS has excellent cycling performance in high oxygen cycling NO removal experiments. [ABSTRACT FROM AUTHOR]

Objetivo: La EHGNA (enfermedad de hígado graso no alcoholica)/NAFLD (Non Alcoholic Fatty Liver Disease) incluye dos trastornos anatomopatológicamente diferentes, que tienen pronósticos distintos: hígado graso no alcohólico (HGNA) y esteatohepatitis no alcohólica (EHNA)/ (NASH)/Non-Alcoholic SteatoHepatitis esta última abarca un amplio espectro de gravedad de la enfermedad, del que forman parte la fibrosis, la cirrosis y el carcinoma hepatocelular (CHC) La prevalencia de NAFLD en América Latina ha aumentado en paralelo con los cambios en la obesidad, la inactividad física y la diabetes tipo 2, con impactos clínicos y económicos directos. Se ha demostrado que el 61% de los pacientes con NAFLD en América del Sur tienen esteatohepatitis no alcohólica (NASH); De aquí la importancia de lograr identificar a los pacientes en riesgo, a través de historia médica, pruebas de laboratorio, y pruebas no invasiva para fibrosis FIB-4. En caso de clasificar con riesgo indeterminado se realizará el Ultrasonido elastografía transitoria controlada por vibración (FibroScan) y lograr corregir los factores que los encaminan a ser diagnosticados con NAFLD con fibrosis avanzada (NASH) que es la causa más rápido de aumento de carcinoma hepatocelular y es una indicación principal para el trasplante de hígado en muchos países de América Latina. Conclusion: La paciente en estudio desde el año 2018, se encontraba en estadios temprano con fib-4 estadio (f2-f3: 1.75) Estadio INTERMEDIO de riesgo. Dada la complejidad de la atención que plantean los pacientes con obesidad, diabetes, enfermedades cardiovasculares y EHGNA con fibrosis, una intervención exitosa requiere un equipo multidisciplinario

Objective(s): Infertility in varicocele may have an adverse outcome on the future life of an infertile male. This study was designed to investigate whether varicocele affects remote organs, including the kidney, liver, and brain. We have also evaluated the protective effects of NaHS administration on the structure and function of these organs.Materials and Methods: Thirty-six rats were randomly assigned to 3 experimental groups: 1) Sham, 2) Varicocele, and 3) Varicocele + sodium hydrosulfide. Varicocele was induced via partial ligation of the left renal veins. Animals in the Varicocele + sodium hydrogen sulfide group received 30 µmol/l NaHS in drinking water for 56 days. On the 57th day of the treatment, blood samples, as well as kidney, liver, and brain tissues, were collected to assess kidney and liver functions, measurement of oxidative stress markers, and histological changes. For evaluation of sperm parameters caudal epididymis was used. The behavioral tests were performed to evaluate the animal’s anxiety-related behaviors. Results: Varicocele caused significant decrease in sperm parameters (motility and viability) and superoxide dismutase activity in the kidney, liver, and brain tissue. Anxiety-related parameters decreased in varicocele. Moreover, varicocele resulted in a significant increase in malondialdehyde levels in the kidney, liver and brain tissue, and liver function enzymes. Varicocele did not alter kidney function parameters. The administration of NaHS improves the above parameters.Conclusion: This study showed that notice to remote organs such as the liver and brain beside reproductive organs in varicocele is important. The administration of NaHS improved remote organ injury in varicocele via its anti-oxidant mechanism.

Hydrogen sulfide (H2S) is involved in many physiological processes and responses to the abiotic types of stress. The aim of the study was to determine the effect of sodium hydrogen sulfide (NaHS) and the time of application on the physiological properties of etiolated wheatgrass plants. Two genotypes of wheatgrass were grown under controlled conditions for five days without light and then with a 12-hour photoperiod, watered for three consecutive days with 100, 200, and 500 mM NaHS solutions. The plants were watered in three variants, 7-9, 10-12, and 13-15 days after sowing, respectively. The highest content of phenols, flavonoids, and hydrogen peroxide was found in wheatgrass plants watered with 100 mM of NaHS solution. The highest proline content and lipid peroxidation levels were found in the plants at 500 mM of NaHS solution. Also, the significant influence of the watering period on the examined physiological parameters was determined. The results show that H2S significantly affects the de-etiolation process and concentration of physiologically active compounds in wheatgrass plants.

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 (H 2 S) 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 H 2 S donor), hydroxocobalamin (an H 2 S 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 H 2 S 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. H 2 S 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. H 2 S modulates platelet autophagy and functions possibly via the PDGFR-α/PI3K/Akt/mTOR signaling pathway., Competing Interests: The authors have no conflicts of interest related to this publication., (© 2024 Authors.)

As a multifunctional signaling molecule, hydrogen sulfide (H2S) has been reported to induce plant responses to a variety of abiotic stresses. However, there are no reports on H2S treatment inducing resistance in apples against Penicillium expansum , a biotic factor, and its possible mechanism of action. In this study, fumigating apples with 5 mM sodium hydrosulfide (NaHS), the exogenous donor of H2S, for 12 h reduced the diameter of lesions in fruit colonized by P. expansum. NaHS treatment markedly promoted the synthesis of endogenous H2S, hydrogen peroxide (H2O2), and nitrogen oxide (NO). In vivo NaHS treatment enhanced the activities of phenylalanine ammonia-lyase, cinnamate 4-hydroxylase, p -coumarate:coenzyme A ligase isoenzymes, caffeoyl-CoA-O-methyltransferase, caffeic acid-O-methyltransferase, ferulic acid-5-hydroxylase, cinnamyl-CoA reductase, and cinnamyl-alcohol dehydrogenase. The treatment also facilitated the production of specific phenolic acids, such as cinnamic acid, p -coumaric acid, caffeic acid, ferulic acid, and sinapic acid; total phenolic compounds; p- coumaryl alcohol; coniferyl alcohol; sinapyl alcohol; and lignin. NaHS treatment induced resistance against P. expansum in apples through H2O2- and NO-mediated activation of phenylpropanoid metabolism. [ABSTRACT FROM AUTHOR]

A high fructose diet (HFD) and advanced age are key factors for the gradual loss of physiological integrity of adipose tissue. Endogenous hydrogen sulfide (H2S) has beneficial effects on cytoprotection and redox balance. But its interactive effects on age-related damage of mesenteric vessels and connective and adipose tissues (MA) during HFD which could be the base of the development of effective physiological-based therapeutic strategy are unknown. The aim of study was to investigate age- and HFD-induced mesenteric cellular changes and activities of enzymes in H2S synthesis and to test the effects of sodium hydrosulfide (NaHS) which is considered an H2S donor on them. Adult and aged male rats on a standard diet (SD) or 4-week HFD were exposed to acute water-immersion restraint stress (WIRS) for evaluation of mesenteric subcellular and cellular adaptive responses by electron microscopy. The effects of exogenous NaHS (5.6 mg/kg/day for 9 days) versus vehicle on mesentery changes were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS), thiosulfate-dithiol sulfurtransferase (TST), and sulfite oxidase (SO) were examined by spectrophotometry. In both adult and aged SD groups, treatment with NaHS protected mesenteric cells after WIRS. In both groups, the treatment with NaHS also protected MA mitochondria, microvascular endothelial and sub-endothelial structures, and fibroblasts versus the vehicle-treated group that had signs of damage. HFD increased MA injury and mitochondrial changes in both aged and adult rats. HFD-associated malfunction is characterized by low activities of CSE, CBS, TST, SO, and increased TBARS. Finally, we demonstrated that pretreatment with NaHS inhibited MA and mitochondria alterations in aged rats exposed to HFD and WIRS, lowered TBARS, and enhanced H2S enzyme activities in contrast to the vehicle-treated group. Mitochondrial integrity alterations, endothelial damage, and redox imbalance are key factors for rat mesenteric adipose tissue damage during advanced age. These alterations and MA hypertrophic changes retain the central for HFD-induced damage. Moreover, H2S signaling contributes to MA and mitochondria redox balance that is crucial for advanced age and HFD injury. The future study of H2S donors' effects on mesenteric cells is fundamental to define novel therapeutic strategies against metabolic changes. [ABSTRACT FROM AUTHOR]

As a multifunctional signaling molecule, hydrogen sulfide (H2S) has been reported to induce plant responses to a variety of abiotic stresses. However, there are no reports on H2S treatment inducing resistance in apples against Penicillium expansum, a biotic factor, and its possible mechanism of action. In this study, fumigating apples with 5 mM sodium hydrosulfide (NaHS), the exogenous donor of H2S, for 12 h reduced the diameter of lesions in fruit colonized by P. expansum. NaHS treatment markedly promoted the synthesis of endogenous H2S, hydrogen peroxide (H2O2), and nitrogen oxide (NO). In vivo NaHS treatment enhanced the activities of phenylalanine ammonia-lyase, cinnamate 4-hydroxylase, p-coumarate:coenzyme A ligase isoenzymes, caffeoyl-CoA-O-methyltransferase, caffeic acid-O-methyltransferase, ferulic acid-5-hydroxylase, cinnamyl-CoA reductase, and cinnamyl-alcohol dehydrogenase. The treatment also facilitated the production of specific phenolic acids, such as cinnamic acid, p-coumaric acid, caffeic acid, ferulic acid, and sinapic acid; total phenolic compounds; p-coumaryl alcohol; coniferyl alcohol; sinapyl alcohol; and lignin. NaHS treatment induced resistance against P. expansum in apples through H2O2- and NO-mediated activation of phenylpropanoid metabolism.

Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction.

The use of cyclosporine A (CsA) in transplant recipients is limited due to its side effects of causing severe hypertension. We have previously shown that CsA increases the activity of the epithelial sodium channel (ENaC) in cultured distal nephron cells. However, it remains unknown whether ENaC mediates CsA-induced hypertension and how we could prevent hypertension. Our data show that the open probability of ENaC in principal cells of split-open cortical collecting ducts was significantly increased after treatment of rats with CsA; the increase was attenuated by lovastatin. Moreover, CsA also elevated the levels of intracellular cholesterol (Cho), intracellular reactive oxygen species (ROS) via activation of NADPH oxidase p47phox, serum- and glucocorticoid-induced kinase isoform 1 (Sgk1), and phosphorylated neural precursor cell–expressed developmentally downregulated protein 4–2 (p-Nedd4-2) in the kidney cortex. Lovastatin also abolished CsA-induced elevation of α-, ß-, and γ-ENaC expressions. CsA elevated systolic blood pressure in rats; the elevation was completely reversed by lovastatin (an inhibitor of cholesterol synthesis), NaHS (a donor of H2S which ameliorated CsA-induced elevation of reactive oxygen species), or amiloride (a potent ENaC blocker). These results suggest that CsA elevates blood pressure by increasing ENaC activity via a signaling cascade associated with elevation of intracellular ROS, activation of Sgk1, and inactivation of Nedd4-2 in an intracellular cholesterol-dependent manner. Our data also show that NaHS ameliorates CsA-induced hypertension by inhibition of oxidative stress.

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Objectives. Acute pancreatitis (AP) is a life-threatening condition. Using antioxidants in AP is insufficient and conflicting. Therefore, this study compared the effect of hydrogen sulfide (H2S) donor, sodium hydrosulfide (NaHS), leptin or curcumin pretreatment on AP induced by L-arginine.

Sunflower seeds (hybrid Luka) were primed with water (hydropriming) or sodium hydrosulphide (NaHS) solutions (0.1, 0.5, 1.0 and 1.5 mM NaHS) and subsequently dried to initial moisture content. Unprimed (control) and primed seeds were germinated in a growth chamber on paper towels moistened with water or polyethylene glycol (PEG) 6000 solutions (2.5, 5.0 and 10%), mimicking different drought stress levels. To evaluate the response of the primed seeds to drought in the germination stage, the germination energy (GE), germination rate (SG), seedling fresh mass (SW), hydrogen peroxide and free proline content (PRO), as well as lipid peroxidation rate (malondialdehyde; MDA) were established. The results show strong effects of the imposed drought stress and the metabolic response to oxidative stress through lower germinability and proline accumulation in seedlings. NaHS priming showed some positive effects on seed germination depending on stress level and the concentration of NaHS. Sunflower seeds were also germinated in pots filled with soil, at optimal (70% of field water capacity [FWC 70%]) and drought conditions (FWC 30%), in natural outdoors conditions. When plantlets developed the first pair of leaves, the number of plants (emergence rate [ER]), shoot mass (SM) and leaves mass (LM) were determined, as well as the total activities of catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR) and dehydroascorbate reductase (DHAR). There was a significant influence of an interaction between drought stress and priming, whereas drought stress inhibited plant emergence and early growth (SW and LW), and strong antioxidative enzymatic response to drought stress was clearly established in the leaves. Although seed priming showed some influence on enzyme activities, it was mostly related to seed hydropriming effects, while NaHS seed priming was less effective, influencing only DHAR. Altogether, the results imply that sunflower seed priming with NaHS may not have a prolonged impact on the antioxidative defence mechanism based on CAT and ascorbate/glutathione cycle during sunflower early growth in drought conditions. [ABSTRACT FROM AUTHOR]

Copyright of Agriculture / Poljoprivreda is the property of Josip Juraj Strossmayer University of Osijek, Faculty of Agriculture in Osijek and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

AIMS: Hypoxic ischemic encephalopathy is one of the main causes of neonatal deaths. The objective of this study was to evaluate the neuroprotective effect of antioxidant and anti-inflammatory properties of sodium hydrosulfide (NaHS) in neonatal rats with hypoxic ischemic encephalopathy, as well as its effect on neuronal apoptosis through histopathological and biochemical tests. METHODS: Forty-seven-day-old rats with induced hypoxia-ischemia (HI) were randomly separated into four groups. Half an hour after the induction of hypoxic-ischemia, serum physiological (SF), 50 μmol/kg NaHS, or 100 μmol/kg NaHS were intraperitoneally given to the rats. RESULTS: Apoptotic cells in the brain tissue of rats in HI + NaHS 50 μmol/kg, and HI + NaHS 100 μmol/kg groups decreased compared to HI group (p = 0.00). While HI + NaHS 50 μmol/kg and HI + NaHS 100 μmol/ kg groups yielded no difference in TNF-α, IL-6, and iNOS levels as compared to the HI group, an increase in NGF was detected in the 50 μmol/kg and 100 μmol/kg NaHS groups (p = 0.34, p = 0.24, p = 0.26, p = 0.026, p = 0.017). When TOS, TAS and OSI levels were compared, an increase in TAS and OSI and a decrease in TOS were observed in the treatment groups as compared to HI group. CONCLUSIONS: NaHS given to hypoxic-ischemic encephalopathy model significantly decreased apoptosis in neurons and had a neuroprotective efficacy with an increase in NGF levels (Tab. 1, Fig. 3, Ref. 25). [ABSTRACT FROM AUTHOR]

T cell-mediated adaptive immunity is designed to respond to non-self antigens and pathogens through the activation and proliferation of various T cell populations. T helper 1 (Th1), Th2, Th17 and Treg cells finely orchestrate cellular responses through a plethora of paracrine and autocrine stimuli that include cytokines, autacoids, and hormones. Hydrogen sulfide (H2S) is one of these mediators able to induce/inhibit immunological responses, playing a role in inflammatory and autoimmune diseases, neurological disorders, asthma, acute pancreatitis, and sepsis. Both endogenous and exogenous H2S modulate numerous important cell signaling pathways. In monocytes, polymorphonuclear, and T cells H2S impacts on activation, survival, proliferation, polarization, adhesion pathways, and modulates cytokine production and sensitivity to chemokines. Here, we offer a comprehensive review on the role of H2S as a natural buffer able to maintain over time a functional balance between Th1, Th2, Th17 and Treg immunological responses.

Indigo and indirubin are effective medicinal components in Isatis indigotica and belong to indole alkaloids . 1-Deoxy-D-xylulose reductoisomerase ( DXR), SKikimate kinase (SK) and anthranilate synthase (AS) are three important enzymes in the indole alkaloid synthesis pathway, which is indigo Synthetic precursor of indirubin. This paper analyzes the relative expression of BcSK,BcDXR,BcASAl,BcASA2,and BcASB in leaves and roots of Isatis indigotica by real-time quantitative PCR,and explores the effect of NaHS on its expression. The NaHS concentration was 150 μmol/L,and the treatment time was 3 h,6 h,and 9 h,respectively. The results showed that NaHS (a hydrogen sulfide donor) significantly up-regulated the expression of related genes in leaves and roots of Isatis indigotica at 3 h. Among them, only the relative expression level of BcASB was down-regulated in the leaves, and showed different degrees of inhibition and induction of the expression of pharmacodynamic genes at 6 h and 9 h. In summary, Na HS may increase the content of indigo and indigo red by inducing the expression of the pharmacodynamicgene of lsatis indigotica seedlings, thereby enhancing the effective pharmacodynamic components of Isatis indigotica. [ABSTRACT FROM AUTHOR]

Objective(s): Infertility in varicocele may have an adverse outcome on the future life of an infertile male. This study was designed to investigate whether varicocele affects remote organs, including the kidney, liver, and brain. We have also evaluated the protective effects of NaHS administration on the structure and function of these organs. Materials and Methods: Thirty-six rats were randomly assigned to 3 experimental groups: 1) Sham, 2) Varicocele, and 3) Varicocele + sodium hydrosulfide. Varicocele was induced via partial ligation of the left renal veins. Animals in the Varicocele + sodium hydrogen sulfide group received 30 µmol/l NaHS in drinking water for 56 days. On the 57th day of the treatment, blood samples, as well as kidney, liver, and brain tissues, were collected to assess kidney and liver functions, measurement of oxidative stress markers, and histological changes. For evaluation of sperm parameters caudal epididymis was used. The behavioral tests were performed to evaluate the animal's anxiety-related behaviors. Results: Varicocele caused significant decrease in sperm parameters (motility and viability) and superoxide dismutase activity in the kidney, liver, and brain tissue. Anxiety-related parameters decreased in varicocele. Moreover, varicocele resulted in a significant increase in malondialdehyde levels in the kidney, liver and brain tissue, and liver function enzymes. Varicocele did not alter kidney function parameters. The administration of NaHS improves the above parameters. Conclusion: This study showed that notice to remote organs such as the liver and brain beside reproductive organs in varicocele is important. The administration of NaHS improved remote organ injury in varicocele via its anti-oxidant mechanism. [ABSTRACT FROM AUTHOR]

Copyright of Nonferrous Metals (Mineral Processing Section) is the property of Beijing Research Institute of Mining & Metallurgy Technology Group and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective(s): Transforming growth factor alpha (TGF-α) has been shown to modulate the gastric acid secretion. Therefore, the aim of the present study was to investigate the effect of sodium hydrosulfide (NaHS) on TGF-α expression in gastric mucosa in rats. Materials and Methods: Eighteen rats were randomly divided into 3 groups (6 per group). To determine the effect of NaHS on gene and protein expression of TGF-α in gastric mucosa in response to gastric acid, the acid output induced by gastric distension. At the end of experiment, rats were euthanized by anesthetics, and gastric effluents, in addition to mucosa were collected to measure the pH of gastric effluents and to quantify protein and gene expression of TGF-α. Results: The stimulated gastric acid upregulated expression levels of TGF-α in gastric mucosa. These levels were higher in animals pretreated with NaHS. Conclusion: TGF-α upregulatory effect of sodium hydrosulfate implied that TGF-α is involved in the acid inhibitory effect of NaHS.

Background: Hydrogen sulfide (H2S) has been shown to have a protective role in various kidney disorders. Objectives: This study investigated the molecular mechanism of NaHS (a H2S donor) in treating on the renal damage induced by cisplatin (CP).Materials and Methods: Thirty-two male rats were randomly divided into 4 groups: Normal control group (group A)‚ NaHS group (group B) which received 200 µg/kg/d (intraperitoneal injection; i.p.) for 15 days‚ CP group (group C) which rats were injected with CP (5 mg/kg, single dose, i.p.), and CP + NaHS group (group D) (5 mg/kg and 200 µg/kg, respectively, i.p.). Samples of urine and serum, tissue of kidney were collected for analysis after treatments for 15 days. Morphological changes were elevated under light microscope‚ protein expression of desmin and nephrin were determined by immunohistochemistry and western blotting and also malondialdehyde (MDA) level was determined by spectrophotometer. Results: Compared to the CP group, NaHS treatment mitigated histological damages, decreased 24-hour urine protein excretion, serum urea and creatinine as well as MDA level. NaHS treatment increased protein levels of nephrin. Moreover, NaHS treatment decreased protein levels of desmin. Conclusions: NaHS can ameliorate CP -induced renal damage in rats which is associated with the increase in nephrin protein expression, and the decrease in MDA level and desmin protein expression.

Abstract Hydrogen sulfide (H2S), previously only considered a toxic environmental air pollutant, is now increasingly recognized as an important signaling molecule able to modulate several cellular pathways in many human tissues. As demonstrated in recent studies, H2S is produced endogenously in response to different cellular stimuli and plays different roles in controlling a number of physiological responses. The precise role of H2S in inflammation is still largely unknown. In particular, the role of H2S in the regulation of the inflammatory response in acute and chronic infections is being actively investigated because of its potential therapeutic use. To study the effect of H2S as an anti-inflammatory mediator during bacterial infections, we developed an ex vivo model of primary cells and cell lines infected with Mycoplasma. Our data demonstrate a dichotomic effect of H2S on the NF-kB and Nrf-2 molecular pathways, which were inhibited and stimulated, respectively.

Stem cell therapy represents a promising therapeutic avenue for cardiac disorders, including heart failure. Although stem cell transplantation showed encouraging preliminary results, the outcomes of clinical studies are still unsatisfactory. This study aimed to compare the outcomes of two therapeutic approaches, in vivo co-delivery of sodium hydrogen sulfide (NaHS) concomitant with bone marrow-derived mesenchymal stem cell (BMSC) transplantation and in vitro preconditioning of BMSCs with NaHS, both of which are intended to promote the success of stem cell therapy in rats with isoprenaline-induced heart failure. Heart failure developed 4 weeks after the subcutaneous injection of isoprenaline (170 mg/kg) for 4 consecutive days. The in vivo approach involved the co-delivery of intraperitoneally administered NaHS concomitant with BMSC transplantation for a period of 14 days. The in vitro approach involved preconditioning BMSCs with NaHS for 30 min before transplantation. Compared to treatment with BMSCs alone, in vitro preconditioning of BMSCs with NaHS improved left ventricular function as measured by echocardiography and electrocardiography and enhanced stem cell homing, proliferation and differentiation as manifested by higher cardiac expression of GATA-4 and myocyte enhancer factor 2. Moreover, the measurement of cardiac transforming growth factor beta 1 levels and histopathological investigation revealed mitigated fibrosis and myocardial injury scores. Compared with BMSC therapy alone, the in vivo approach enhanced stem cell homing and differentiation, alleviated fibrosis and augmented vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expression. In conclusion, NaHS can potentiate the efficiency of BMSC therapy for heart failure by in vitro preconditioning or in vivo co-delivery. The in vitro approach is superior with regard to improving cardiac function in addition to enhancing stem cell proliferation, while the in vivo approach is superior with regard to increasing cardiac VEGF and eNOS expression.

Highlights • Hydrogen sulfide (H 2 S) is an important component of cell signalling pathways. • Plants produce H 2 S and use it as an integral part of sulfur metabolism. • H 2 S is produced in response to numerous plant stresses, including heavy metal exposure, temperature, drought and salt stress. • H 2 S may have intracellular effects through the modification of thiols and antioxidants. • Interactions of H 2 S with other reactive signals, such as nitric oxide and reactive oxygen species, need to be considered. Abstract Hydrogen sulfide (H 2 S) is part of a suite of small reactive molecules which are known to be involved in cell signaling events in plants. It is produced by cells, can move around, including through membranes, and can be removed when no longer needed. It is perceived by cells, partly through persulfidation of proteins. Along with nitric oxide (NO) and reactive oxygen species (ROS) H 2 S is involved in a range of stress responses, including following treatment with heavy metals, salt, temperature change and pathogen challenge. H 2 S can lead to changes in the activity of antioxidants, cell signaling proteins such as mitogen activated protein kinases (MAPKs) and gene expression. Understanding how H 2 S fits into cell signaling pathways may lead to advances in how treatment with H 2 S or H 2 S releasing donors may improve plant tolerance to stress, and hence plant growth and agricultural outputs. [ABSTRACT FROM AUTHOR]

Introduction and aim : Hydrogen sulfide (H2S) is an endogenously produced gas-structure mediator. It is proposed to have antioxidant, anti-inflammatory and antiapoptotic effects. Acetaminophen (N-acetyl-P-aminophenol; APAP) is an antipyretic and analgesic medication known as paracetamol. When taken at therapeutic doses there are few side-effects, but at high doses APAP can cause clear liver and kidney damage in humans and experimental animals. In this study, the effects of the H2S donor of sodium hydrosulfide (NaHS) on acute renal toxicity induced by APAP in rats were researched in comparison with N-acetyl cysteine (NAC). Method : Rats were divided into six groups (n = 7) as control. APAP, APAP + NAC, APAP + NaHS 25 µmol/kg, NaHS 50 µmol/kg and NaHS 100 µmol/kg. After oral dose of 2 g/kg APAP, NAC and NaHS were administered via the i.p. route for 7 days. In renal homogenates, KIM-1 (Kidney Injury Molecule-1), NGAL (neutrophil gelatinase-associated lipocalin), TNF-α and TGFβ levels were measured with the ELISA method for tissue injury and inflammation. In renal tissue, oxidative stress levels were identified by spectrophotometric measurement of TAS and TOS. Histopathologic investigation of renal tissue used caspase 3 staining for apoptotic changes, Masson trichrome and H&E staining for variations occurring in glomerular and tubular systems. Results : NaHS lowered KIM-1, NGAL, TNF-α, TGF-β and TOS levels elevated in renal tissue linked to APAP and increased TAS values. NaHS prevented apoptosis in the kidney and was identified to ensure histologic amelioration in glomerular and tubular structures. NaHS at 50 µmol/kg dose was more effective, with the effect reduced with 100 µmol/kg dose. Conclusion : H2S shows protective effect against acute renal injury linked to APAP. This protective effect reduces with high doses of H2S. The anti-inflammatory and antioxidant activity of H2S may play a role in the renoprotective effect. [ABSTRACT FROM AUTHOR]

Highlights • NaHS and Na 2 S augmented high stretch-induced ANP secretion whereas GYY4137 and sodium thiosulfate did not. • NaHS-stimulated ANP secretion was blocked by the pretreatment with inhibitor for K ATP channel, NOS, sGC, PI3K or protein kinase B. • The attenuation of NaHS-induced ANP secretion in ISP-treated rat atria may be due to the low expression of eNOS protein. • These findings clarify that NaHS stimulates ANP secretion through the K ATP channel and PI3K/Akt/NOS/sGC pathway. Abstract Hydrogen sulfide (H 2 S) is normally produced from l -cysteine in mammalian tissues and related to the pathogenesis of cardiovascular diseases. The aim of this study is to investigate the effects of H 2 S donor on atrial natriuretic peptide (ANP) secretion and define its mechanism using normal and isoproterenol (ISP)-treated rats. Several H 2 S donors were perfused into isolated beating rat atria, and atrial pressure (AP) and ANP secretion were measured. NaHS augmented high stretch-induced ANP secretion and decreased AP in a dose-dependent manner. The high stretch-induced ANP secretion was stimulated by Na 2 S but was not changed by GYY4137 and sodium thiosulfate. NaHS and Na 2 S produced very high amount of H 2 S rapidly whereas GYY4137 produced very low amount of H 2 S slowly. NaHS-stimulated ANP secretion was blocked by the pretreatment with inhibitor for K ATP channel, nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC), phosphoinositol 3 kinase (PI3K) or protein kinase B. H 2 S synthesis enzyme inhibitor (DL-propargylglycine) did not show any significant changes in atrial parameters. However, the response of ANP secretion to NaHS markedly attenuated and DL-propargylglycine suppressed ANP secretion in ISP-treated rat atria. The expression of eNOS protein was decreased but the expression of cardiomyocyte-specific H 2 S producing enzyme, cystathione γ-lyase, was not changed in ISP-treated rat atria. The attenuation of NaHS-induced ANP secretion in ISP-treated rat atria may be due to the low expression of eNOS protein. These findings clarify that NaHS stimulates ANP secretion via the K ATP channel and the PI3K/Akt/NOS/sGC pathway in rat atria. [ABSTRACT FROM AUTHOR]

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 (H 2 S), 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 H 2 S 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 H 2 S-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 H 2 S donor on regeneration and the muscle fiber type composition. Overall, the H 2 S 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. [Display omitted] • The expression of H 2 S-generating enzymes is decreased in dystrophic mdx mice. • Markers of dystrophic conditions (CK, LDH, OPN) are improved after treatment with an H 2 S donor. • H 2 S donor exerts anti-inflammatory and anti-oxidative effects. • NaHS restores the expression of key angiogenic mediators in mdx animals and the number of blood vessels. • H 2 S has the potential to alleviate the hallmarks of Duchenne muscular dystrophy. [ABSTRACT FROM AUTHOR]

Introduction: Multiple sclerosis (MS) is generally known as a manageable but not yet curable autoimmune disease affecting central nervous system. A potential therapeutic approach should possess several properties: Prevent immune system from damaging the brain and spinal cord, promote differentiation of oligodendrocyte progenitor cells (OPCs) into mature oligodendrocytes to produce myelin, prevent the formation of fibronectin aggregates by astrocytes to inhibit scar formation, and enhance function of healthy endothelial cells (ECs). Methods: To determine if an increase in sulfur contents through H2S, a potent antioxidant known to induce protective autophagy in cells, could provide the above desired outcomes, peripheral blood mononuclear cells (PBMNCs), OCPs, astrocytes, and ECs were treated with NaHS (50 μM) in vitro. Results: Transmigration assay using EC monolayer showed that serotonin increased migration of PBMNC while pretreatment of EC with NaHS inhibited the migration induced by serotonin treatment. NaHS upregulated proteins involved in immune system response and downregulated PBMNCs- and EC-related adhesion molecules (LFA-1 and VCAM-1). Furthermore, it had a cell expansion inducing effect, altering EC morphology. The effects of NaHS on OPCs and astrocytes were studied compared to mTOR inhibitor rapamycin. In NaHS treated astrocytes the induced fibronectin production was partially inhibited while rapamycin almost fully inhibited fibronectin production. NaHS slowed but did not inhibit the differentiation of OCPs or the production of myelin compared to rapamycin. Conclusion: The in vitro results point to the potential therapeutic application of hydrogen sulfide releasing molecules or health-promoting sulfur compounds in MS.