Na2S Treatment Research Articles

Density functional theory calculation of catalytic sulfidization on the azurite (0 1 1) surface by ammonium salts and its effect on flotation

In this study, we performed microflotation experiments and density functional theory (DFT) calculations to investigate the effect of ammonium salts on azurite sulfidization. The flotation recovery of azurite with ammonium salt and Na2S treatment was higher than that with Na2S treatment alone. The DFT calculation showed that the S atom in HS− could bond to Cu atoms on the azurite (011) surface, i.e., it chemically adsorbed on the azurite (011) surface to form copper sulfide species. In the presence of NH3, the adsorption energy decreased from −149.42 kJ/mol to −187.26 kJ/mol compared with only HS− adsorption, and the bond length of CuS increased from 2.17 Å to 2.30 Å, indicating enhanced adsorption of the S species. The Cu 3d and S 2p energy-level overlap range became wider, and the formed CuS species became complex after catalytic sulfidization by ammonium salts, enhancing the stability of the CuS species. During catalytic sulfidization, NH3 species desorbed from the azurite surface and returned to the solution, so ammonium species acted as a catalyst in azurite sulfidization. This work elucidated the role of ammonium salts in the enhanced sulfidization flotation of azurite at an atomic level and further supplemented our previous experimental statement.

Adsorption characteristics of Cu2+ species on cerussite surfaces and implications for sulfidization flotation

Metal ions are unavoidable in pulp solution, and they frequently influence the flotation recovery of minerals, such as by activation or depression. In this work, we systematically investigated the adsorption characteristics of Cu2+ species on cerussite surfaces and the concomitant effect on sulfidization flotation by micro-flotation experiments and surface analysis. The flotation results indicated that the flotation recovery of cerussite was almost unchanged at low Cu2+ concentration in the presence of Na2S, but it decreased at high Cu2+ concentration. X-ray photoelectron spectroscopy indicated that CuCO3 species formed on cerussite surface in the presence of Cu2+, and Pb–S species and Cu–S species formed after Cu2+–Na2S treatment. Time-of-flight-secondary-ion mass spectrometry indicated that the distribution of lead species narrowed and that of copper species broadened with increasing Cu2+ concentration, which demonstrated that Cu2+ covered the mineral surfaces and inherent Pb2+ was shield. Ultraviolet–visible spectroscopy indicated that the stability of cerussite surface increased with increasing amount of added Na2S. Compared with only Na2S treatment, consumption of xanthate was almost unchanged at low Cu2+ concentration, whereas consumption of xanthate considerably increased at high Cu2+ concentration, which may be because xanthate was consumed by the residual copper ions in the pulp solution. Zeta potential measurements indicated that Cu2+ can chemisorb on cerussite surfaces and increasing the Cu2+ concentration facilitates adsorption of copper species, but it inhibits adsorption of Na2S and BX. Therefore, sulfidization flotation of cerussite is not substantially affected by low concentrations of Cu2+, but is greatly affected by high concentrations of Cu2+.

High-expression and characterization of a novel serine protease from Ornithinibacillus caprae L9T with eco-friendly applications.

In the current work, a novel thermophilic serine protease gene (P3862) from Ornithinibacillus caprae L9T was functionally expressed in Bacillus subtilis SCK6. The monomeric enzyme of about 29 kDa was purified to homogeneity with 43.91% of recovery and 2.81-folds of purification. Characterization of the purified protease revealed the optimum activity at pH 7 and 65 °C. The protease exhibited excellent activity and stability in the presence of Na+, Mg2+, Ca2+, ethanediol, n-hexane, Tween-20, Tween-80 and Triton X-100. P3862 displayed favorable caseinolytic activity, moderate keratinolytic activity but no collagenolytic activity. Besides, the homology model of P3862 possessed a globular configuration and characteristic of α/β hydrolase fold, and displayed stable interactions with casein, glycoprotein and keratin rather than collagen. Moreover, the crude enzyme could completely dehair goatskin within 6 h, resulting in decrease in BOD5, COD and TSS loads by 72.86, 74.07, and 73.79%, respectively, as compared with Na2S treatment. Biocatalytic applications revealed that it could effectively remove egg-stains from fabrics at 37 °C for 30 min with low supplementation (300 U/mL), and was able to degrade the feathers of duck and chicken. Overall, these outstanding properties make P3862 valuable in the development of environmentally friendly biotechnologies .

Enhanced flotation of hemimorphite: Adjusting mineral surface potential with sodium thiocyanate as activator

In this paper, sodium thiocyanate (NaSCN) has been used for the first time as an activator of heteromorphite. In the flotation of heteromorphite, 93% recovery was obtained at the concentration of collector ODA 0.4 × 10–4 mol/L in the presence of NaSCN, while the concentration of collector should be 2.5 × 10–4 mol/L and 0.6 × 10–4 mol/L for the non-activator or Na2S treatment, respectively. The Micro-flotation results showed that heteromorphite can be effectively activated by NaSCN. Nay, the activation effect was better than sodium sulfide, and was slightly affected by activation time. FTIR analysis, Zeta-potential measurements and XPS analysis were conducted to determine the activation mechanism of sodium thiocyanate on heteromorphite. The result of FTIR analysis showed that after NaSCN treatment, the collector ODA can be chemisorbed on the heteromorphite surface via forming zinc-ammonium complex, and physically adsorbed simultaneously by electrostatic attraction. Note that the physisorption effect is more significant. Zeta-potential measurements and XPS analysis showed that the ambidentate ligand SCN− can chemisorbed on the heteromorphite surface via forming zinc-thiocyanate complex anions by S or N elements. What's more, the value of zeta potential of minerals was more negative, which enhanced the physisorption of collector on the mineral surface. Ultimately, the surface hydrophobicity of the heteromorphite was enhanced, and better flotation recovery effect was obtained. The results of this paper can provide a new idea for the activation of minerals.

Modification of malachite surfaces with lead ions and its contribution to the sulfidization flotation

Malachite is a common copper-oxide resource, and it is usually enriched by sulfidization flotation. Its floatability and recovery are greatly determined by the surface sulfidization results. In this paper, Pb(NO3)2 is used to pretreat malachite, and the sulfidization mechanism of malachite was studied through microflotation experiments, zeta-potential determination, adsorption tests, XPS and ToF-SIMS. The flotation and adsorption results show that the malachite floatability after pretreatment with Pb ions improved significantly. Compared with Na2S treatment, the maximum recovery increased by 42.6% after treatment with lead ions and Na2S. The zeta potential results showed that lead ions (such as Pb(OH)+) could adsorb on the malachite surface, and the surface active sites of malachite were increased. XPS results indicate that lead ions adsorbed onto the mineral surface through the interaction between Pb species, S species and O species. The formation for new species (such as Pb-S) enhanced the malachite sulfidization. ToF-SIMS was used to visualize the three-dimensional distribution of lead- and sulfur-species adsorbed on the malachite surface. It demonstrated that the sulfidization layer increased after pretreatment with Pb(NO3)2, facilitating the surface hydrophobicity and flotation recovery of malachite.

Hydrogen Sulfide Therapy Suppresses Cofilin-2 and Attenuates Ischemic Heart Failure in a Mouse Model of Myocardial Infarction.

Hydrogen sulfide (H2S) protects against ischemic and inflammatory injury following myocardial ischemia via induction of microRNA (miR)-21. We sought to determine whether H2S attenuates ischemic heart failure with reduced ejection fraction (HFrEF) and interrogate the role of cofilin-2, a target of miR-21, in this protective process. Adult male mice underwent myocardial infarction (MI) by coronary artery ligation after baseline echocardiography. Following MI, mice were treated with Na2S (100 μg/kg/day; intraperitoneal [IP]) or saline up to 28 days. End-diastolic pressure, measured by Millar catheter, was significantly increased (P < .05 vs sham) at 3 days post-MI in the saline group, which was attenuated with Na2S. Left ventricular (LV) fractional shortening decreased significantly at 28 days post-MI in the saline group but was preserved with Na2S and LV infarct scar size was smaller in Na2S group as compared to control. Apoptotic signaling, measured by Bcl-2/Bax ratio, was significantly increased in the saline group but was mitigated with Na2S. Survival rate was 2-fold higher in Na2S group compared to saline control (P < .05). Proteomic analysis and Matrix-Assisted Laser Desorption/Ionization-Time of Flight (TOF)/TOF tandem mass spectrometry identified significant changes in proapoptotic cofilin-2 expression, a specific target of miR-21, between saline- and sodium sulfide -treated mice at 28 days post-MI. Western blot analysis confirmed a significant increase in cofilin-2 after MI, which was suppressed with Na2S treatment. Chronic Na2S treatment also attenuated inflammasome formation and activation leading to reduction of maladaptive signaling. Na2S treatment after MI preserves LV function and improves survival through attenuation of inflammasome-mediated adverse remodeling. We propose H2S donors as promising therapeutic tools for ischemic HFrEF.

Significant photoluminescence enhancement in WS2 monolayers through Na2S treatment.

Tungsten disulfide monolayers have attracted extensive attention in nanoelectronics and optoelectronics applications due to their remarkable electronic and optical properties. High-quality WS2 monolayers with a scalable size and uniform thickness can be synthesized by a chemical vapor deposition method (CVD). However, they commonly contain intrinsic structural defects and different populations of charge carriers, which are responsible for different contributions of excitons, trions, and biexcitons to their photoluminescence (PL) emission. Here, we adopt sodium sulphide (Na2S) solution to chemically treat CVD-grown WS2 monolayers by a simple immersing method. The results show that WS2 monolayers have a significantly enhanced PL emission by a factor of 25-fold and an obvious red-shift of the PL wavelength, resulting from the different excitonic states induced by effective n-type doping after Na2S treatment. This work provides a simple but promising chemical doping route to significantly improve the optical properties of WS2 monolayers and paves the way for the realization of practical WS2 monolayer based optoelectronic applications.

Toxic effects and possible mechanisms of hydrogen sulfide and/or ammonia on porcine oocyte maturation in vitro

Previous studies suggest that hydrogen sulfide (H2S) and ammonia (NH3) are two major air pollutants which can cause damage to porcine health. However, the mechanisms underlying toxic effects of these compounds on porcine oocyte maturation are not clear. To clarify the mechanism, we evaluated the oocyte quality by detecting some events during oocytes maturation. In our study, porcine oocytes were cultured with different concentrations of Na2S and/or NH4Cl in vitro and the rate of the first polar body extrusion decreased significantly. Also, actin filament was seriously disrupted to damage the cytoskeleton which resulted in reduced rate of oocyte maturation. We explored the reactive oxygen species (ROS) generation and found that the ROS level was increased significantly after Na2S treatment but not after NH4Cl treatment. Moreover, early stage apoptosis rate was significantly increased and autophagy protein LC3 B expression level was higher in oocytes treated with Na2S and/or NH4Cl, which might be caused by ROS elevation. Additionally, exposure to Na2S and/or NH4Cl also caused ROS generation and early apoptosis in cumulus cells, which might further affect oocyte maturation in vitro. In summary, our data suggested that exposure to H2S and/or NH3 decreased porcine oocyte maturation in vitro, which might be caused by actin disruption, ROS generation, early apoptosis and autophagy.

2014 AHA Late-Breaking Basic Science Abstracts

### 24178 ### MAVS Mediates Protection against Myocardial Ischemic Injury with Hydrogen Sulfide David Durrant, Adolfo G Mauro, Juan Valle Raleigh, Anindita Das, Jun He, Khoa Nguyen, Stefano Toldo, Antonio Abbate, Fadi N Salloum; Virginia Commonwealth Univ, Richmond, VA Background : Hydrogen sulfide (H2S) has been shown to protect against myocardial ischemic and inflammatory injury in part by preserving mitochondrial integrity. Since mitochondrial antiviral signaling (MAVS) protein has been implicated in attenuating Bax-mediated cytochrome c release from mitochondria caused by oxidative stress or ischemia, we sought to determine whether MAVS mediates the cardioprotective effects of H2S. Methods and Results : After baseline echocardiography, adult male wild type (WT) or MAVS KO mice underwent myocardial infarction (MI) by coronary artery ligation for 30 min. followed by 24 h reperfusion. Mice were pretreated with Na2S (100 μg/kg; ip ) or saline 1 h before MI. Infarct size, measured with TTC staining, was reduced and LV fractional shortening (FS) was preserved with Na2S at 24h post MI in WT mice as compared to saline-treated mice, but not in MAVS KO mice (Figs. A and B). The risk area was not different between the groups. Western blot analysis revealed a significant decline in myocardial MAVS expression at 24h post MI, which was preserved with Na2S (Fig. C). Another subset of mice was subjected to permanent coronary artery occlusion and treated with Na2S or saline daily for 28 days. LVFS decreased significantly at 28 days post-MI in the saline group, but was significantly preserved with Na2S (Fig. D). Moreover, LV infarct scar size, assessed by trichrome staining, was smaller in Na2S group (22.4 ± 2.7%) as compared to control (33.5 ± 2.1%, P<0.05). Survival rate was 2 fold higher with Na2S compared to saline (P<0.05). Western blot analysis confirmed a significant …

Effects of sulfide reduction on adsorption affinities of colloidal graphene oxide nanoparticles for phenanthrene and 1-naphthol

The abiotic transformation of nanomaterials in the natural environment can significantly affect their fate, transport, and effects. We observed that the adsorption affinities of graphene oxide nanoparticles (GONPs) for both phenanthrene and 1-naphthol were profoundly enhanced in the presence of sulfide, an environmentally relevant reductant, with doses as low as 0.5 mM Na2S per 10 mg/L GONPs. For phenanthrene adsorption enhancement was predominantly caused by the increased surface hydrophobicity from Na2S treatment. For 1-naphthol, however, adsorption enhancement was caused mainly by the conversion of the epoxy/ether groups on the surface of graphene oxide (GO) to the phenolic hydroxyl and carbonyl groups, which allowed more significant H-bonding between 1-naphthol and GONPs. The findings of this study underline that abiotic transformation of GO not only affects the stability and mobility of GONPs, but also influences the adsorptive interactions between GONPs and environmental contaminants, and consequently, may increase the environmental risks of GONPs.

N-(2-hydroxy phenyl) acetamide produces profound inhibition of c-Fos protein and mRNA expression in the brain of adjuvant-induced arthritic rats

Chronic pain and cognitive decline are characteristic symptoms of rheumatoid arthritis. One of the immediate early gene c-fos is overexpressed during peripheral and central noxious conditions and can be used as a marker for neuronal activity/excitability. In the adjuvant-induced arthritis Sprague-Dawley rat model, we examined the dynamics of c-Fos protein and mRNA expression in the amygdala, cortex, hippocampus, and thalamus and evaluated the effects of N-(2-hydroxy phenyl) acetamide (NA-2), a derivative of salicylic acid. The paw volume was assessed as an indicator of peripheral edema and the hyperalgesia associated with arthritis was monitored by gait analysis. The region of interests of the brain from arthritic and non-arthritic animals were used to isolate the RNA and were then reverse transcribed into cDNA. The PCR products were electrophoresed on 1% agarose gel and the gels were visualized in gel-doc system. The frozen brain sections were stained for c-Fos using immunohistochemistry. Negative control experiments were performed without the primary and secondary antibodies to rule out the nonspecific tissue binding of antibodies. We report a significant increase in the c-Fos expression in the arthritic control animals. In comparison to the control group, the treatment of NA-2 treatment was found to block the development of the arthritis-induced c-Fos protein and mRNA expression and peripheral edema. It also significantly reduces the gait deficits which were otherwise observed in the arthritic control group. Both the immunohistochemistry and PCR analysis revealed NA-2 to be more potent in comparison to member of non-steroidal anti-inflammatory drug.

P35 Sodium sulfide therapy attenuates myocardial ischemia–reperfusion injury in the type-2 diabetic heart via the activation of Nrf2 signaling

Background Hydrogen sulfide (H2S) therapy protects non-diabetic animals in various models of myocardial injury, including acute myocardial infarction and heart failure. However, it has yet to be determined if H2S therapeutic strategies have similar cardioprotective effects in the setting of type-2 diabetes. Here we sought to examine if H2S therapy could provide cardioprotection in the db/db diabetic mouse model. Methods Diabetic (db/db; 12 weeks of age) mice were subjected to transient myocardial ischemia for a period of 30 min followed by reperfusion. Sodium Sulfide (Na2S) or vehicle (saline) was administered either daily for 7 days before ischemia or 24 h prior to ischemia. Results Na2S therapy significantly decreased myocardial injury in the db/db diabetic mouse, as evidenced by a reduction in infarct size, circulating troponin-I levels, oxidative stress, and cleaved caspase-3 expression. In an effort to evaluate the signaling mechanism responsible for the observed cardioprotection, mice were administered (via tail vein) a single injection of Na2S or daily injections of either vehicle or Na2S for 7 days. Heart tissue was then excised and processed for Western blot analysis. Analysis uncovered a complication in the ability of Na2S to activate a Nuclear factor erythroid 2-related factor (Nrf2) signaling cascade in the diabetic heart. Specifically, the results indicate that the ability of Na2S to increase the nuclear localization of Nrf2 is not altered by diabetes. However, we did find that diabetes impaired Nrf2 transcriptional activity, as evidenced by the finding that it takes 7 days of Na2S therapy to increase Heme oxygenase-1 (HO-1) levels in the diabetic heart. Further analysis revealed that Nrf2 was unable to bind to the antioxidant response element (ARE). This appears to have been caused by Bach1, a known repressor of HO-1 transcription, as evidenced by the increased levels of Bach1 in the nucleus of the diabetic heart and the finding that 7 days of Na2S treatment reduced its nuclear expression. Conclusions Our findings demonstrate that Na2S therapy attenuates myocardial ischemia–reperfusion injury in the db/db diabetic mouse model, confirming the therapeutic potential of using Na2S to treat a heart attack in the setting of diabetes. Our results also demonstrate that Na2S activates Nrf2 signaling in the diabetic heart by removing Bach1 from the nucleus.

Abstract 96: Thioredoxin-1 Is Essential for Hydrogen Sulfide-Mediated Cardioprotection in the Setting of Ischemic-Induced Heart Failure

Background: Numerous studies have reported the cytoprotective effects of hydrogen sulfide (H2S) in various models of myocardial injury. Here we examined the role that thioredoxin-1 (Trx1) plays in mediating the protective effects of H2S in a model of heart failure. Methods and Results: Mice were subjected to 60 min of left coronary artery ischemia followed by 4 wks of reperfusion (R) at which time left ventricular dimensions and function were assessed. Mice received saline (Veh) or H2S in the form of sodium sulfide (Na2S, 100 μ g/kg) at the time of R followed by daily i.v. injections for the first 7 days of R. Mice treated with Na2S experienced less left ventricular dilatation and hypertrophy, displayed improved left ventricular ejection fraction, and displayed improved contractility and relaxation when compared to Veh-treated mice. Studies aimed at evaluating the underlying cardioprotective mechanisms found that Na2S treatment increased the expression of Trx1. Further analysis revealed that this was accompanied by an increase in phosphorylation of apoptosis signaling kinase-1 (ASK1) at serine residue 966 (inhibitory site), as well as a decrease in the phosphorylation of JNK and p38 (downstream targets of ASK1). We also found that Na2S treatment did not improve cardiac dilatation, cardiac dysfunction, or cardiac hypertrophy in cardiac specific Trx1 dominant negative transgenic (Trx1 dnTg) mice when compared to Veh-treated mice. Conclusion: These findings provide important information that the upregulation of cardiac Trx1 by H2S in the setting of ischemic-induced heart failure sets into motion events, including ASK1 inhibition, which ultimately leads to cardioprotection.

CARDIOPROTECTION BY HYDROGEN SULFIDE

CARDIOPROTECTION BY HYDROGEN SULFIDE