Hydrogen Sulfide Levels Research Articles

Improving Air Quality in Broiler Rooms Using an Electrostatic Particle Ionization System

Highlights An EPI system reduced PM and bacteria in broiler houses by up to 50% and 48%, on average, respectively. The system had no significant effect on animal productivity. The performance of the system decreased towards the end of the rearing cycle. Abstract. Air quality in poultry operations is important for animal and human health. This study evaluated an electrostatic particle ionization (EPI) system for improving air quality in mechanically ventilated broiler rooms (11.7 m long, 6.4 m wide, and 2.9 m high), each with 800 birds. The study evaluated the impact of the EPI system on the levels of particulate matter (PM), ammonia (NH3), and hydrogen sulfide (H2S), as well as on animal performance. On average, the EPI system reduced PM fractions (PM1, PM2.5, PM4, PM10, and PM15) by approximately 50%. Average reductions for total PM and bacteria were 40% and 48%, respectively. No significant reduction was observed for NH3, and no measurable H2S was detected during the entire study period. No significant effects on feed conversion ratio and animal mortality were observed. Reductions in PM and total culturable bacteria decreased over time, which could possibly be due to increased contaminant concentration, ventilation rate, and accumulated dust on collection surfaces towards the end of the rearing cycle. Further assessments are required to determine if additional EPI units or collection surfaces could improve the efficiency of the system. Overall, the system reduced airborne PM and bacteria and improved the air quality in broiler houses. Keywords: Animal performance, Air quality, Bacteria, Broiler houses, Electrostatic particle ionization, Particulate matter.

Protective Effect of Sodium Hydrosulfide on Lipopolysaccharide Induced Myocardial Cell Injury Model: Involvement of Oxidative Stress and Endoplasmic Reticulum Stress

Lipopolysaccharide can induce myocardial cell injury, which has been widely used in the preparation of septic cardiomyopathy models. We herein aimed to evaluate the protective effects of sodium hydrosulfide against oxidative stress and endoplasmic reticulum stress on the cell model of septic cardiomyopathy and to explore whether the protein kinase RNA-like endoplasmic reticulum kinase-eukaryotic initiation factor 2 alpha signaling pathways was involved. The sepsis induced cardiomyopathy model which was established by inducing rat cardiomyoblast cell line H9c2 cells with lipopolysaccharide and sodium hydrosulfide and endogenous hydrogen sulfide inhibitor (DL-propargylglycine) were used for intervention treatment. Then, cell viability, endogenous hydrogen sulfide levels, lactate dehydrogenase, reactive oxygen species, superoxide dismutase, glutathione and malondialdehyde were determined using commercial assay kits; enzyme-linked immunosorbent assay was used to determine creatine kinase-myoglobin binding, interleukin-6, tumor necrosis factor alpha and interleukin-10; reverse transcription-polymerase chain reaction was used to determine cystathionine gamma-lyase messenger RNA expression; and Western blot was used to determine glucose-regulated protein 78, protein kinase RNA-like endoplasmic reticulum kinase, phosphorylated protein kinase RNA-like endoplasmic reticulum kinase, eukaryotic initiation factor alpha, phosphorylated eukaryotic initiation factor alpha, activating transcription factor 4 and C/EBP-homologous protein levels. Sodium hydrosulfide increased the hydrogen sulfide contents of cells, but did not affect the messenger RNA expression of cystathionine gamma-lyase. It attenuated the decrease in cell viability caused by lipopolysaccharide; reduced the release of the myocardial enzymes like lactate dehydrogenase and creatine kinase-myoglobin binding; reduced the level of inflammatory factors like interleukin-6 and tumor necrosis factor alpha; reduced the level of oxidative stress; inhibited the expression of protein kinase RNA-like endoplasmic reticulum kinase pathway proteins. Sodium hydrosulfide treatment improves septic cardiomyopathy by inhibiting oxidative stress and endoplasmic reticulum stress via the protein kinase RNA-like endoplasmic reticulum kinaseeukaryotic initiation factor alpha pathway, which may be a theory for the treatment of septic cardiomyopathy.

The level of hydrogen sulfide and morphological changes in the aorta of rats under the influence of vitamin D under the conditions of modulation of the H2S / cystathionine-γ-lyase system

Annotation. Vitamin D and hydrogen sulfide (H2S) belong to pleitropic regulators, which are involved in the control of many cellular functions and biochemical processes, determine the adaptive potential of the cardiovascular system. The relationship between vitamin D and the H2S system is not fully investigated. The aim of the study was to evaluate the effect of the active form of vitamin D - calcitriol (1,25 (OH)2D3) on the morphological state of the thoracic aorta of rats and the level of it’s saturation with hydrogen sulfide under the conditions of the H2S / cystathionine-γ-lyase system modulation. The experiments were performed on 90 white male laboratory rats in accordance with the principles of bioethics (Strasbourg, 1986). 1,25(OH)2D3 was administered in doses of 0.1 μg/kg and 1 μg/kg for 4 weeks. Propargylglycine (50 mg/kg) and NaHS (1 mg/kg) were used to modulate the state of the H2S/cystathionine-γ-lyase system. The content of H2S was determined in the thoracic aorta and morphological changes were evaluated. Statistical calculations were performed in IBM Statistics SPSS 26, differences were evaluated in the Mann-Whitney test at the significance level of p<0.05. It was established that 1,25 (OH)2D3 in a dose of 1.0 μg/kg leads to the formation of H2S deficiency and a complex of morphological changes in the aorta, which are manifested by damage of epithelial cells and stromal elements, and the formation of calcifications. Modulation of the H2S / cystathionine-γ-lyase system is a factor that modifies the effect of high doses of 1,25 (OH)2D3 on vessels: H2S deficiency increases damage of the vascular wall, while increasing tissue H2S saturation has the opposite effect. 1,25 (OH)2D3 in a dose of 0.1 μg/kg shows the ability to increase the level of endogenous H2S and reduces the development of pathological changes in blood vessels under the conditions of long-term inhibition of the H2S / cystathionine-γ-lyase system.

Improvement of the technology of disposal of pig waste products at the industrial complex

The aim. To determine the degree of completeness of air purification and the suitability of the developed experimental samples of the chamber for its use to reduce the content of polluting gases during the removal of air from the premises of the industrial complex. Methods. The research was conducted on the basis of the pig farm of Agroprime Holding LLC of the Odesa region. The determination of the level of methyl mercaptan (mg/m3) in air emissions outside the premises was carried out using a portable gas analyzer Dräger X-am 5600. The determination of the level of ammonia (mg/m3), hydrogen sulfide (mg/m3) was carried out using a portable multi-component gas analyzer ANKAT - 7664 Micro. The measurement of the content of polluting gases in the air before and after passing the air through the purification chamber was carried out in the pig fattening shop of the pig complex. The concentration level of ammonia and hydrogen sulfide was recorded using a certified and certified device: a multicomponent individual alarm-analyzer of gases "DOZOR-S-M". The results. It was established that the level of hydrogen sulfide in the air of the room at a height of 0.5 m from the floor was 3.34 mg/m3, above the manure bath – 9.72, at the entrance to the upper filter from below - 2.46, at the entrance to the upper filter from the side – 3.03, at the exit from the air exchange shafts on the roof – 2.83, and at the entrance to the side filter – 5.66 mg/m3. The level of ammonia at a height of 0.5 m from the floor was 1.84 mg/m3, above the manure bath – 5.28, at the entrance to the upper filter from below – 1.34, at the entrance to the upper filter from the side – 1.64, at the exit from the air exchange ventilation shaft on the roof – 1.54, at the entrance to the side filter – 3.08 mg/m3. Hydrogen sulfide and ammonia were not detected at the exit from the ventilation ducts, where air purification chambers were installed. Conclusions. The obtained results indicate that, during the tests, the air contaminated with foul-smelling gases, after passing through the purification chamber, was completely freed from gases, and the presence of ammonia and hydrogen sulfide was not detected either by apparatus or organoleptically. Purification of polluted indoor air with the help of a developed chamber makes it possible to completely remove ammonia and hydrogen sulfide. Therefore, it is possible to ventilate the premises without polluting the environment. Key words: pig complex, pig farm, air pollution, hydrogen sulfide, ammonia, air purification, ecological state of the environment

Theoretical investigation on FRET strategy of ratio metric fluorescent probe sensing hydrogen sulfide

The level of hydrogen sulfide (H2S) in human body is related to many diseases, such as Alzheimer's disease, Down syndrome, etc. Therefore, the detection of H2S level in biological systems is very important and has attracted great attention from scientific and clinical researchers. Understanding the design and working mechanism of fluorescent probes for H2S level detection is important for building new highly efficient fluorescent probe. The mechanisms of a recently reported efficient small molecule fluorescent probe based on the Fluorescence Resonance Energy Transfer (FRET) were investigated thoroughly in this work. The theoretical results would provide the insights for designing new efficient and multi-functional fluorescent probe applicable in the biological systems.

MLN-4760 Induces Oxidative Stress without Blood Pressure and Behavioural Alterations in SHRs: Roles of Nfe2l2 Gene, Nitric Oxide and Hydrogen Sulfide.

Reduced angiotensin 1-7 bioavailability due to inhibition of angiotensin-converting enzyme 2 (ACE2) may contribute to increased mortality in hypertensive individuals during COVID-19. However, effects of ACE2 inhibitor MLN-4760 in brain functions remain unknown. We investigated the selected behavioural and hemodynamic parameters in spontaneously hypertensive rats (SHRs) after a 2-week s.c. infusion of MLN-4760 (dose 1 mg/kg/day). The biochemical and molecular effects of MLN-4760 were investigated in the brainstem and blood plasma. MLN-4760 had no effects on hemodynamic and behavioural parameters. However, MLN-4760 increased plasma hydrogen sulfide (H2S) level and total nitric oxide (NO) synthase activity and conjugated dienes in the brainstem. Increased NO synthase activity correlated positively with gene expression of Nos3 while plasma H2S levels correlated positively with gene expressions of H2S-producing enzymes Mpst, Cth and Cbs. MLN-4760 administration increased gene expression of Ace2, Sod1, Sod2, Gpx4 and Hmox1, which positively correlated with expression of Nfe2l2 gene encoding the redox-sensitive transcription factor NRF2. Collectively, MLN-4760 did not exacerbate pre-existing hypertension and behavioural hyperactivity/anxiety in SHRs. However, MLN-4760-induced oxidative damage in brainstem was associated with activation of NO- and H2S-mediated compensatory mechanisms and with increased gene expression of antioxidant, NO- and H2S-producing enzymes that all correlated positively with elevated Nfe2l2 expression.

Variability in Background Urinary Concentrations of the Hydrogen Sulfide Biomarker Thiosulfate.

Hydrogen sulfide is a toxic gas at high concentrations but has recently attracted attention as a naturally produced gaseous signaling molecule in various tissues of the human body, playing key physiological roles at low nanomolar concentrations. This has wide implications for chronic exposure to this gas in air at low levels far below toxicity. Thiosulfate is the currently used biomarker for exposure to hydrogen sulfide via inhalation but has been mainly employed for acute exposure. It is unknown how background thiosulfate concentrations vary on an intraindividual and interindividual basis in humans at normal ambient hydrogen sulfide levels (<1 μg m-3), which is key for the interpretation of its levels as biomarker for low-level hydrogen sulfide exposure. In the current work, the variability in thiosulfate urinary excretion in a total of 168 urine samples collected from eight volunteers over a period of 8 weeks was investigated. The determination of thiosulfate in urine was carried out by UHPLC-MS/MS. The total average concentration ± SD was 16 ± 6 μM (n = 168). Average urinary thiosulfate concentrations in the studied volunteers were within the range of 10-20 μM, but it was found that urinary thiosulfate can show significant day-to-day and week-to-week variability in some individuals (up to 10-fold), despite adjusting for urine specific gravity. In light of the presented variability data and previous studies about the lack of consistent response of thiosulfate to low levels of hydrogen sulfide inhalation exposure, and based on a review of the biochemistry of the production of thiosulfate and its various biological sources, it can be argued that thiosulfate might not be suitable as a biomarker for chronic environmental exposure to low levels of hydrogen sulfide via inhalation.

Changes in the Metabolism of Nitric Oxide, Hydrogen Sulfide of the Oral Fluid Taking into Account Age and Dental Status

The relevance of the study is conditioned by the prevalence of dental pathology, its complicated course in senior age and the search for the age-associated metabolic markers of oral fluid.&#x0D; Objective. The aim of the study is: to determine the age peculiarities of the content of nitric oxide and hydrogen sulfide metabolism in the oral fluid of patients, taking into account their dental status.&#x0D; Materials and Methods. Indicators of nitric oxide metabolism, L-arginine/arginase, hydrogen sulfide content in oral fluid, dental status of different aged people under conditions of intact dentitions, their defects and against the background of correction with different types of dentures, were studied.&#x0D; Results. It was determined that with age, changes in oral fluid are characterized by an increase in nitrite ion, the amount of nitrites and nitrates, increasing the formation of peroxynitrite against the background of lower levels of L-arginine and hydrogen sulfide, inhibition of arginase activity. The results obtained are confirmed by the presence of close correlations between the concentrations of hydrogen sulfide and peroxynitrite (reverse, strong), caries intensity and: the total level of nitrites and nitrates (direct, strong), peroxynitrite content (direct, medium strength).&#x0D; Conclusion. The studied biomarkers of oral fluid depend more on age, hygienic condition of the oral cavity, intensity of dental caries and defects of dentitions than types of dentures. Therefore, age-related changes in the biochemical composition of oral fluid, metabolic, somatic, comorbid pathologies are likely to be a trigger for structural-functional disorders of the dental-maxillofacial system.

Hydrogen sulfide and miR21 are suitable biomarkers of hypoxic exposure.

Hypoxia is the reduction of alveolar partial pressure of oxygen ([Formula: see text]). Military members and people who practice recreational activities from moderate to high altitudes are at risk for hypoxic exposure. Hypoxemia's signs and symptoms vary from asymptomatic to severe responses, such as excessive hypoxic ventilatory responses and residual neurobehavioral impairment. Therefore, it is essential to identify hypoxia-induced biomarkers to indicate people with exposure to hypoxia. Advances have been made in understanding physiological responses to hypoxia, including elevations in circulating levels of endothelin 1 (ET-1) and microRNA 21 (miR-21) and reduction in circulating levels of hydrogen sulfide (H2S). Although the levels of these factors change upon exposure to hypoxia, it is unclear if these changes are sustained on return to normoxia. We hypothesize that hypoxia-induced ET-1 and miR-21 remain elevated, whereas hypoxia-reduction in H2S sustains after returning to normoxic conditions. To test this hypothesis, we exposed male rats to 6 h of 12% O2 and measured circulating levels of ET-1 and miR-21, pre, during, and posthypoxia. We found that ET-1 plasma levels increased in response to hypoxia but returned to normal levels within 30 min after the restoration of normoxia. miR-21 plasma levels and transdermal H2S emissions decreased in response to hypoxia, remaining decreased on return to normoxia, thus following the biomarker criteria. Therefore, this study supports a unique role for plasma miR21 and transdermal H2S as hypoxia biomarkers that could be used to identify individuals after exposure to hypoxia.

Targeting hepatic sulfane sulfur/hydrogen sulfide signaling pathway with α-lipoic acid to prevent diabetes-induced liver injury via upregulating hepatic CSE/3-MST expression

BackgroundDiabetes-induced liver injury is a complication of diabetes mellitus of which there are no approved drugs for effective treatment or prevention. This study investigates possible hepatoprotective effect of alpha-lipoic acid (ALA), and sulfane sulfur/hydrogen sulfide pathway as a novel protective mechanism in a rat model of type 2 diabetes-induced liver injury.MethodsThirty Sprague–Dawley rats underwent fasting for 12 h after which fasting blood glucose was measured and rats were randomly assigned to diabetic and non-diabetic groups. Type 2 diabetes mellitus (T2DM) was induced in diabetic group by administration of nicotinamide (110 mg/kg) and streptozotocin (55 mg/kg). Diabetic rats were treated daily with ALA (60 mg/kg/day p.o.) or 40 mg/kg/day DL-propargylglycine (PPG, an inhibitor of endogenous hydrogen sulfide production) for 6 weeks and then sacrificed. Liver, pancreas and blood samples were collected for analysis. Untreated T2DM rats received distilled water.ResultsHypoinsulinemia, hyperglycemia, hepatomegaly and reduced hepatic glycogen content were observed in untreated T2DM rats compared to healthy control group (p < 0.001). Also, the pancreas of untreated T2DM rats showed severely damaged pancreatic islets while liver damage was characterized by markedly increased hepatocellular vacuolation, sinusoidal enlargement, abnormal intrahepatic lipid accumulation, severe transaminitis, hyperbilirubinemia, and impaired hepatic antioxidant status and inflammation compared to healthy control rats (p < 0.01). While pharmacological inhibition of hepatic sulfane sulfur/hydrogen sulfide with PPG administration aggravated these pathological changes (p < 0.05), ALA strongly prevented these changes. ALA also significantly increased hepatic expression of hydrogen sulfide-producing enzymes (cystathionine γ-lyase and 3-mecaptopyruvate sulfurtransferase) as well as hepatic sulfane sulfur and hydrogen sulfide levels compared to all groups (p < 0.01).ConclusionsTo the best of our knowledge, this is the first experimental evidence showing that ALA prevents diabetes-induced liver injury by activating hepatic sulfane sulfur/hydrogen sulfide pathway via upregulation of hepatic cystathionine γ-lyase and 3-mecaptopyruvate sulfurtransferase expressions. Therefore, ALA could serve as a novel pharmacological agent for the treatment and prevention of diabetes-induced liver injury, with hepatic sulfane sulfur/hydrogen sulfide as a novel therapeutic target.

Utilisation of Ammonium Carbonate in a Solid Oxide Cell

In this work, the utilisation of aqueous ammonium carbonate, (NH4)2CO3, has been investigated as a fuel for solid oxide cell technology for the first time. In its pure form, ammonium carbonate is a solid white power that can easily be stored. It is easily dissolved in water to create an ammonium-rich aqueous solution and can therefore potentially be utilised as a fuel for solid oxide cell technology 1. Aqueous ammonium carbonate is produced as a waste stream from the coke production processes required for steelmaking. Coke is needed as a fuel for blast furnaces and is typically produced via dry distillation of coal in the absence of oxygen, which yields a waste gas stream known as coke oven gas (COG). Cleaning and treatment of COG yields an aqueous waste stream containing ammonia (28 wt%), water (61 wt%), phenol-based tars (5 wt%), carbon dioxide (3.9 wt%), hydrogen sulfide (0.6 wt%) and trace levels of hydrogen cyanide and sodium hydroxide. Due to the presence of carbon dioxide, a significant fraction of the ammonia is present in the form of ammonium carbonate. Significant amounts of COG are produced due to steelmaking, with 44,000 Nm3 produced every hour at the Tata Steel Port Talbot (UK) site alone, corresponding to 264 kg of ammonia every hour 2. Presently, ammonia waste is disposed via incineration, wasting energy and a valuable resource, and contributing to air pollution and greenhouse gas emissions.Ammonia is a well-established chemical commodity used mainly for the manufacture of mineral fertiliser 3. Recently, ammonia has gained more interest in the energy sector since it is a carbon-free hydrogen carrier and can be used directly and efficiently in fuel cells and gas turbines without emitting CO2 4. It also has a high energy density (12.7 MJ L-1) and its storage as a liquid requires less energy-intensive conditions (-33 ˚C) in comparison with hydrogen (-253 ˚C) 5. The high volumetric hydrogen density of ammonia (17.8 wt%) and ease of liquefication make it ideal for capturing, storing, and transporting hydrogen.This work investigates the utilisation of aqueous ammonium carbonate solutions in a solid oxide cell. The electrical performance and gaseous outputs of an anode-supported solid oxide cell operating in fuel cell and electrolysis mode at 750 °C have been established. The cell performance was characterised by current-voltage (I-V) curves and the dried gaseous outputs were characterised by online quadrupole mass spectrometry (QMS).QMS measurements showed that upon delivery to the anode, ammonium carbonate decomposed to form gaseous hydrogen, carbon dioxide and nitrogen, with no NO x emissions detected. No carbon monoxide was detected due to the presence of the water-gas shift reaction. In fuel cell mode, QMS measurements showed the cell utilised hydrogen to produce electrical power. The I-V curves (see Figure) showed the electrical power output was lower than pure hydrogen, due to greater open circuit voltage and concentration losses caused by dilution of hydrogen in the steam, carbon dioxide and nitrogen present. The activation losses observed under aqueous ammonium carbonate were very low.In electrolysis mode, the cell utilised steam to produce hydrogen, which was diluted in carbon dioxide and nitrogen. At 1.4 V, QMS measurements showed the output gases were composed of 60 vol% hydrogen, 29 vol% nitrogen and 11 vol% carbon dioxide. No co-electrolysis of carbon dioxide was observed, and no carbon monoxide was produced. The main losses under ammonium carbonate were ohmic overpotentials (see Figure), with no activation or concentration losses observed. Whilst this work has focussed on the short-term performance and outputs of the cell, no potential causes of long-term deactivation were identified. M. Ragu, C. J. Laycock, G. Owen, G. Lloyd, and A. Guwy, ECS Trans., 103 (1), 2173-2184 (2021). doi.org/10.1149/10301.2173ecstS. C. J. Van Acht, C. J. Laycock, S. J. W. Carr, J. Maddy, A. J. Guwy, G. Lloyd, and L. F. J. M. Raymakers, Int. J. Hydrogen Energy, 45, 15196-15212 (2020) doi.org/10.1016/j.ijhydene.2020.03.211.M. A. de Graaff, N. Hornslein, H. L. Throop, P. Kardol, and L. T. A. van Diepen, Adv. Agron., 155, 1-44 (2019). doi.org/10.1016/bs.agron.2019.01.001A. Valera-Medina, H. Xiao, M. Owen-Jones, W. I. F. David, and P. J. Bowen, Prog. Energy Combust. Sci., 69, 63–102 (2018). doi.org/10.1016/j.pecs.2018.07.001.M. Cheliotis, E. Boulougouris, N. L. Trivyza, G. Theotokatos, G. Livanos, G. Mantalos, A. Stubos, E. Stamatakis, and A. Venetsanos, Energies, 14(11), 3023-3042 (2021). doi.org/10.3390/en14113023 Figure. I-V and power curves of an anode-supported solid oxide cell operating on mixtures of hydrogen and aqueous ammonium carbonate at 750 °C. The mixtures indicated are balanced in pure hydrogen. Figure 1

Effects of exogenous taurine on growth, photosynthesis, oxidative stress, antioxidant enzymes and nutrient accumulation by Trifolium alexandrinum plants under manganese stress

Plants essentially require manganese (Mn) for their normal metabolic functioning. However, excess Mn in the cellular environment is detrimental to plant growth, development, and physio-biochemical functions. Taurine (TAU) is an amino acid with potent antioxidant and anti-inflammatory properties in animals and humans. However, no previous study has investigated the potential of TAU in plant metal stress tolerance. The current study provides some novel insights into the effect of TAU in modulating the defense system of Trifolium alexandrinum plants under Mn toxicity. Manganese toxicity resulted in higher oxidative stress and membrane damage through increased superoxide radical, hydrogen peroxide, malondialdehyde, and methylglyoxal generation alongside enhanced lipoxygenase (LOX) activity. Mn toxicity also resulted in limited uptake of potassium (K+), phosphorus (P), calcium (Ca2+), and increased the accumulation of Mn in both leaf and roots. However, TAU circumvented the Mn-induced oxidative stress by upregulating the activities of antioxidant enzymes (ascorbate peroxidase, peroxidase, catalase, glutathione reductase, glutathione-S-transferase, and superoxide dismutase) and levels of ascorbic acid, proline, anthocyanins, phenolics, flavonoids and glutathione (GSH). Taurine conspicuously improved the growth, photosynthetic pigments, hydrogen sulphide (H2S), and nitric oxide (NO) levels of Mn stressed plants. Taurine also improved the uptake of K+, Ca2+, P and reduced the Mn content in stressed plants. Overall, exogenous taurine might be a suitable strategy to combat Mn stress in T. alexandrinum plants but applications at field levels for various crops and metal toxicities and economic suitability need to be addressed before final recommendations.

Methanogens and Hydrogen Sulfide Producing Bacteria Guide Distinct Gut Microbe Profiles and Irritable Bowel Syndrome Subtypes.

Irritable bowel syndrome (IBS) includes diarrhea-predominant (IBS-D) and constipation-predominant (IBS-C) subtypes. We combined breath testing and stool microbiome sequencing to identify potential microbial drivers of IBS subtypes. IBS-C and IBS-D subjects from 2 randomized controlled trials (NCT03763175 and NCT04557215) were included. Baseline breath carbon dioxide, hydrogen (H 2 ), methane (CH 4 ), and hydrogen sulfide (H 2 S) levels were measured by gas chromatography, and baseline stool microbiome composition was analyzed by 16S rRNA sequencing. Microbial metabolic pathways were analyzed using Kyoto Encyclopedia of Genes and Genomes collection databases. IBS-C subjects had higher breath CH 4 that correlated with higher gut microbial diversity and higher relative abundance (RA) of stool methanogens, predominantly Methanobrevibacter , as well as higher absolute abundance of Methanobrevibacter smithii in stool. IBS-D subjects had higher breath H 2 that correlated with lower microbial diversity and higher breath H 2 S that correlated with higher RA of H 2 S-producing bacteria, including Fusobacterium and Desulfovibrio spp. The predominant H 2 producers were different in these distinct microtypes, with higher RA of Ruminococcaceae and Christensenellaceae in IBS-C/CH 4 + (which correlated with Methanobacteriaceae RA) and higher Enterobacteriaceae RA in IBS-D. Finally, microbial metabolic pathway analysis revealed enrichment of Kyoto Encyclopedia of Genes and Genomes modules associated with methanogenesis and biosynthesis of methanogenesis cofactor F420 in IBS-C/CH 4 + subjects, whereas modules associated with H 2 S production, including sulfate reduction pathways, were enriched in IBS-D. Our findings identify distinct gut microtypes linked to breath gas patterns in IBS-C and IBS-D subjects, driven by methanogens such as M. smithii and H 2 S producers such as Fusobacterium and Desulfovibrio spp, respectively.

Hydrogen Sulfide Attenuates High-Fat Diet-Induced Obesity: Involvement of mTOR/IKK/NF-κB Signaling Pathway.

Obesity has become a public health epidemic worldwide and is associated with many diseases with high mortality including hypertension, diabetes, and heart disease. High-fat diet (HFD)-induced energy imbalance is one of the primary causes of obesity, but the underlying mechanisms are not fully elucidated. Our study showed that HFD reduced the level of hydrogen sulfide (H2S) and its catalytic enzyme cystathionine β-synthase (CBS) in mouse hypothalamus and plasma. We found that HFD activated mTOR, IKK/NF-κB, the main pathway regulating inflammation. Activation of inflammatory pathway promoted the production of pro-inflammatory cytokines including IL-6, IL-1β, and TNF-α, which caused cell damage and loss in the hypothalamus. The disturbance of the hypothalamic neuron circuits resulted in body weight gain in HFD-induced mice. Importantly, we also showed that restoration of H2S level with NaHS or activation of CBS with SAMe attenuated HFD-induced activation of mTOR, IKK/NF-κB signaling, which reduced the inflammation and the neuronal cell loss in the hypothalamus, and also inhibited body weight gain in mice. The same effects were obtained by inhibiting mTOR or NF-κB, which suggested that mTOR and NF-κB were the critical molecular factors involved in hypothalamic inflammation. Taken together, this study identified that HFD-induced hypothalamus inflammation plays a critical role in the development of obesity. Moreover, the inhibition of hypothalamic inflammation by regaining H2S level could be a potential therapeutic to prevent the development of obesity.

Dietary molybdenum may stimulate the growth of colonic sulfur reducing bacteria, increasing hydrogen sulfide levels in the human colon and the possible health effects of an excess of colonic sulfides

Molybdenum is a trace mineral needed in small quantities by most life forms. In living organisms, a molybdenum atom is found within molybdenum-dependent enzymes or molybdoenzymes. Molybdoenzymes catalyze reactions in carbon, sulfur, and nitrogen metabolism. Only four molbdoenzymes have been identified in humans. Most of the known molybdoenzymes are found in bacteria. Dietary molybdenum can be administrated to humans, to treat Wilson disease and tungsten poisoning; and it may be useful in arthritis. Sulfur-reducing bacteria are the bacterial group that reduces certain sulfur molecules to hydrogen sulfide. These bacteria can inhabit anaerobic parts of the gastrointestinal tract of mammals and are the predominant producer of hydrogen sulfide in the human colon. Hydrogen sulfide plays a major role in the malodor of human flatus. Some individuals have reported an increase in foul odoriferous gases from the colon after molybdenum supplementation. The underlying mechanism as to how this occurs is currently not known. Possible bacteria that are involved could be sulfur-reducing bacteria and methionine dissimilating bacteria. Supplementing sheep with molybdenum and with sulfur exclusively in the form of methionine can stimulate the growth of sulfur-reducing bacteria and increase the level of sulfides in the rumen. The molybdoenzyme, thiosulfate reductase, is found in sulfur-reducing bacteria and catalyzes the reduction of thiosulfate to hydrogen sulfide. The source of thiosulfate could be from ruminal epithelial cells detoxifying methanethiol, produced by methionine dissimilating bacteria, degrading the dietary methionine to methanethiol. Therefore, the molybdenum could be activating thiosulfate reductases of sulfur-reducing bacteria in the rumen of these animals. The human colon can also harbor sulfur-reducing bacteria, and dietary molybdenum and methionine can reach this organ. Therefore, dietary molybdenum may be stimulating the growth of sulfur-reducing bacteria in some individuals. Sulfides in the human colon could have beneficial and detrimental effects on health. Such effects could include the already mentioned malodor of flatus, the stabilizing of the microbiome-mucosa interface in an intestinal dysbiosis, the treatment of hypertension and the promotion of inflammation in ulcerative colitis.

SODIUM SELENITE ABROGATES THE EFFECTS OF ARSENIC TOXICITY ON ORGAN INJURY BIOMARKERS IN THE BLOOD

Heavy metals are becoming ubiquitous in our environment due to its natural abundance and anthropogenic uses. Arsenic an example of heavy metal, can cause deleterious effects in numerous organs and biochemical pathways. Use of noninvasive testing procedures had been used in diagnosis, monitoring of pathological events during treatment. In order to investigate the effects of sodium selenite on biomarkers of organ injury in arsenic-exposed rats for a period of 5 weeks, twenty-four male albino rats divided into four groups (n = 6) were exposed to sodium arsenite (SA) and sodium selenite (SS). Group I (control) received only distilled water, groups II and III were exposed to 40 ppm SA in drinking water ad libtum, in addition group III received 0.25 mg/kg bwt SS orally and group IV received 0.25 mg/kg bwt SS orally only. Activities and levels of organ-injury markers were determined in the blood using spectrophotometric method. In the SA exposed group (group II), there were significant increases (p ˂ 0.05) in the activities of plasma xanthine oxidase, lactate dehydrogenase, aldolase, glutamate dehydrogenase, NAD glycohydrolase, aspartate and alanine aminotransferases, and levels of plasma nitric oxide and hydrogen sulphide (in plasma and erythrocyte) when compared to control. Sodium selenite administration abrogated the observed effects of SA exposure by decreasing the measured biomarkers to the normal level as observed in group III and IV. In conclusion, this results suggests the use of SS is safe and non-invasive approach for the prevention of SA-induced toxicity in humans.

Simultaneous Sensing of H2S and ATP with a Two-Photon Fluorescent Probe in Alzheimer's Disease: toward Understanding Why H2S Regulates Glutamate-Induced ATP Dysregulation.

Energy deprivation and reduced levels of hydrogen sulfide (H2S) in the brain is closely associated with Alzheimer's disease (AD). However, there is currently no fluorescent probe for precise exploration of both H2S and adenosine triphosphate (ATP) to directly demonstrate their relationship and their dynamic pattern changes. Herein, we developed a two-photon fluorescent probe, named AD-3, to simultaneously image endogenous H2S and ATP from two emission channels of fluorescent signals in live rat brains with AD. The probe achieved excellent selectivity and good detection linearity for H2S in the 0-100 μM concentration range and ATP in the 2-5 mM concentration range, respectively, with a detection limit of 0.19 μM for H2S and 0.01 mM for ATP. Fluorescence imaging in live cells reveals that such probe could successfully apply for simultaneous imaging and accurate quantification of H2S and ATP in neuronal cells. Further using real-time quantitative polymerase chain reaction and Western blots, we confirmed that H2S regulates ATP synthesis by acting on cytochrome C, cytochrome oxidase subunit 3 of complex IV, and protein 6 of complex I in the mitochondrial respiratory chain. Subsequently, we constructed a high-throughput screening platform based on AD-3 probe to rapidly screen the potential anti-AD drugs to control glutamate-stimulated oxidative stress associated with abnormal H2S and ATP levels. Significantly, AD-3 probe was found capable of imaging of H2S and ATP in APP/PS1 mice, and the concentration of H2S and ATP in the AD mouse brain was found to be lower than that in wild-type mice.

Heating and emission characteristics from combustion of charcoal and co-combustion of charcoal with faecal char-sawdust char briquettes in a ceramic cook stove

Over reliance on charcoal has accelerated deforestation in sub-Saharan Africa. Seeking alternative sustainable and environmentally friendly sources of biomass energy to meet the escalating energy demand is therefore vital. However, limited evidence exists on the concentrations of toxic emissions of different biomass fuels. Herein, dried human faeces and sawdust were pyrolyzed at 350 °C to produce biochar and mixed in equal ratio to produce briquettes through densification, with molasses (10 wt.%) used as a binder. A comparative study on the heating properties and emission level of carbon monoxide (CO), nitric oxide (NO), and hydrogen sulphide (H2S) during combustion of charcoal, and co-combustion (50:50 wt. %) of charcoal with briquettes was conducted. The thermal profile of the flue gases indicated rapid combustion of volatile gases followed by slow oxidation of the char. Co-combustion significantly (P < 0.05) enhanced the amount of heat energy released with flue gases temperatures reaching a peak of 475 °C. The briquettes had a gross calorific value of 19.8 MJ/kg which was lower than 25.7 MJ/kg for charcoal. Combustion of charcoal did not emit NO, however the concentration of CO was above the critical short term limits of 35 ppm. The concentration of CO and H2S was above the short term exposure limits of 35 ppm, and 0.005 ppm, respectively, during co-combustion, whereas NO concentration was below dangerous exposure levels of 100 ppm. These results suggest that co-combustion of charcoal with the briquettes is a promising approach to generate safe and sufficient heat energy for cooking and reduce deforestation.

PENGARUH GAS HIDROGEN SULFIDA (H2S) TERHADAP KELUHAN SUBYEKTIF PETUGAS PENGOLAHAN SAMPAH DI PUSAT DAUR ULANG JAMBANGAN SURABAYA

The Jambangan Recycling Center (PDU) in Surabaya is a waste management site that applies the 3R principles, namely Reuse, Reduce, Recycle. The amount of waste that comes in every day is 5-6 tons. The waste processing officer complained of subjective complaints in the form of influenza, cough, sore throat and chest pain. The purpose of the study was to determine the effect of H2S gas on subjective complaints of waste processing officers at the Jambangan Recycling Center Surabaya. This research is an analytic observational research with a cross sectional approach. This research was conducted at the Jambangan Recycling Center. Sampling of respondents and ambient air was carried out by saturated sampling with a total population and sample of 27 people. Data collection techniques in this study used measurements, observations, and interviews. Data analysis using SPSS application with Spearman Correlation Test. The results showed that the average level of Hydrogen Sulfide (H2S) in the Jambangan Recycling Center Surabaya was 0.00054 ppm which was included in the eligible category according to the East Java Governor Regulation Number 10 of 2009. This study also showed that 27 waste processing officers who 2 people experienced severe complaints, 25 people had mild complaints, and there were no waste processing officers who had no complaints. The conclusion of the study is that there is no effect between levels of Hydrogen Sulfide on subjective complaints of waste processing officers at the Jambangan Recycling Center Surabaya (P = 0.336) so it is recommended to the relevant agencies to monitor air quality regularly. Waste processing officers are also advised to use personal protective equipment when in the Surabaya Jambangan Recycling Center environment.

Myricetin Improves Impaired Nerve Functions in Experimental Diabetic Rats.

Diabetic peripheral neuropathy (DPN) is considered as one of the most important complications of diabetes mellitus. At present, effective treatments that might improve the damaged neurological function in DPN are sorely needed. As myricetin has been proved to possess excellent neuroprotective and antioxidant effects, it might have therapeutic potential for DPN. Therefore, the purpose of our study was to detect the potential beneficial effect of myricetin on DPN. A single dose of 50 mg/kg of streptozotocin was applied in rats for the establishment of diabetic models. Different doses of myricetin (0.5 mg/kg/day, 1.0 mg/kg/day, and 2.0 mg/kg/day) were intraperitoneally injected for 2 weeks from the 21st day after streptozotocin injection. After the final myricetin injection, behavioral, electrophysiological, biochemical, and protein analyses were performed. In the present study, myricetin significantly ameliorated diabetes-induced impairment in sensation, nerve conduction velocities, and nerve blood flow. In addition, myricetin significantly reduced the generation of advanced glycation end-products (AGEs) and reactive oxygen species (ROS), and elevated Na+, K+-ATPase activity and antioxidant activities in nerves in diabetic animals. Additional studies revealed that myricetin significantly raised the hydrogen sulfide (H2S) levels, and elevated the expression level of heme oxygenase-1 (HO-1) as well as nuclear factor-E2-related factor-2 (Nrf2) in diabetic rats. In addition, myricetin has the capability of decreasing plasma glucose under diabetic conditions. The findings in our present study collectively indicated that myricetin could restore the impaired motor and sensory functions under diabetic conditions. The Nrf2-dependent antioxidant action and the capability of decreasing plasma glucose might be the underlying mechanisms for the beneficial effect of myricetin on impaired neural functions. Our study showed the therapeutic potential of myricetin in the management of DPN.