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48 results for “hydrogen sulfide”
Hydrogen sulfide release via the ACE inhibitor Zofenopril prevents intimal hyperplasia in human vein segments and in a mouse model of carotid artery stenosis
<p>The current strategies to reduce intimal hyperplasia (IH) principally rely on local drug delivery, in endovascular approach. The oral angiotensin converting enzyme inhibitor (ACEi) Zofenopril has additional effects compared to other non-sulfyhydrated ACEi to prevent intimal hyperplasia and restenosis. Given the number of patients treated with ACEi worldwide, these findings call for further prospective clinical trials to test the benefits of sulfhydrated ACEi over classic ACEi for the prevention of restenosis in hypertensive patients.</p> <p>Abstract</p> <p>Objectives</p> <p>Hypertension is a major risk factor for intimal hyperplasia (IH) and restenosis following vascular and endovascular interventions. Pre-clinical studies suggest that hydrogen sulfide (H2S), an endogenous gasotransmitter, limits restenosis. While there is no clinically available pure H2S releasing compound, the sulfhydryl-containing angiotensin-converting enzyme inhibitor Zofenopril is a source of H2S. Here, we hypothesized that Zofenopril, due to H2S release, would be superior to other non-sulfhydryl containing angiotensin converting enzyme inhibitor (ACEi), in reducing intimal hyperplasia in the context of hypertension.</p> <p>Materials</p> <p>Spontaneously hypertensive male Cx40 deleted mice (Cx40-/-) or WT littermates were randomly treated with Enalapril 20 mg (Mepha Pharma) or Zofenopril 30 mg (Mylan SA). Discarded human vein segments and primary human smooth muscle cells (SMC) were treated with the active compound Enalaprilat or Zofenoprilat.</p> <p>Methods</p> <p>IH was evaluated in mice 28 days after focal carotid artery stenosis surgery and in human vein segments cultured for 7 days ex vivo. Human primary smooth muscle cell (SMC) proliferation and migration were studied in vitro.</p> <p>Results</p> <p>Compared to control animals (intima/media thickness=2.3±0.33), Enalapril reduced IH in Cx40-/- hypertensive mice by 30% (1.7±0.35; p=0.037), while Zofenopril abrogated IH (0.4±0.16; p<.0015 vs. Ctrl and p>0.99 vs. sham-operated Cx40-/-mice). In WT normotensive mice, enalapril had no effect (0.9665±0.2 in control vs 1.140±0.27; p>.99), while Zofenopril also abrogated IH (0.1623±0.07, p<.008 vs. Ctrl and p>0.99 vs. sham-operated WT mice). Zofenoprilat, but not Enalaprilat, also prevented intimal hyperplasia in human veins segments ex vivo. The effect of Zofenopril on carotid and SMC correlated with reduced SMC proliferation and migration. Zofenoprilat inhibited the MAPK and mTOR pathways in SMC and human vein segments.</p> <p>Conclusion</p> <p>Zofenopril provides extra beneficial effects compared to non-sulfhydryl ACEi to reduce SMC proliferation and restenosis, even in normotensive animals. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases and hypertension.</p>
Raw data from Qin et al. (2018) "Modeling the kinetics of hydrogen formation by zerovalent iron: Effects of sulfidation on micro- and nano-scale particles"
<p>Raw hydrogen concentration vs. time data from Qin, H., X. Guan, J. Z. Bandstra, R. L. Johnson, and P. G. Tratnyek (2018) “Modeling the kinetics of hydrogen formation by zerovalent iron: Effects of sulfidation on micro- and nano-scale particles” Environ. Sci. Technol. 52(23): 13887-13896. [10.1021/acs.est.8b04436]</p> <p>This manuscript reports a large set of new concentration vs. time data for dihydrogen (H2) produced by corrosion of granular zerovalent iron (i.e., the hydrogen evolution reaction, HER) in aqueous media relevant to groundwater remediation. Four alternative kinetic models are evaluated by fitting the data using global non-linear regression. Details are given in the main text and supporting information of the (open access) manuscript. </p> <p>The data provided here are in two formats: (i) a .csv file that contains only data and labels, and (ii) a .pxp file that includes the data and graphs (without fits) in the same layout as figures in the original manuscript. The .pxp file was prepared with Igor Pro 8.02 (https://www.wavemetrics.com).</p>
Data from: Nascent transcription reveals regulatory changes in extremophile fishes inhabiting hydrogen sulfide-rich environments
<p>Regulating transcription allows organisms to respond to their environment, both within a single generation (plasticity) and across generations (adaptation). We examined transcriptional differences in gill tissues of fishes in the Poecilia mexicana species complex (family Poeciliidae), which have colonized toxic springs rich in hydrogen sulfide (H2S) in southern Mexico. There are gene expression differences between sulfidic and non-sulfidic populations, yet regulatory mechanisms mediating this gene expression variation remain poorly studied. We combined capped-small RNA sequencing (csRNA-seq), which captures actively transcribed (i.e., nascent) transcripts, and traditional messenger RNA sequencing (mRNA-seq) to examine how variation in transcription, enhancer activity, and associated transcription factor binding sites may facilitate adaptation to extreme environments. csRNA-seq revealed thousands of differentially initiated transcripts between sulfidic and non-sulfidic populations, many of which are involved in H2S detoxification and response. Analyses of transcription factor binding sites in promoter and putative enhancer csRNA-seq peaks identify a suite of transcription factors likely involved in regulating H2S-specific shifts in gene expression, including several key transcription factors known to respond to hypoxia. Our findings uncover a complex interplay of regulatory processes that reflect the divergence of extremophile populations of P. mexicana from their non-sulfidic ancestors and suggest shared responses among evolutionarily independent lineages.</p>
Data from: Nascent transcription reveals regulatory changes in extremophile fishes inhabiting hydrogen sulfide-rich environments
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Data from: Metabolomic profiles of acute and chronic ambient hydrogen sulfide exposure in a mouse model
<p>Hydrogen sulfide (H<sub>2</sub>S) is an environmental toxicant of health concern following acute or chronic human exposures. Male 6-8 week-old C57BL/6J mice were exposed by whole-body inhalation to 1000 ppm H<sub>2</sub>S for 45 min and euthanized at 5 min and 72 h for acute exposure. For subchronic study, mice were exposed to 5 ppm H<sub>2</sub>S 2 h/day, 5 days/week for 5 weeks. The brainstem was removed for metabolomic analysis. The metabolomics analyses consisted of three assays, (1) primary metabolism by GC-TOF MS, (2) biogenic amines (hydrophilic compounds) by HILIC-MS/MS and (3) lipidomics by RPLC-MS/MS. Metabolomics were performed in West Coast Metabolomics Center, University of California at Davis, CA, USA. 348, 311, and 565 known metabolites were detected and analyzed by primary metabolism, biogenic amines, and lipidomic metabolomics assays. 33, 19, and 46 metabolites were increased at 5 min and 72 h post acute H<sub>2</sub>S exposures and subchronic ambient H<sub>2</sub>S exposures, respectively, compared to room air control group. 22, 17, and 32 metabolites were decreased at 5 min and 72 h post acute H<sub>2</sub>S exposures and subchronic ambient H<sub>2</sub>S exposures, respectively, compared to room air control group. Acute H<sub>2</sub>S exposure decreased excitatory neurotransmitters aspartate and glutamate concentrations while the inhibitory neurotransmitter serotonin was increased. Glutamate and serotonin were also decreased after ambient H<sub>2</sub>S exposure. Branched-chain amino acids, fructose, and glucose were increased by acute H<sub>2</sub>S exposure. In ambient H<sub>2</sub>S exposure, glucose was decreased while MUFAs, PUFAs, inosine, and hypoxanthine were increased. Collectively, these results provide important mechanistic clues of acute and subchronic ambient H<sub>2</sub>S poisonings and show that H<sub>2</sub>S alters neurotransmission homeostasis.</p>
Assessing the Safety and Ability of SG1002 to Overcome Deficits in Hydrogen Sulfide in Heart Failure Patients
ClinicalTrials.gov study NCT01989208. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Host-microbiome associations in livebearing fishes adapted to toxic streams rich in hydrogen sulfide: Code for analyzing 16S rRNA dataset
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Data from: Metabolomic profiles of acute and chronic ambient hydrogen sulfide exposure in a mouse model
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Hydrogen sulfide exposure reduces thermal set point in zebrafish
<p>Behavioural flexibility allows ectotherms to exploit the environment to govern their metabolic physiology, including in response to environmental stress. Hydrogen sulfide (H<sub>2</sub>S) is a widespread environmental toxin that can lethally inhibit metabolism. However, H<sub>2</sub>S can also alter behaviour and physiology, including a hypothesised induction of hibernation-like states characterised by downward shifts of the innate thermal setpoint (anapyrexia). Support for this hypothesis has proved controversial because it is difficult to isolate active and passive components of thermoregulation, especially in animals with high resting metabolic heat production. Here, we directly test this hypothesis by leveraging the natural behavioural thermoregulatory drive of fish to move between environments of different temperatures in accordance with their current physiological state and thermal preference. We observed a decrease in adult zebrafish (<i>Danio rerio</i>) preferred body temperature with exposure to 0.02% H<sub>2</sub>S, which we interpret as a shift in thermal setpoint. Individuals exhibited consistent differences in shuttling behaviour and preferred temperatures, which were reduced by a constant temperature magnitude during H<sub>2</sub>S exposure. Seeking lower temperatures alleviated H<sub>2</sub>S-induced metabolic stress, as measured by reduced rates of aquatic surface respiration. Our findings highlight the interactions between individual variation and sublethal impacts of environmental toxins on behaviour.</p>
Products for "Hydrogen sulfide and metal-enriched atmosphere for a Jupiter-mass exoplanet"
<p>Data and model for JWST transit observation of HD 189733b using NIRCam (GO 1633, PI: Drake Deming) from paper "Hydrogen sulfide and metal-enriched<br>atmosphere for a Jupiter-mass exoplanet" (Fu et al. 2024).</p>
Short-Term Endogenous Hydrogen Sulfide Upregulation For Vein Graft Disease
ClinicalTrials.gov study NCT05457881. IPD Sharing: NO. Countries: 1. Publications: 95.
Hydrogen Sulfide as Prognostic Factor
ClinicalTrials.gov study NCT01088490. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Plasma Hydrogen Sulfide as a Biomarker for Alzheimer's Disease and Related Dementias
ClinicalTrials.gov study NCT05060848. IPD Sharing: NO. Countries: 1. Publications: 1.
Hydrogen Sulfide and Peripheral Arterial Disease
ClinicalTrials.gov study NCT01407172. IPD Sharing: Not stated. Countries: 1. Publications: 5.
Measurement of Distinct Biological Pools of Hydrogen Sulfide in Women With Cardiovascular Disease
ClinicalTrials.gov study NCT02180074. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Short-Term Endogenous Hydrogen Sulfide Upregulation
ClinicalTrials.gov study NCT03303534. IPD Sharing: NO. Countries: 1. Publications: 8.
Hydrogen sulfide exposure reduces thermal set point in zebrafish
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Data from: Hydrogen sulfide regulates cardiovascular function by influencing the excitability of subfornical organ neurons
Hydrogen sulfide (H2S), a gasotransmitter endogenously found in the central nervous system, has recently been suggested to act as a signalling molecule in the brain having beneficial effects on cardiovascular function. This study was thus undertaken to investigate the effect of NaHS (an H2S donor) in the subfornical organ (SFO), a central nervous system site important to blood pressure regulation. We used male Sprague-Dawley rats for both in vivo and in vitro experiments. We first used RT-PCR to confirm our previous microarray analyses showing that mRNAs for the enzymes required to produce H2S are expressed in the SFO. We then used microinjection techniques to investigate the physiological effects of NaHS in SFO, and found that NaHS microinjection (5 nmol) significantly increased blood pressure (mean AUC = 853.5±105.7 mmHg*s, n = 5). Further, we used patch-clamp electrophysiology and found that 97.8% (88 of 90) of neurons depolarized in response to NaHS. This response was found to be concentration dependent with an EC50 of 35.6 µM. Coupled with the depolarized membrane potential, we observed an overall increase in neuronal excitability using an analysis of rheobase and action potential firing patterns. This study has provided the first evidence of NaHS and thus H2S actions and their cellular correlates in SFO, implicating this brain area as a site where H2S may act to control blood pressure.
Electron microscopy images of thalamus from acutely hydrogen sulfide poisoned mice
<p class="MsoNormal"><span>To date, the mitochondrial morphological changes that take place after an acute H<sub>2</sub>S exposure are not well described. In the present study, we analyzed images of transmission electron microscopy of thalami from mice subjected to a single acute (1000 ppm) H<sub>2</sub>S exposure and euthanized at various time points to assess the mitochondrial structure and morphometric parameters over time. From our observations, changes induced by H<sub>2</sub>S up to 48 h were mostly limited to increased cristae and matrix compartments' disorganization in mainly accumulated round-shaped mitochondria. At 72 h, H<sub>2</sub>S induced a spectrum of morphological cellular changes. Impaired H<sub>2</sub>S-mediated energy-producing capacity of mitochondria relative to their normal-sized counterparts was inferred from our observations of disorganization and paucity of the inner mitochondrial membrane, the infoldings of which—into cristae—are well-documented to increase the surface area for ATP production, the evaluation of a disorganized network, and likely a disrupted mitophagy because of changes in mitochondrial shape. </span></p>
Plasma Hydrogen Sulfide, Nitric Oxide and Stress Hyperglycemia in Acute Myocardial Infarction
ClinicalTrials.gov study NCT03829605. IPD Sharing: Not stated. Countries: 0. Publications: 4.
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