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Antioxidants
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Role of Hydrogen Sulfide in Health and Disease
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Role of Hydrogen Sulfide in Health and Disease

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 20162

Special Issue Editors

Dr. Emma Mitidieri

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Guest Editor
Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, via Domenico Montesano, 49, 80131 Naples, Italy
Interests: gaseous mediators; cardiovascular pathophysiology; inflammation; erectile dysfunction; urogenital tract pathophysiology
Dr. Vincenzo Brancaleone

E-Mail Website
Co-Guest Editor
Department of Science, University of Basilicata, via Ateneo Lucano, 10, 85100 Potenza, Italy
Interests: endothelial and vascular dysfunction; resolution of inflammation; gender pharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As Guest Editors, we invite you to contribute to the Special Issue entitled “Role of Hydrogen Sulfide in Health and Disease”. Original research reports and reviews will be published online in Antioxidants.

Hydrogen sulfide (H2S), for a long time recognized as a putrid, toxic gas, is actually considered the third gasotransmitter alongside nitric oxide (NO) and carbon monoxide (CO) in mammalian systems. It is endogenously produced from the amino acid L-cysteine (L-Cys) through the activation of two pyridoxal-5-phosphate-dependent enzymes, i.e., cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) or 3-mercaptopyruvate-sulfurtransferase (3-MST). H2S is a small, reactive signaling molecule that can freely diffuse through membranes participating in the modulation of multiple physiological and pathological processes. The current literature reports conflicting data with respect to its biological effects. In particular, H2S, similarly to NO and CO, exhibits pleiotropic and dose-dependent effects on a variety of physiological pathways. Indeed, it is involved in angiogenesis, neuronal activity, vascular homeostasis, glucose metabolism, energy production, and the inflammatory response. Interestingly, an altered H2S biosynthesis is associated with a number of diseases, including heart failure, hypertension, atherosclerosis, asthma, diabetes, neurodegenerative diseases, autoimmunity, and chronic inflammation.

Due to the ambiguous data reported in the literature and possible undiscovered mechanisms underlying H2S driven effects, there is the need to better understand its role in physiology and diseases.

Thus, we invite investigators to contribute to this Special Issue with original research and review articles. In order to improve the current knowledge, papers describing novel mechanism(s) of action and/or interaction that help to clarify whether H2S is friend or foe for human health will be especially welcome and published online in Antioxidants.

Dr. Emma Mitidieri
Guest Editor

Dr. Vincenzo Brancaleone
Co-Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Hydrogen sulfide
  • New pharmacological approaches
  • Cardiovascular disease
  • Inflammation
  • Cancer
  • Urogenital tract
  • Immunity

Published Papers (9 papers)

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Research

23 pages, 4832 KiB  
Article
Hydrogen Sulfide Metabolizing Enzymes in the Intestinal Mucosa in Pediatric and Adult Inflammatory Bowel Disease
by Nathalie Stummer, Daniel Weghuber, René G. Feichtinger, Sara Huber, Johannes A. Mayr, Barbara Kofler, Daniel Neureiter, Eckhard Klieser, Sarah Hochmann, Wanda Lauth and Anna M. Schneider
Antioxidants 2022, 11(11), 2235; https://doi.org/10.3390/antiox11112235 - 12 Nov 2022
Cited by 4 | Viewed by 2123
Abstract
Hydrogen sulfide (H2S) is a toxic gas that has important regulatory functions. In the colon, H2S can be produced and detoxified endogenously. Both too little and too much H2S exposure are associated with inflammatory bowel disease (IBD), [...] Read more.
Hydrogen sulfide (H2S) is a toxic gas that has important regulatory functions. In the colon, H2S can be produced and detoxified endogenously. Both too little and too much H2S exposure are associated with inflammatory bowel disease (IBD), a chronic intestinal disease mainly classified as Crohn’s disease (CD) and ulcerative colitis (UC). As the pathogenesis of IBD remains elusive, this study’s aim was to investigate potential differences in the expression of H2S-metabolizing enzymes in normal aging and IBD. Intestinal mucosal biopsies of 25 adults and 22 children with IBD along with those of 26 healthy controls were stained immunohistochemically for cystathionine-γ-lyase (CSE), 3-mercapto-sulfurtransferase (3-MST), ethylmalonic encephalopathy 1 protein (ETHE1), sulfide:quinone oxidoreductase (SQOR) and thiosulfate sulfurtransferase (TST). Expression levels were calculated by multiplication of the staining intensity and percentage of positively stained cells. Healthy adults showed an overall trend towards lower expression of H2S-metabolizing enzymes than healthy children. Adults with IBD also tended to have lower expression compared to controls. A similar trend was seen in the enzyme expression of children with IBD compared to controls. These results indicate an age-related decrease in the expression of H2S-metabolizing enzymes and a dysfunctional H2S metabolism in IBD, which was less pronounced in children. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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12 pages, 1557 KiB  
Article
Role of Cholesterol in the Regulation of Hydrogen Sulfide Signaling within the Vascular Endothelium
by Perenkita J. Mendiola, Emily E. Morin, Laura V. Gonzalez Bosc, Jay S. Naik and Nancy L. Kanagy
Antioxidants 2022, 11(9), 1680; https://doi.org/10.3390/antiox11091680 - 28 Aug 2022
Cited by 1 | Viewed by 1659
Abstract
H2S is a gaseous signaling molecule enzymatically produced in mammals and H2S-producing enzymes are expressed throughout the vascular wall. We previously reported that H2S-induced vasodilation is mediated through transient receptor potential cation channel subfamily V member 4 [...] Read more.
H2S is a gaseous signaling molecule enzymatically produced in mammals and H2S-producing enzymes are expressed throughout the vascular wall. We previously reported that H2S-induced vasodilation is mediated through transient receptor potential cation channel subfamily V member 4 (TRPV4) and large conductance (BKCa) potassium channels; however, regulators of this pathway have not been defined. Previous reports have shown that membrane cholesterol limits activity of TRPV4 and BKCa potassium channels. The current study examined the ability of endothelial cell (EC) plasma membrane (PM) cholesterol to regulate H2S-induced vasodilation. We hypothesized that EC PM cholesterol hinders H2S-mediated vasodilation in large mesenteric arteries. In pressurized, U46619 pre-constricted mesenteric arteries, decreasing EC PM cholesterol in large arteries using methyl-β-cyclodextrin (MBCD, 100 µM) increased H2S-induced dilation (NaHS 10, 100 µM) but MBCD treatment had no effect in small arteries. Enface fluorescence showed EC PM cholesterol content is higher in large mesenteric arteries than in smaller arteries. The NaHS-induced vasodilation following MBCD treatment in large arteries was blocked by TRPV4 and BKCa channel inhibitors (GSK219384A, 300 nM and iberiotoxin, 100 nM, respectively). Immunohistochemistry of mesenteric artery cross-sections show that TRPV4 and BKCa are both present in EC of large and small arteries. Cholesterol supplementation into EC PM of small arteries abolished NaHS-induced vasodilation but the cholesterol enantiomer, epicholesterol, had no effect. Proximity ligation assay studies did not show a correlation between EC PM cholesterol content and the association of TRPV4 and BK. Collectively, these results demonstrate that EC PM cholesterol limits H2S-induced vasodilation through effects on EC TRPV4 and BKCa channels. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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13 pages, 1403 KiB  
Article
β3 Relaxant Effect in Human Bladder Involves Cystathionine γ-Lyase-Derived Urothelial Hydrogen Sulfide
by Emma Mitidieri, Annalisa Pecoraro, Erika Esposito, Vincenzo Brancaleone, Carlotta Turnaturi, Luigi Napolitano, Vincenzo Mirone, Ferdinando Fusco, Giuseppe Cirino, Raffaella Sorrentino, Giulia Russo, Annapina Russo and Roberta d’Emmanuele di Villa Bianca
Antioxidants 2022, 11(8), 1480; https://doi.org/10.3390/antiox11081480 - 28 Jul 2022
Cited by 2 | Viewed by 1466
Abstract
It is now well established that the urothelium does not act as a passive barrier but contributes to bladder homeostasis by releasing several signaling molecules in response to physiological and chemical stimuli. Here, we investigated the potential contribution of the hydrogen sulfide (H [...] Read more.
It is now well established that the urothelium does not act as a passive barrier but contributes to bladder homeostasis by releasing several signaling molecules in response to physiological and chemical stimuli. Here, we investigated the potential contribution of the hydrogen sulfide (H2S) pathway in regulating human urothelium function in β3 adrenoceptor-mediated relaxation. The relaxant effect of BRL 37344 (0.1–300 µM), a selective β3 adrenoceptor agonist, was evaluated in isolated human bladder strips in the presence or absence of the urothelium. The relaxant effect of BRL 37344 was significantly reduced by urothelium removal. The inhibition of cystathionine-γ-lyase (CSE), but not cystathionine-β-synthase (CBS), significantly reduced the BRL 37344 relaxing effect to the same extent as that given by urothelium removal, suggesting a role for CSE-derived H2S. β3 adrenoceptor stimulation in the human urothelium or in T24 urothelial cells markedly increased H2S and cAMP levels that were reverted by a blockade of CSE and β3 adrenoceptor antagonism. These findings demonstrate a key role for urothelium CSE-derived H2S in the β3 effect on the human bladder through the modulation of cAMP levels. Therefore, the study establishes the relevance of urothelial β3 adrenoceptors in the regulation of bladder tone, supporting the use of β3 agonists in patients affected by an overactive bladder. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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14 pages, 1373 KiB  
Article
The Combined Partial Knockdown of CBS and MPST Genes Induces Inflammation, Impairs Adipocyte Function-Related Gene Expression and Disrupts Protein Persulfidation in Human Adipocytes
by Jessica Latorre, Angeles Aroca, José Manuel Fernández-Real, Luis C. Romero and José María Moreno-Navarrete
Antioxidants 2022, 11(6), 1095; https://doi.org/10.3390/antiox11061095 - 31 May 2022
Cited by 5 | Viewed by 2130
Abstract
Recent studies in mice and humans demonstrated the relevance of H2S synthesising enzymes, such as CTH, CBS, and MPST, in the physiology of adipose tissue and the differentiation of preadipocyte into adipocytes. Here, our objective was to investigate the combined role [...] Read more.
Recent studies in mice and humans demonstrated the relevance of H2S synthesising enzymes, such as CTH, CBS, and MPST, in the physiology of adipose tissue and the differentiation of preadipocyte into adipocytes. Here, our objective was to investigate the combined role of CTH, CBS, and MPST in the preservation of adipocyte protein persulfidation and adipogenesis. Combined partial CTH, CBS, and MPST gene knockdown was achieved treating fully human adipocytes with siRNAs against these transcripts (siRNA_MIX). Adipocyte protein persulfidation was analyzed using label-free quantitative mass spectrometry coupled with a dimedone-switch method for protein labeling and purification. Proteomic analysis quantified 216 proteins with statistically different levels of persulfidation in KD cells compared to control adipocytes. In fully differentiated adipocytes, CBS and MPST mRNA and protein levels were abundant, while CTH expression was very low. It is noteworthy that siRNA_MIX administration resulted in a significant decrease in CBS and MPST expression, without impacting on CTH. The combined partial knockdown of the CBS and MPST genes resulted in reduced cellular sulfide levels in parallel to decreased expression of relevant genes for adipocyte biology, including adipogenesis, mitochondrial biogenesis, and lipogenesis, but increased proinflammatory- and senescence-related genes. It should be noted that the combined partial knockdown of CBS and MPST genes also led to a significant disruption in the persulfidation pattern of the adipocyte proteins. Although among the less persulfidated proteins, we identified several relevant proteins for adipocyte adipogenesis and function, among the most persulfidated, key mediators of adipocyte inflammation and dysfunction as well as some proteins that might play a positive role in adipogenesis were found. In conclusion, the current study indicates that the combined partial elimination of CBS and MPST (but not CTH) in adipocytes affects the expression of genes related to the maintenance of adipocyte function and promotes inflammation, possibly by altering the pattern of protein persulfidation in these cells, suggesting that these enzymes were required for the functional maintenance of adipocytes. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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20 pages, 2217 KiB  
Article
Reduced Levels of H2S in Diabetes-Associated Osteoarthritis Are Linked to Hyperglycaemia, Nrf-2/HO-1 Signalling Downregulation and Chondrocyte Dysfunction
by María Piñeiro-Ramil, Elena F. Burguera, Tamara Hermida-Gómez, Beatriz Caramés, Natividad Oreiro-Villar, Rosa Meijide-Faílde, Francisco J. Blanco and Carlos Vaamonde-García
Antioxidants 2022, 11(4), 628; https://doi.org/10.3390/antiox11040628 - 25 Mar 2022
Cited by 7 | Viewed by 2297
Abstract
Different findings indicate that type 2 diabetes is an independent risk factor for osteoarthritis (OA). However, the mechanisms underlying the connection between both diseases remain unclear. Changes in the balance of hydrogen sulphide (H2S) are thought to play an important role [...] Read more.
Different findings indicate that type 2 diabetes is an independent risk factor for osteoarthritis (OA). However, the mechanisms underlying the connection between both diseases remain unclear. Changes in the balance of hydrogen sulphide (H2S) are thought to play an important role in the pathogenesis of diabetes and its complications, although its role is still controversial. In this study, we examined the modulation of H2S levels in serum and chondrocytes from OA diabetic (DB) and non-diabetic (non-DB) patients and in cells under glucose stress, in order to elucidate whether impairment in H2S-mediated signalling could participate in the onset of DB-related OA. Here, we identified a reduction in H2S synthesis in the cartilage from OA-DB patients and in cells under glucose stress, which is associated with hyperglycaemia-mediated dysregulation of chondrocyte metabolism. In addition, our results indicate that H2S is an inductor of the Nrf-2/HO-1 signalling pathway in cartilage, but is also a downstream target of Nrf-2 transcriptional activity. Thereby, impairment of the H2S/Nrf-2 axis under glucose stress or DB triggers chondrocyte catabolic responses, favouring the disruption of cartilage homeostasis that characterizes OA pathology. Finally, our findings highlight the benefits of the use of exogeneous sources of H2S in the treatment of DB-OA patients, and warrant future clinical studies. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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11 pages, 2014 KiB  
Article
Elemental Sulfur Inhibits Yeast Growth via Producing Toxic Sulfide and Causing Disulfide Stress
by Tianqi Wang, Yuqing Yang, Menghui Liu, Honglei Liu, Huaiwei Liu, Yongzhen Xia and Luying Xun
Antioxidants 2022, 11(3), 576; https://doi.org/10.3390/antiox11030576 - 17 Mar 2022
Cited by 11 | Viewed by 2551
Abstract
Elemental sulfur is a common fungicide, but its inhibition mechanism is unclear. Here, we investigated the effects of elemental sulfur on the single-celled fungus Saccharomyces cerevisiae and showed that the inhibition was due to its function as a strong oxidant. It rapidly entered [...] Read more.
Elemental sulfur is a common fungicide, but its inhibition mechanism is unclear. Here, we investigated the effects of elemental sulfur on the single-celled fungus Saccharomyces cerevisiae and showed that the inhibition was due to its function as a strong oxidant. It rapidly entered S. cerevisiae. Inside the cytoplasm, it reacted with glutathione to generate glutathione persulfide that then reacted with another glutathione to produce H2S and glutathione disulfide. H2S reversibly inhibited the oxygen consumption by the mitochondrial electron transport chain, and the accumulation of glutathione disulfide caused disulfide stress and increased reactive oxygen species in S. cerevisiae. Elemental sulfur inhibited the growth of S. cerevisiae; however, it did not kill the yeast for up to 2 h exposure. The combined action of elemental sulfur and hosts’ immune responses may lead to the demise of fungal pathogens. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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18 pages, 2848 KiB  
Article
Uremic Toxin Indoxyl Sulfate Impairs Hydrogen Sulfide Formation in Renal Tubular Cells
by Chien-Lin Lu, Chun-Hou Liao, Wen-Bin Wu, Cai-Mei Zheng, Kuo-Cheng Lu and Ming-Chieh Ma
Antioxidants 2022, 11(2), 361; https://doi.org/10.3390/antiox11020361 - 11 Feb 2022
Cited by 2 | Viewed by 1750
Abstract
Hydrogen sulfide (H2S) was the third gasotransmitter to be recognized as a cytoprotectant. A recent study demonstrated that exogenous supplementation of H2S ameliorates functional insufficiency in chronic kidney disease (CKD). However, how the H2S system is impaired [...] Read more.
Hydrogen sulfide (H2S) was the third gasotransmitter to be recognized as a cytoprotectant. A recent study demonstrated that exogenous supplementation of H2S ameliorates functional insufficiency in chronic kidney disease (CKD). However, how the H2S system is impaired by CKD has not been elucidated. The uremic toxin indoxyl sulfate (IS) is known to accumulate in CKD patients and harm the renal tubular cells. This study therefore treated the proximal tubular cells, LLC-PK1, with IS to see how IS affects H2S formation. Our results showed that H2S release from LLC-PK1 cells was markedly attenuated by IS when compared with control cells. The H2S donors NaHS and GYY-4137 significantly attenuated IS-induced tubular damage, indicating that IS impairs H2S formation. Interestingly, IS downregulated the H2S-producing enzymes cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3-MST), and these effects could be reversed by inhibition of the IS receptor, aryl hydrocarbon receptor (AhR). As transcription factor specificity protein 1 (Sp1) regulates the gene expression of H2S-producing enzymes, we further showed that IS significantly decreased the DNA binding activity of Sp1 but not its protein expression. Blockade of AhR reversed low Sp1 activity caused by IS. Moreover, exogenous H2S supplementation attenuated IS-mediated superoxide formation and depletion of the cellular glutathione content. These results clearly indicate that IS activates AhR, which then attenuates Sp1 function through the regulation of H2S-producing enzyme expression. The attenuation of H2S formation contributes to the low antioxidant defense of glutathione in uremic toxin-mediated oxidative stress, causing tubular cell damage. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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9 pages, 1115 KiB  
Article
Sodium Thiosulfate Improves Hypertension in Rats with Adenine-Induced Chronic Kidney Disease
by Chien-Ning Hsu, Chih-Yao Hou, Guo-Ping Chang-Chien, Sufan Lin, Hung-Wei Yang and You-Lin Tain
Antioxidants 2022, 11(1), 147; https://doi.org/10.3390/antiox11010147 - 11 Jan 2022
Cited by 9 | Viewed by 2123
Abstract
Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2S-based therapy, can exert a protective [...] Read more.
Hypertension is highly prevalent in chronic kidney disease (CKD). Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with vasodilator properties. We, hence, investigated whether oral administration of sodium thiosulfate (STS), a clinically applicable H2S-based therapy, can exert a protective effect against hypertension in an adenine-induced CKD rat model. Eight-week-old male Sprague–Dawley rats were fed with 0.5% adenine chow for 3 weeks to induce CKD. After 1 week, the rats were divided into two groups: one without and one with STS (2 g/kg body weight/day) in drinking water for 2 weeks. Treatment with STS lowered systolic and diastolic blood pressure by 7 and 9 mm Hg, respectively. Renal H2S-generating enzyme expression was inhibited by CKD, while STS therapy increased plasma levels of H2S and thiosulfate. Additionally, restoration of nitric oxide bioavailability and rebalance of the renin–angiotensin system may contribute to the protective effects of STS. Our data suggest that the oral administration of STS improves hypertension in an adenine-induced CKD model, which brings us closer to the clinical translation of H2S-targeting therapy in CKD-induced hypertension. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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21 pages, 3367 KiB  
Article
Hydrogen Sulfide Inhibits Inflammatory Pain and Enhances the Analgesic Properties of Delta Opioid Receptors
by Aina Porta, Laura Rodríguez, Xue Bai, Gerard Batallé, Gerard Roch, Enric Pouso-Vázquez, Gianfranco Balboni and Olga Pol
Antioxidants 2021, 10(12), 1977; https://doi.org/10.3390/antiox10121977 - 11 Dec 2021
Cited by 11 | Viewed by 2652
Abstract
Chronic inflammatory pain is present in many pathologies and diminishes the patient’s quality of life. Moreover, most current treatments have a low efficacy and significant side effects. Recent studies demonstrate the analgesic properties of slow-releasing hydrogen sulfide (H2S) donors in animals [...] Read more.
Chronic inflammatory pain is present in many pathologies and diminishes the patient’s quality of life. Moreover, most current treatments have a low efficacy and significant side effects. Recent studies demonstrate the analgesic properties of slow-releasing hydrogen sulfide (H2S) donors in animals with osteoarthritis or neuropathic pain, but their effects in inflammatory pain and related pathways are not completely understood. Several treatments potentiate the analgesic actions of δ-opioid receptor (DOR) agonists, but the role of H2S in modulating their effects and expression during inflammatory pain remains untested. In C57BL/6J male mice with inflammatory pain provoked by subplantar injection of complete Freund’s adjuvant, we evaluated: (1) the antiallodynic and antihyperalgesic effects of different doses of two slow-releasing H2S donors, i.e., diallyl disulfide (DADS) and phenyl isothiocyanate (P-ITC) and their mechanism of action; (2) the pain-relieving effects of DOR agonists co-administered with H2S donors; (3) the effects of DADS and P-ITC on the oxidative stress and molecular changes caused by peripheral inflammation. Results demonstrate that both H2S donors inhibited allodynia and hyperalgesia in a dose-dependent manner, potentiated the analgesic effects and expression of DOR, activated the antioxidant system, and reduced the nociceptive and apoptotic pathways. The data further demonstrate the possible participation of potassium channels and the Nrf2 transcription factor signaling pathway in the pain-relieving activities of DADS and P-ITC. This study suggests that the systemic administration of DADS and P-ITC and local application of DOR agonists in combination with slow-releasing H2S donors are two new strategies for the treatment of inflammatory pain. Full article
(This article belongs to the Special Issue Role of Hydrogen Sulfide in Health and Disease)
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