TST

Last update 23 Jan 2025

Basic Info

Synonyms

RDS, Rhodanese, thiosulfate sulfurtransferase

+ [1]

Introduction

Formation of iron-sulfur complexes, cyanide detoxification or modification of sulfur-containing enzymes. Other thiol compounds, besides cyanide, can act as sulfur ion acceptors. Also has weak mercaptopyruvate sulfurtransferase (MST) activity (By similarity). Together with MRPL18, acts as a mitochondrial import factor for the cytosolic 5S rRNA. Only the nascent unfolded cytoplasmic form is able to bind to the 5S rRNA.

100 Clinical Results associated with TST

100 Translational Medicine associated with TST

0 Patents (Medical) associated with TST

1,576

Literatures (Medical) associated with TST

01 Feb 2025·Pharmacology & Therapeutics

Essential role of sulfide oxidation in brain health and neurological disorders

Review

Author: Kanemaru, Eiki ; Ichinose, Fumito

Hydrogen sulfide (H₂S) is an environmental hazard well known for its neurotoxicity. In mammalian cells, H₂S is predominantly generated by transsulfuration pathway enzymes. In addition, H₂S produced by gut microbiome significantly contributes to the total sulfide burden in the body. Although low levels of H₂S is believed to exert various physiological functions such as neurotransmission and vasomotor control, elevated levels of H₂S inhibit the activity of cytochrome c oxidase (i.e., mitochondrial complex IV), thereby impairing oxidative phosphorylation. To protect the electron transport chain from respiratory poisoning by H₂S, the compound is actively oxidized to form persulfides and polysulfides by a mitochondrial resident sulfide oxidation pathway. The reaction, catalyzed by sulfide:quinone oxidoreductase (SQOR), is the initial and critical step in sulfide oxidation. The persulfide species are subsequently oxidized to sulfite, thiosulfate, and sulfate by persulfide dioxygenase (ETHE1 or SDO), thiosulfate sulfurtransferase (TST), and sulfite oxidase (SUOX). While SQOR is abundantly expressed in the colon, liver, lung, and skeletal muscle, its expression is notably low in the brains of most mammals. Consequently, the brain's limited capacity to oxidize H₂S renders it particularly sensitive to the deleterious effects of H₂S accumulation. Impaired sulfide oxidation can lead to fatal encephalopathy, and the overproduction of H₂S has been implicated in the developmental delays observed in Down syndrome. Our recent findings indicate that the brain's limited capacity to oxidize sulfide exacerbates its sensitivity to oxygen deprivation. The beneficial effects of sulfide oxidation are likely to be mediated not only by the detoxification of H₂S but also by the formation of persulfide, which exerts cytoprotective effects through multiple mechanisms. Therefore, pharmacological agents designed to scavenge H₂S and/or enhance persulfide levels may offer therapeutic potential against neurological disorders characterized by impaired or insufficient sulfide oxidation or excessive H₂S production.

01 Jan 2025·Journal of Medical Toxicology

Cyanide Medical Countermeasure Development: Assessing the Efficacy of Intramuscular Sodium Tetrathionate for the Treatment of Acute, Severe Cyanide Toxicity in Swine (Sus scrofa)

Article

Author: Boss, Gerry R ; Maddry, Col Joseph K ; Mireles, Allyson A. ; Hendry-Hofer, Tara ; Ng, Patrick C. ; Ng, Patrick C ; Bebarta, Vikhyat S. ; Maddry, Col Joseph K. ; Paredes, R Madelaine ; Bebarta, Vikhyat S ; Paredes, R. Madelaine ; Mireles, Allyson A ; Choi, Jae-Hyek ; Boss, Gerry R.

INTRODUCTIONGiven its availability and lethality, cyanide has potential for weaponization and thus has the attention of several governmental agencies. In large scale exposure scenarios, an effective countermeasure that can be administered quickly and in low volume intramuscularly may prove valuable because IV medications may have limited practical applications in these situations. Sodium tetrathionate, a potential cyanide antidote, is a compound that provides sulfur to rhodanese, the enzyme that detoxifies cyanide endogenously. Additionally, sodium tetrathionate has been reported to directly react with cyanide and is effective when administered intramuscularly. In this study, we assess the efficacy of sodium tetrathionate, when administered intramuscularly for the treatment of acute, oral cyanide poisoning in swine.METHODSWe conducted a prospective trial approved by the 59th Medical Wing Institutional Animal Care and Use Committee comparing intramuscular sodium tetrathionate (n=6) to no treatment control (n=4) in animals (Sus scrofa) exposed to a lethal dose of oral potassium cyanide. Survival at 120 minutes was the primary outcome. Lactate, a cyanide toxicity biomarker, was measured. At the study end, all animals were euthanized in compliance with the Animal Welfare Act and the American Association for Accreditation of Laboratory Animal Care. Survival between groups was summarized using a Kaplan-Meier survival curve after comparing survival by log-rank, Mantel-Cox analysis. The Mann-Whitney U test was used for comparison of other variables between groups.RESULTSAt baseline animals were similar. There was 100% survival in the treatment group and 0% survival in the control group (P=0.0011). Serum lactate significantly increased in the control group (control: 5±0.9 vs. treatment: 2.1 ± 0.5 mmol/L at 20 minutes).CONCLUSIONSodium tetrathionate (intramuscular) significantly improved survival in a large, swine model of acute, oral cyanide poisoning. Future studies will be directed at further assessing sodium tetrathionate as a potential medical countermeasure for cyanide poisoning.

01 Jan 2025·Pharmacological Research

Protective role of 3-mercaptopyruvate sulfurtransferase (MPST) in the development of metabolic syndrome and vascular inflammation

Article

Author: Psarras, Stelios ; Davos, Constantinos H ; Lefer, David J ; Varela, Aimilia ; Li, Zhen ; Zampas, Paraskevas ; Katsouda, Antonia ; Papapetropoulos, Andreas

Metabolic syndrome (MetS) is a cluster of metabolic abnormalities that occur concurrently and increase the risk of cardiovascular disease. 3-mercaptopyruvate sulfurtransferase (MPST) is a cysteine-catabolizing enzyme that yields pyruvate and hydrogen sulfide (H₂S) and plays a central role in the regulation of energy homeostasis. Herein, we seek to investigate the role of MPST/H₂S in MetS and its cardiovascular consequences using a mouse model of the disease. Mice were fed a high-fat diet (HFD) for 15 weeks to induce obesity and hyperglycemia and administrated a nitric oxide synthase inhibitor, during the last 5 weeks to induce hypertension and MetS. This model caused a mild left ventricular (LV) diastolic dysfunction and vascular endothelial dysfunction. Free H₂S and sulfane-sulfur levels were decreased in the aorta, but unaltered in the heart. Also, downregulation of MPST and thiosulfate sulfuretransferase (TST) were observed in the aorta. Global deletion of Mpst (Mpst^-/-) resulted in increased body weight and greater glucose intolerance in mice with MetS, without affecting their blood pressure, and caused an upregulation of genes involved in immune responses in the vasculature suggestive of T-cell infiltration and activation. Pharmacological restoration of H₂S levels ameliorated the comorbidities of MetS; GYY4137 administration reduced body weight and blood pressure, attenuated cardiac fibrosis and improved glucose handling and endothelium-dependent relaxation. In conclusion, this study found that reduced MPST/H₂S exacerbates the pathological changes associated with MetS and contributes to vascular inflammation. H₂S supplementation emerges as a potential therapeutic approach to treat the abnormalities associated with MetS.

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