MPST

Last update 08 May 2025

Basic Info

Synonyms

3-mercaptopyruvate sulfurtransferase, human liver rhodanese, mercaptopyruvate sulfurtransferase

+ [5]

Introduction

Transfer of a sulfur ion to cyanide or to other thiol compounds. Also has weak rhodanese activity. Detoxifies cyanide and is required for thiosulfate biosynthesis. Acts as an antioxidant. In combination with cysteine aminotransferase (CAT), contributes to the catabolism of cysteine and is an important producer of hydrogen sulfide in the brain, retina and vascular endothelial cells. Hydrogen sulfide H(2)S is an important synaptic modulator, signaling molecule, smooth muscle contractor and neuroprotectant. Its production by the 3MST/CAT pathway is regulated by calcium ions.

100 Clinical Results associated with MPST

100 Translational Medicine associated with MPST

0 Patents (Medical) associated with MPST

523

Literatures (Medical) associated with MPST

01 Jun 2025·Brain Research

Therapeutic importance of hydrogen sulfide in cognitive impairment diseases

Review

Author: Tan, Hui-Ying ; Zhou, Gui-Juan ; Cao, Jian-Ping ; Jiang, Li ; He, Juan ; Xiao, Fan ; Wei, Hai-Jun ; Zhang, Qing-Li

The brain naturally synthesizes hydrogen sulfide (H₂S) via enzymes such as cystathionine-β-synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3-MST), cysteine aminotransferase (CAT), and cystathionine-γ-lyase (CSE). From a physiological point of view, H₂S serves as a neuromodulator with antioxidant and neuroprotective properties. Recent research suggests that H₂S is crucial in regulating learning and memory, as its downregulation is commonly observed in cognitive impairment diseases. Preclinical studies suggest that external supplementation, through donors like sodium hydrosulfide (NaHS), can improve cognitive impairment in various cognitive disorder models. Moreover, numerous molecular mechanisms have been proposed to explain the effects of these H₂S donors. This review aims to detail the roles of H₂S in various models of cognitive impairment and in human subjects, highlighting its potential mechanisms and providing experimental support for its use as a novel therapeutic approach in treating cognitive disorders. Overall, H₂S plays a significant role in the treatment of cognitive impairment diseases, but further large-scale studies are still required to support the results of current research.

01 Jun 2025·Redox Biology

Cth/Mpst double ablation results in early onset fatty liver disease in lean mice

Article

Author: Valakos, Dimitrios ; Papapetropoulos, Andreas ; Markou, Maria ; Katsouda, Antonia ; Theodorou, Ioannis

Metabolic dysfunction-associated fatty liver disease (MAFLD), a condition that stems from hepatic lipid accumulation in the absence of liver damage and overt inflammation, has become the most common hepatic disorder worldwide. Hydrogen sulfide (H₂S), a gasotrasmitter, endogenously generated mainly by cystathionine-γ lyase (CTH), cystathionine-β synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (MPST) enzymes, exhibits protective effect in steatosis. Herein, we have demonstrated that CTH and MPST play a central role in MAFLD pathogenesis. Young Cth/Mpst knockout (Cth/Mpst^-/-) mice, fed a normal diet, had increased liver mass caused by enhanced hepatic lipid accumulation. Decreased insulin and glucose sensitivity was observed in CTH/MPST-deficient mice. At the cellular level, CTH/MPST inhibition resulted in increased lipid deposition and glucose uptake in hepatocytes. Transcriptome analysis revealed significant upregulation of cholesterol biosynthesis and SREBP-related genes in the liver of Cth/Mpst^-/- mice. Transcription factor enrichment analysis of differentially expressed genes between two genotypes, revealed a major impact of LXR, RXR and PPARA in the observed phenotype. Sulfide donor (SG1002) treatment attenuated the fatty liver disease of CTH/MPST-deficient mice. Our findings underline the importance of endogenously produced H₂S in the pathogenesis of MAFLD and introduce the Cth/Mpst^-/- mouse as a new animal model of early onset hepatic steatosis.

01 May 2025·Biochimie

The modulation of low molecular weight sulfur compounds levels in visceral adipose tissue of TLR2-deficient mice on a high-fat diet

Article

Author: Bronowicka-Adamska, Patrycja ; Bentke-Imiolek, Anna ; Majewska-Szczepanik, Monika ; Kaszuba, Kinga ; Szlęzak, Dominika

Obesity treatment requires an individualized approach, emphasizing the need to identify metabolic pathways of diagnostic relevance. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play a crucial role in metabolic disorders, as receptor deficiencies improves insulin sensitivity and reduces obesity-related inflammation. Additionally, hydrogen sulfide (H₂S) influences lipolysis, adipogenesis, and adipose tissue browning through persulfidation. This study investigates the impact of a high-fat diet (HFD) on low molecular weight sulfur compounds in the visceral adipose tissue (VAT) of C57BL/6 and TLR2-deficient mice. It focuses on key enzymes involved in H₂S metabolism: cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CGL), 3-mercaptopyruvate sulfurtransferase (MPST), and thiosulfate sulfurtransferase (TST). In C57BL/6 mice on HFD, MPST activity decreased, while CBS level increased, potentially compensating for H₂S production. In contrast, TLR2-deficient mice on HFD exhibited higher MPST activity but reduced level of CBS and CGL activity, suggesting that TLR2 deficiency mitigates HFD-induced changes in sulfur metabolism. TST activity was lower in TLR2-deficient mice, indicating an independent regulatory role of TLR2 in TST activity. Elevated oxidative stress, reflected by increased glutathione levels, was observed in wild-type mice. Interestingly, cysteine and cystine were detectable only in the VAT of the C57BL/6 ND group and were absent in all other groups. The capacity for hydrogen sulfide production in tissues from TLR2-/-B6 HFD group was significantly lower than in the C57BL/6 HFD group. In conclusion, TLR2 modulates sulfur metabolism, oxidative stress, and inflammation in obesity. TLR2 deficiency disrupts H₂S production and redox balance, potentially contributing to metabolic dysfunction, highlighting TLR2 as a potential therapeutic target for obesity-related metabolic disorders.

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