A concentration dependent auto-relay-recognition by the same analyte: a dual fluorescence switch-on by hydrogen sulfide via Michael addition followed by reduction and staining for bio-activity

2016 ◽  
Vol 14 (2) ◽  
pp. 570-576 ◽  
Author(s):  
Avijit Kumar Das ◽  
Shyamaprosad Goswami ◽  
Gorachand Dutta ◽  
Sibaprasad Maity ◽  
Tarun kanti Mandal ◽  
...  

H2S is shown, for the first time, to play an extraordinary dual role due to its nucleophilicity and reducing property with a single chemosensor.

Synlett ◽  
2018 ◽  
Vol 29 (12) ◽  
pp. 1589-1592 ◽  
Author(s):  
Abolfazl Olyaei ◽  
Mahnaz Saraei ◽  
Reyhaneh Khoeiniha

A high-yielding cyclocondensation of 4-hydroxycoumarin, phenylglyoxal monohydrate, and heteroarylamines proceeds without catalysis, which gives novel functionalized furo[3,2-c]coumarins and heteroarylamino alkylation of coumarin products in acetonitrile under reflux, is reported for the first time. This tandem process involves sequentially an aldol condensation, Michael addition, a ring closure, and dehydration reaction.


2015 ◽  
Vol 309 (11) ◽  
pp. E925-E935 ◽  
Author(s):  
Li Sun ◽  
Song Zhang ◽  
Chengyuan Yu ◽  
Zhenwei Pan ◽  
Yang Liu ◽  
...  

Autophagy plays an important role in liver triglyceride (TG) metabolism. Inhibition of autophagy could reduce the clearance of TG in the liver. Hydrogen sulfide (H2S) is a potent stimulator of autophagic flux. Recent studies showed H2S is protective against hypertriglyceridemia (HTG) and noalcoholic fatty liver disease (NAFLD), while the mechanism remains to be explored. Here, we tested the hypothesis that H2S reduces serum TG level and ameliorates NAFLD by stimulating liver autophagic flux by the AMPK-mTOR pathway. The level of serum H2S in patients with HTG was lower than that of control subjects. Sodium hydrosulfide (NaHS, H2S donor) markedly reduced serum TG levels of male C57BL/6 mice fed a high-fat diet (HFD), which was abolished by coadministration of chloroquine (CQ), an inhibitor of autophagic flux. In HFD mice, administration of NaSH increased the LC3BII-to-LC3BI ratio and decreased the p62 protein level. Meanwhile, NaSH increased the phosphorylation of AMPK and thus reduced the phosphorylation of mTOR in a Western blot study. In cultured LO2 cells, high-fat treatment reduced the ratio of LC3BII to LC3BI and the phosphorylation of AMPK, which were reversed by the coadministration of NaSH. Knockdown of AMPK by siRNA in LO2 cells blocked the autophagic enhancing effects of NaSH. The same qualitative effect was observed in AMPKα2−/− mice. These results for the first time demonstrated that H2S could reduce serum TG level and ameliorate NAFLD by activating liver autophagy via the AMPK-mTOR pathway.


1980 ◽  
Vol 26 (2) ◽  
pp. 232-234
Author(s):  
Nell C. Roberts ◽  
Beverly O. Freeman ◽  
Henry B. Bradford Jr.

For the first time in nearly 4 decades of surveillance, H2S positive Escherichia coli have been isolated from Calcasieu Lake and River. These results are reported because of recent clinical interest in these organisms.


Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 946
Author(s):  
Tom E. Forshaw ◽  
Julie A. Reisz ◽  
Kimberly J. Nelson ◽  
Rajesh Gumpena ◽  
J. Reed Lawson ◽  
...  

Human peroxiredoxins (Prx) are a family of antioxidant enzymes involved in a myriad of cellular functions and diseases. During the reaction with peroxides (e.g., H2O2), the typical 2-Cys Prxs change oligomeric structure between higher order (do)decamers and disulfide-linked dimers, with the hyperoxidized inactive state (-SO2H) favoring the multimeric structure of the reduced enzyme. Here, we present a study on the structural requirements for the repair of hyperoxidized 2-Cys Prxs by human sulfiredoxin (Srx) and the relative efficacy of physiological reductants hydrogen sulfide (H2S) and glutathione (GSH) in this reaction. The crystal structure of the toroidal Prx1-Srx complex shows an extended active site interface. The loss of this interface within engineered Prx2 and Prx3 dimers yielded variants more resistant to hyperoxidation and repair by Srx. Finally, we reveal for the first time Prx isoform-dependent use of and potential cooperation between GSH and H2S in supporting Srx activity.


Nanoscale ◽  
2014 ◽  
Vol 6 (5) ◽  
pp. 2937-2944 ◽  
Author(s):  
Raj Kumar Koninti ◽  
Abhigyan Sengupta ◽  
Krishna Gavvala ◽  
Nirmalya Ballav ◽  
Partha Hazra

Sensing of bio-molecules using the fluorescence-switch/dual fluorescence property of an eminent anticancer drug, ellipticine, has been explored to directly monitor its efficient loading onto graphene oxide and subsequent release to biomolecules like DNA/RNA.


2009 ◽  
Vol 388 (3) ◽  
pp. 595-600 ◽  
Author(s):  
Wang Hua ◽  
Jianbin Jiang ◽  
Xing Rong ◽  
Rongzhou Wu ◽  
Huixian Qiu ◽  
...  
Keyword(s):  

2020 ◽  
Vol 245 (14) ◽  
pp. 1280-1289
Author(s):  
Rui Yang ◽  
Qiang Jia ◽  
Yan Li ◽  
Shomaila Mehmood

Diabetes mellitus has been shown to impair respiratory function. The diaphragm is an important skeletal muscle involved in respiration. Hydrogen sulfide (H2S) is one of the three endogenous gas messengers in mammals, which exhibits anti-fibrotic activity in some types of diabetes-related complications. However, whether and how H2S exerts its anti-fibrotic activity on the diabetic diaphragmatic muscle remains unclear. In this study, we explored the anti-fibrotic activity of exogenous H2S on the diaphragm using a streptozotocin (STZ)-induced diabetic rat model. The results showed that diaphragmatic biomechanical parameters were decreased, whereas the levels of inflammatory cytokines, collagen, and nucleotide-binding oligomerization domain-like receptor protein (NLRP) 3 inflammasome-related protein expression were increased in diabetic diaphragms. This implies that diabetes causes fibrosis of the diaphragm muscle through activation of NLRP3 inflammasome. After supplementation with exogenous H2S, the diaphragmatic biomechanical and pathological alterations were ameliorated and activation of NLRP3 inflammasome was inhibited, followed by a decline in diaphragm muscle inflammation and fibrosis. These results demonstrate for the first time that exogenous H2S effectively attenuates STZ-induced diabetic diaphragm muscle fibrosis, and that the underlying mechanism may be associated with suppression of the NLRP3 inflammasome-mediated inflammatory reaction. Impact statement Diabetes mellitus is a group of chronic metabolic disorders, which causes serious damage to a variety of organs, such as the retina, heart, and skeletal muscle. The diaphragm is an important skeletal muscle involved in respiration in mammals. Fibrosis of the diaphragm muscle affects its contractility, which in turn impairs respiratory function. Accumulating evidence suggests that exogenous hydrogen sulfide (H2S) exhibits anti-fibrotic activity in diabetes mellitus, but whether and how H2S exerts this anti-fibrotic effect in the diabetic diaphragm remains unclear. The current work for the first time reveals that exogenous H2S attenuates hyperglycemia-induced fibrosis of the diaphragm muscle and strengthens diaphragmatic biomechanical properties in diabetes mellitus, and the mechanism may involve the alleviation of collagen deposition by suppression of the nucleotide-binding oligomerization domain-like receptor protein (NLRP) 3 inflammasome-mediated inflammatory reaction. Therefore, H2S supplementation could be used as an efficient targeted therapy against the NLRP3 inflammasome in the diabetic diaphragm.


2018 ◽  
Vol 54 (65) ◽  
pp. 8960-8963 ◽  
Author(s):  
Xingxing Ma ◽  
Shaoyu Mai ◽  
Yao Zhou ◽  
Gui-Juan Cheng ◽  
Qiuling Song

An efficient one-pot cascade process via unprecedented quadruple cleavage of BrCF2COOEt with primary amines to afford valuable fluorine-containing heterocycles is described, in which BrCF2COOEt plays a dual role as a C1 synthon and a difluoroalkylating reagent for the first time.


RSC Advances ◽  
2014 ◽  
Vol 4 (19) ◽  
pp. 9856-9865 ◽  
Author(s):  
Ana Alcaine ◽  
Eugenia Marqués-López ◽  
Raquel P. Herrera

The synthesis of interesting β-nitrohydrazides, as the target product of our reaction, is reached for the first time under organocatalytic enantioselective conditions.


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