Sigma-Aldrich

Ammonium persulfate ACS reagent, ≥98.0%; CAS Number: 7727-54-0; EC Number: 231-786-5; Synonyms: Ammonium peroxydisulfate,PER,Ammonium peroxodisulfate,APS,AP; Linear Formula: (NH4)2S2O8; find Sigma-Aldrich-248614 MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich

Ammonium persulfate ACS reagent, = 98.0 7727-54-0

Ammonium persulfate ACS reagent, &#8805;98.0%

Ammonium persulfate

After a decade of work to address cellular uptake, the principal obstacle to RNAi-based therapeutics, there is now well-deserved, renewed optimism about RNAi-based drugs. Phase I and II studies have shown safe, strong, and durable-gene knockdown (80-90%, lasting for a month after a single injection) and/or clinical benefit in treating several liver pathologies. Although promising, these studies have also highlighted the need for robust delivery techniques to develop RNAi therapeutics for treating other organ systems and diseases. Conjugation of siRNAs to cell-specific, synthetic RNA ligands (aptamers) is being proposed as a viable solution to this problem. While encouraging, the extended use of RNA aptamers as a delivery tool for siRNAs awaits the identification of RNA aptamer sequences capable of targeting and entering the cytoplasm of many different cell types. We describe a cell-based selection process for the rapid identification and characterization of RNA aptamers suited for delivering siRNA drugs into the cytoplasm of target cells. This process, termed "cell-internalization SELEX (Systematic Evolution of Ligands by Exponential Enrichment)," entails the combination of multiple sophisticated technologies, including cell culture-based SELEX procedures, next-generation sequencing (NGS), and novel bioinformatics tools.

Cell-internalization SELEX: method for identifying cell-internalizing RNA aptamers for delivering siRNAs to target cells.

Solid state deoximation with ammonium persulfate-silica gel: Regeneration of carbonyl compounds using microwaves.	

Electrical conductivity response of polypyrrole to acetone vapor: effect of dopant anions and interaction mechanisms.	

The chloric acid method is most commonly used to obtain accurate and reproducible measurements of iodine and remove interfering substances. Unfortunately chloric acid is a potential hazard, requiring an explosion-proof hood, among other precautions. We have developed a simple, convenient, and economic method for measuring urinary iodine by using 1 mol/L ammonium persulfate, a nonexplosive, nonhazardous chemical, as the oxidizing reagent. The oxidation procedure can be completed in 30 min at a temperature of 91-95 degrees C. The iodine in the urine is then measured by a modification of the traditional colorimetric method of Sandell and Kolthoff. Urine samples (110) collected from a mixed population of healthy males and females, ranging in age from 6 to 79 years and living in the US, were analyzed for urine iodine content by two methods: the proposed ammonium persulfate method and the chloric acid method. The ammonium persulfate method has an intraassay CV of 9.1% at 0.42 +/- 0.04 micromol/L (mean +/- SD), 7.8% at 1.46 +/- 0.11 micromol/L, and 4.0% at 3.54 +/- 0.14 micromol/L. The interassay CV is 10.2% at 0.46 +/- 0.05 micromol/L, and 7.9% at 3.27 +/- 0.26 micromol/L. Recovery of iodine added to urine in vitro was 107%, 94%, and 97% for 0.42 micromol/L, 0.77 micromol/L and 3.64 micromol/L, respectively. The lower limit of detectability was 0.0034 microgram of iodine. Values for iodine in 110 urines measured by the reference chloric acid method ranged from 0.06 to 8.03 micromol/L and by the ammonium persulfate method from 0.05 to 7.4 micromol/L. The persulfate method (y) correlated extremely closely with the reference chloric acid method (x) by the Pearson correlation (y = 0.923x + 0.810 micromol/L, and r = 0.994, Sy/x = 1.841).

Ammonium persulfate: a safe alternative oxidizing reagent for measuring urinary iodine.

Ammonium persulfate, a common polymerizing agent for acrylamide gels, can inactivate yeast enolase and produce increased electrophoretic heterogeneity during disc electrophoresis in gels containing 8M urea. The use of riboflavin and light for polymerization or thioglycolate for removal of the persulfate are feasible alternatives.

Artifact produced in disc electrophoresis by ammonium persulfate.

The c-myc oncogene is one of the most commonly malfunctioning genes in human cancers, and is an attractive target for anti-gene therapy. Although synthetic oligonucleotides designed to silence c-myc expression via one of its major control elements function well in vitro, their mode of action has been indefinite. Here we show that the targeted control element adopts an intrastrand fold-back DNA tetraplex, which requires potassium ions for stability in vitro. We believe formation of the tetraplex is important for c-myc activation in vivo, and propose a transcription initiation mechanism that explains how anti-gene therapy silence c-myc at the molecular level.

DNA tetraplex formation in the control region of c-myc.

Chronic kidney disease is characterized by a gradual decline in renal function that progresses toward end-stage renal disease. Podocytes are highly specialized glomerular epithelial cells which form with the glomerular basement membrane (GBM) and capillary endothelium the glomerular filtration barrier. GBM is an extracellular matrix (ECM) that acts as a mechanical support and provides biophysical signals that control normal podocytes behavior in the process of glomerular filtration. Thus, the ECM stiffness represents an essential characteristic that controls podocyte function. Hydrolyzed Polyacrylamide (PAAm) hydrogels are smart polyelectrolyte materials. Their biophysical properties can be tuned as desired to mimic the natural ECM. Therefore, these hydrogels are investigated as new ECM-like constructs to engineer a podocyte-like basement membrane that forms with cultured human podocytes a functional glomerular-like filtration barrier. Such ECM-like PAAm hydrogel construct will provide unique opportunity to reveal podocyte cell biological responses in an in vivo-like setting by controlling the physical properties of the PAAm membranes. In this work, Hydrolyzed PAAm scaffolds having different stiffness ranging between 0.6-44 kPa are prepared. The correlation between the hydrogel structural and mechanical properties and Podocyte morphology, elasticity, cytoskeleton reorganization, and podocin expression is evaluated. Results show that hydrolyzed PAAm hydrogels promote good cell adhesion and growth and are suitable materials for the development of future 3D smart scaffolds. In addition, the hydrogel properties can be easily modulated over a wide physiological range by controlling the cross-linker concentration. Finally, tuning the hydrogel properties is an effective strategy to control the cells function. This work addressed the complexity of podocytes behavior which will further enhance our knowledge to develop a kidney-on-chip model much needed in kidney function studies in both healthy and diseased states.

Influence of Hydrolyzed Polyacrylamide Hydrogel Stiffness on Podocyte Morphology, Phenotype, and Mechanical Properties.

This paper investigates the structure of the products obtained from the polymerization of aniline with ammonium persulfate in a citrate/phosphate buffer solution at pH 3 by resonance Raman, NMR, FTIR, and UV-vis-NIR spectroscopies. All the spectroscopic data showed that the major product presented segments that were formed by a 1,4-Michael reaction between aniline and p-benzoquinone monoimine, ruling out the formation of polyazane structure that has been recently proposed. The characterization of samples obtained at different stages of the reaction indicated that, as the reaction progressed, phenazine units were formed and 1,4-Michael-type adducts were hydrolyzed/oxidized to yield benzoquinone. Raman mapping data suggested that phenazine-like segments could be related to the formation of the microspheres morphology.

Spectroscopic characterization of oligoaniline microspheres obtained by an aniline-persulfate approach.

Graphite intercalation compounds (GICs) can be considered stacks of individual doped graphene layers. Here we demonstrate a reversible formation of sulfuric acid-based GICs using ammonium persulfate as the chemical oxidizing agent. No covalent chemical oxidation leading to the formation of graphite oxide occurs, which inevitably happens when other compounds such as potassium permanganate are used to charge carbon layers. The resulting acid/persulfate-induced stage-1 and stage-2 GICs are characterized by suppression of the 2D band in the Raman spectra and by unusually strong enhancement of the G band. The G band is selectively enhanced at different doping levels with different excitations. These observations are in line with recent reports for chemically doped and gate-modulated graphene and support newly proposed theories of Raman processes. At the same time GICs have some advantageous differences over graphene, which are demonstrated in this report. Our experimental observations, along with earlier reported data, suggest that at high doping levels the G band cannot be used as the reference peak for normalizing Raman spectra, which is a commonly used practice today. A Fermi energy shift of 1.20-1.25 eV and ∼1.0 eV was estimated for the stage-1 and stage-2 GICs, respectively, from the Raman and optical spectroscopy data.

Reversible formation of ammonium persulfate/sulfuric acid graphite intercalation compounds and their peculiar Raman spectra.

Strigolactones (SLs) are endogenous hormones and exuded signaling molecules in plant responses to low levels of mineral nutrients. Key mediators of the SL signaling pathway in rice include the α/β-fold hydrolase DWARF 14 (D14) and the F-box component DWARF 3 (D3) of the ubiquitin ligase SCF(D3) that mediate ligand-dependent degradation of downstream signaling repressors. One perplexing feature is that D14 not only functions as the SL receptor but is also an active enzyme that slowly hydrolyzes diverse natural and synthetic SLs including GR24, preventing the crystallization of a binary complex of D14 with an intact SL as well as the ternary D14/SL/D3 complex. Here we overcome these barriers to derive a structural model of D14 bound to intact GR24 and identify the interface that is required for GR24-mediated D14-D3 interaction. The mode of GR24-mediated signaling, including ligand recognition, hydrolysis by D14, and ligand-mediated D14-D3 interaction, is conserved in structurally diverse SLs. More importantly, D14 is destabilized upon the binding of ligands and D3, thus revealing an unusual mechanism of SL recognition and signaling, in which the hormone, the receptor, and the downstream effectors are systematically destabilized during the signal transduction process.

Destabilization of strigolactone receptor DWARF14 by binding of ligand and E3-ligase signaling effector DWARF3.

Persulfates have been reported to cause both delayed-type and immediate skin reactions. They may also cause immediate reactions of the mucous membranes of the bronchial system through inhalation, leading to asthma and rhinitis. Anaphylactic reactions caused by contact with persulfates are rare. The mechanism of immediate reactions caused by persulfates is unclear. To report 2 cases with systemic reactions after skin contact with persulfates, and to propose a test protocol for diagnosing immediate reactions caused by persulfates. Prick tests with serial dilutions of ammonium and potassium persulfate were performed. Patch tests were also performed with the two agents. Persulfate-specific IgE was detected with two different IgE immunoblotting techniques. Prick tests were positive with ammonium and potassium persufate, but no specific IgE was detected in the serum. Patch tests showed early positive reactions to both persulfates in 1 patient. Prick tests and patch tests can be valuable in the testing of patients with a suspicion of an immediate-type reaction caused by persulfates. The mechanism of these reactions remains unclear.

Anaphylaxis and severe systemic reactions caused by skin contact with persulfates in hair-bleaching products.

Stimuli-responsive hydrogels were recently proposed for energy-saving forward osmosis (FO) process. However, their low water flux and dewatering ability for reuse make them less attractive for industrial desalination process. In this work, the co-polymer microgels of N-isopropylacrylamide and acrylic acid with different mixing ratios were synthesized using surfactant-free emulsion polymerization to produce submicron-size hydrogels with high surface area and fast swelling-deswelling response. The microgels were employed as draw agents in a laboratory scale FO desalination system. The microgel-based FO process performed a high water flux up to 23.8 LMH and high water recovery ability of 72.4%. In addition, we explored a new conductivity measurement method to online analyze water flux of the FO system. This on-line conductivity analysis approach appeared to be an accurate and efficient method for evaluating microgel-based FO desalination performance. Our experimental data revealed that the stimuli-responsive microgel was an efficient draw agent for FO desalination.

Functionalized thermo-responsive microgels for high performance forward osmosis desalination.

The implant-host interface is a critical element in guiding tissue or organ regeneration. We previously developed hydrogels comprising interpenetrating networks of recombinant human collagen type III and 2-methacryloyloxyethyl phosphorylcholine (RHCIII-MPC) as substitutes for the corneal extracellular matrix that promote endogenous regeneration of corneal tissue. To render them functional for clinical application, we have now optimized their composition and thereby enhanced their mechanical properties. We have demonstrated that such optimized RHCIII-MPC hydrogels are suitable for precision femtosecond laser cutting to produce complementing implants and host surgical beds for subsequent tissue welding. This avoids the tissue damage and inflammation associated with manual surgical techniques, thereby leading to more efficient healing. Although we previously demonstrated in clinical testing that RHCIII-based implants stimulated cornea regeneration in patients, the rate of epithelial cell coverage of the implants needs improvement, e.g. modification of the implant surface. We now show that our 500μm thick RHCIII-MPC constructs comprising over 85% water are suitable for microcontact printing with fibronectin. The resulting fibronectin micropatterns promote cell adhesion, unlike the bare RHCIII-MPC hydrogel. Interestingly, a pattern of 30μm wide fibronectin stripes enhanced cell attachment and showed the highest mitotic rates, an effect that potentially can be utilized for faster integration of the implant. We have therefore shown that laboratory-produced mimics of naturally occurring collagen and phospholipids can be fabricated into robust hydrogels that can be laser profiled and patterned to enhance their potential function as artificial substitutes of donor human corneas.

Functional fabrication of recombinant human collagen-phosphorylcholine hydrogels for regenerative medicine applications.

The origin of fracture in epithelial cell sheets subject to stretch is commonly attributed to excess tension in the cells' cytoskeleton, in the plasma membrane, or in cell-cell contacts. Here, we demonstrate that for a variety of synthetic and physiological hydrogel substrates the formation of epithelial cracks is caused by tissue stretching independently of epithelial tension. We show that the origin of the cracks is hydraulic; they result from a transient pressure build-up in the substrate during stretch and compression manoeuvres. After pressure equilibration, cracks heal readily through actomyosin-dependent mechanisms. The observed phenomenology is captured by the theory of poroelasticity, which predicts the size and healing dynamics of epithelial cracks as a function of the stiffness, geometry and composition of the hydrogel substrate. Our findings demonstrate that epithelial integrity is determined in a tension-independent manner by the coupling between tissue stretching and matrix hydraulics.

Hydraulic fracture during epithelial stretching.

Snake venoms are excellent sources of pharmacologically active proteins and peptides, and hence are potential sources of leads for drug developments. It has been previously established that krait (Bungarus genus) venoms contain mainly neurotoxins. A screening for anticoagulants showed that Bungarus fasciatus venom exhibits potent anticoagulant effect in standard clotting assays. Through sequential fractionation of the venom by size exclusion and high performance liquid chromatographies, coupled with functional screening for anticoagulant activities, we have isolated and purified two anticoagulant proteins, termed BF-AC1 (Bungarus fasciatusanticoagulant 1) and BF-AC2. They have potent inhibitory activities (IC50 of 10 nM) on the extrinsic tenase complex. Structurally, these proteins each has two subunits covalently held together by disulfide bond(s). The N-terminal sequences of the individual subunits of BF-AC1 and BF-AC2 showed that the larger subunit is homologous to phospholipase A2, while the smaller subunit is homologous to Kunitz type serine proteinase inhibitor. Functionally, in addition to their anticoagulant activity, these proteins showed presynaptic neurotoxic effects in both in vivo and ex vivo experiments. Thus, BF-AC1 and BF-AC2 are structurally and functionally similar to β-bungarotoxins, a class of neurotoxins. The enzymatic activity of phospholipase A2 subunit plays a significant role in the anticoagulant activities. This is the first report on the anticoagulant activity ofβ-bungarotoxins and these results expand on the existing catalogue of haemostatically active snake venom proteins.

Identification and characterisation of novel inhibitors on extrinsic tenase complex from Bungarus fasciatus (banded krait) venom.

In Mycobacterium tuberculosis the sulfate activating complex provides a key branching point in sulfate assimilation. The complex consists of two polypeptide chains, CysD and CysN. CysD is an ATP sulfurylase that, with the energy provided by the GTPase activity of CysN, forms adenosine-5'-phosphosulfate (APS) which can then enter the reductive branch of sulfate assimilation leading to the biosynthesis of cysteine. The CysN polypeptide chain also contains an APS kinase domain (CysC) that phosphorylates APS leading to 3'-phosphoadenosine-5'-phosphosulfate, the sulfate donor in the synthesis of sulfolipids. We have determined the crystal structures of CysC from M. tuberculosis as a binary complex with ADP, and as ternary complexes with ADP and APS and the ATP mimic AMP-PNP and APS, respectively, to resolutions of 1.5 Å, 2.1 Å and 1.7 Å, respectively. CysC shows the typical APS kinase fold, and the structures provide comprehensive views of the catalytic machinery, conserved in this enzyme family. Comparison to the structure of the human homolog show highly conserved APS and ATP binding sites, questioning the feasibility of the design of specific inhibitors of mycobacterial CysC. Residue Cys556 is part of the flexible lid region that closes off the active site upon substrate binding. Mutational analysis revealed this residue as one of the determinants controlling lid closure and hence binding of the nucleotide substrate.

Crystal structures of the kinase domain of the sulfate-activating complex in Mycobacterium tuberculosis.

Ischemia-reperfusion (IR) of liver results in hepatocytes (HP) and sinusoidal endothelial cells (LSEC) irreversible damage. Ischemic preconditioning protects IR damage upon adenosine A2a receptor (A2aR) stimulation. Understanding the phenotypic changes that underlie hepatocellular damage and protection is critical to optimize strategies against IR. The proteome of HP and LSEC, isolated from sham or IR exposed mice, receiving or not the A2aR agonist CGS21680 (0.5mg/kg b.w.), was analyzed by 2-D DIGE/MALDI-TOF. We identified 64 proteins involved in cytoprotection, regeneration, energy metabolism and response to oxidative stress; among them, 34 were associated with IR injury and A2aR protection. The main pathways, downregulated by IR and upregulated by CGS21680 in HP and LSEC, were related to carbohydrate, protein and lipid supply and metabolism. In LSEC, IR reduced stress response enzymes that were instead upregulated by CGS21680 treatment. Functional validation experiments confirmed the metabolic involvement and showed that inhibition of pyruvate kinase, 3-chetoacylCoA thiolase, and arginase reduced the protection by CGS21680 of in vitro hypoxia-reoxygenation injury, whereas their metabolic products induced liver cell protection. Moreover, LSEC, but not HP, were sensitive to H2O2-induced oxidative damage and CGS21680 protected against this effect. IR and A2aR stimulation produces pathological and protected liver cell phenotypes, respectively characterized by down- and upregulation of proteins involved in the response to O2 and nutrients deprivation during ischemia, oxidative stress, and reactivation of aerobic energy synthesis at reperfusion. This provides novel insights into IR hepatocellular damage and protection, and suggests additional therapeutic options.

Mouse hepatocytes and LSEC proteome reveal novel mechanisms of ischemia/reperfusion damage and protection by A2aR stimulation.

Podosomes are adhesion structures formed in monocyte-derived cells. They are F-actin-rich columns perpendicular to the substrate surrounded by a ring of integrins. Here, to measure podosome protrusive forces, we designed an innovative experimental setup named protrusion force microscopy (PFM), which consists in measuring by atomic force microscopy the deformation induced by living cells onto a compliant Formvar sheet. By quantifying the heights of protrusions made by podosomes onto Formvar sheets, we estimate that a single podosome generates a protrusion force that increases with the stiffness of the substratum, which is a hallmark of mechanosensing activity. We show that the protrusive force generated at podosomes oscillates with a constant period and requires combined actomyosin contraction and actin polymerization. Finally, we elaborate a model to explain the mechanical and oscillatory activities of podosomes. Thus, PFM shows that podosomes are mechanosensing cell structures exerting a protrusive force.

Protrusion force microscopy reveals oscillatory force generation and mechanosensing activity of human macrophage podosomes.

We have developed a general method for controlling molecular functions using a photodegradable hydrogel; gels containing molecules made from such materials are capable of release and activation by light stimulus. As the elimination of molecular leaching from the gel before irradiation was a barrier to the precise control of molecular function, we optimized the monomer used in gel preparation during this study. The addition of N,N'-methylenebis(acrylamide) (MBAA) inhibited molecular leaching from the gel; the MBAA concentration is a critical factor in controlling the leaching of encapsulated molecules. We succeeded in preparing a gel that halved the leaching of small encapsulated molecules, while the leaching of large molecules, such as albumin (66 kDa) and ferritin (450 kDa), was at negligible levels, or disappeared. The on/off ratios (released amount/leached amount) of albumin and ferritin were 8 and 17, respectively.

Reduction of molecular leaching from a gel matrix for the precisely controlled release of encapsulated molecules by light stimulus.

The Prostaglandin E2 (PGE2) signaling mechanism within fibroblasts is of growing interest as it has been shown to prevent numerous fibrotic features of fibroblast activation with limited evidence of downstream pathways. To understand the mechanisms of fibroblasts producing tremendous amounts of PGE2 with autocrine effects, we apply a strategy of combining a wide-screening of PGE2-induced kinases with quantitative phosphoproteomics. Our large-scale proteomic approach identified a PKA signal transmitted through phosphorylation of its substrates harboring the R(R/X)X(S*/T*) motif. We documented 115 substrates, of which 72 had 89 sites with a 2.5-fold phosphorylation difference in PGE2-treated cells than in untreated cells, where approximately half of such sites were defined as being novel. They were compiled by networking software to focus on highlighted activities and to associate them with a functional readout of fibroblasts. The substrates were associated with a variety of cellular functions including cytoskeletal structures (migration/motility), regulators of G-protein coupled receptor function, protein kinases, and transcriptional/translational regulators. For the first time, we extended the PGE2 pathway into an elaborate network of interconnecting phosphoproteins, providing vital information to a once restricted signalosome. These data provide new insights into eicosanoid-initiated cell signaling with regards to the regulation of fibroblast activation and the identification of new targets for evidenced-based pharmacotherapy against fibrosis.

Quantitative phosphoproteomic analysis of signaling downstream of the prostaglandin e2/g-protein coupled receptor in human synovial fibroblasts: potential antifibrotic networks.

Ammonium persulfate

ACS reagent, ≥98.0%

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