Tert-butyl Hydroperoxide Research Articles

Combination of phenylsilsesquioxane and acetate ligands as an approach to a record high nuclear Cu13Na2-cage. Synthesis, unique structure, and catalytic activity.

Self-assembly synthesis of mixed-ligand (silsesquioxane/acetate) complex allows to isolate record high nuclear copper(II) Cu13-cage (1). In the presence of two additional sodium ions, a unique molecular architecture, with triple combination of ligands (cyclic and acyclic silsesquioxanes as well as acetates), has been formed. The structure was established by single-crystal X-ray diffraction based on the use of synchrotron radiation. Complex 1 was evaluated as precatalyst in the Baeyer-Villiger oxidation of cyclohexanone towards ε-caprolactone, employing hydrogen peroxide, tert-butyl hydroperoxide (TBHP) or m-chloroperoxybenzoic acid (mCPBA) as oxidants, in an aqueous acidic acetonitrile medium. The direct formation of the lactone from cyclohexane via a tandem peroxidative oxidation/Baeyer-Villiger oxidation was also studied. For both substrates, the best results (ε-caprolactone yields up to 100% or 26%, from cyclohexanone or cyclohexane, respectively) were achieved with mCPBA under considerably mild conditions, i.e., conventional heating at 50 °C for 4 h or microwave (MW) irradiation at 80 °C for only 30 minutes.

A Review on Hepatoprotective Effect of Chrysin: Preclinical Implications and Molecular Cascades Came into Focus.

Chrysin, a flavone nutraceutical, possesses several beneficial pharmacological properties, which has gained much emphasis in recent years. The biological effects of chrysin are exerted due to impeding or activating multifarious cellular and molecular pathways. Our findings indicated that chrysin inhibited tumor progression in various cancer cell lines by repressing the formation of a sphere and upregulated protein expression of Src homology region 2 domain-containing phosphatase-1 (SHP-1), alleviating phosphorylated-signal transducer and activator of transcription 3 (p-STAT3) and transaction workflow innovation standards team1 (Twist1), sustaining phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and endorsing mitogen-activated protein kinase kinase1 (MEK1) overexpression, increasing the cytochrome c release, mitochondrial reactive oxygen species (ROS) formation, matrix metalloproteinases (MMP) collapse, and caspase-3 activity, modulating p53/ B-cell lymphoma-2 (Bcl-2)/caspase-9 cascade, cyclooxygenase- 2 (COX-2), nuclear factor kappa B proposition 65 (NF-kB p65) expression and also decreasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Chrysin prevented cyclophosphamide, doxorubicin, cisplatin, methotrexate, paracetamol, alcohol, carbon tetrachloride, tert-butyl hydroperoxide (tBHP) and thioacetamide. Chrysin has protective properties against oxidative stress, inflammation, hepatotoxicity, liver fibrosis, steatosis, and hepatocellular carcinoma. Chrysin's most common hepatoprotective biochemical and molecular mechanisms involve the ability to control enzyme synthesis, scavenge free radicals, boost the antioxidant response, induce apoptosis, and modify the synthesis of proinflammatory and profibrotic cytokines.Chrysin is a valuable nutraceutical with broad therapeutic feasibility, but to confirm its representative hepatoprotective potential, clinical studies are advised. It would also be interesting to use cutting-edge drug delivery techniques or include bio-enhancers.

Oxidants-induced high levels of nitric oxide impair the antioxidative property of molybdenum nanoparticles in HUVE cells

In recent years, there has been significant interest in the biomedical potential of redox-active molybdenum nanoparticles (Mo NPs) due to their varied responses from oxidative to antioxidative. Our knowledge of the bio-response of Mo NPs in endothelial cells is lacking. We, therefore, are prompted to examine the biocompatibility of well-characterized Mo NPs in human endothelial (HUVE) cells and their potential antioxidative response against standard oxidants- tert-butyl hydroperoxide (t-BHP) and hydrogen peroxide (H2O2). The study found that Mo NPs were highly biocompatible in HUVE cells and enhanced cellular antioxidant glutathione (GSH), significantly protecting cells against exogenous oxidants. Moreover, Mo NPs significantly restored the loss of mitochondrial membrane potential (MMP) determined by the Rh123 probe. They decreased reactive oxygen species (ROS) levels as measured by DHE and DCFH-DA probes. In light of Mo involvement in the nitric oxide (NO) metabolism and dependency of HUVE cells on NO signaling, intracellular NO was determined using DAR-2 fluorescent dye and the Griess assay. NO was not produced significantly by Mo NPs alone or t-BHP or H2O2. However, NO generation was significantly high when HUVE cells were co-exposed with Mo NPs and exogenous oxidants. Although the exact mechanism is unclear to us, our study concludes that the enhanced generation of NO under the co-exposure of oxidants with Mo NPs can impair the potential antioxidative property of Mo NPs, especially in endothelial cells. The study also suggests that NO modulatory strategies can improve and broaden the antioxidative properties of Mo-based nanoparticles.

Ergothioneine-rich Lentinula edodes mushroom extract restores mitochondrial functions in senescent HT22 cells

A decline in mitochondrial functions associated with ageing is the key factor of free radical generation which contributes to age-related pathologies. Protecting healthy functional mitochondrial networks with antioxidants is critical in promoting healthy ageing. This study aimed to investigate the protective effect of ergothioneine (EGT)-rich Lentinula edodes extract (LE-ETH) against tert-butyl hydroperoxide (t-BHP) assaulted senescent HT22 cells. Mitochondrial function was evaluated by measuring mitochondrial membrane potential (MMP), ATP levels and mitochondrial toxicity. The protective mechanisms were elucidated via the exploration of antioxidant and mitochondrial biogenesis signalling pathways. Our results revealed that a low dose of t-BHP increases mitochondrial toxicity. The pretreatment with 100 µg/mL of LE-ETH and the equimolar concentration of EGT for 8 h significantly improve the mitochondrial function and reduced inflammation. Through gene expression studies, we demonstrated that pretreatment of LE-ETH significantly improves the antioxidant and mitochondrial biogenesis pathway via Nrf2 signaling axis. However, the downstream genes of the mitochondrial biogenesis pathway were unaffected by equimolar EGT concentration. Gas chromatography-mass spectrum (GC–MS) analysis was carried out to identify the bioactive compounds that are present in LE-ETH extract which contributed to its efficacy in improving the mitochondrial functions. A total of 23 compounds consisting of phenols, fatty acids, and sterols were identified in the ethanolic extract. Pentanoic acid was the major compound identified in LE-ETH. These findings demonstrated that EGT-rich L.edodes mushroom is a potential neuroprotective agent which could serve as a potential therapeutic strategy for the preservation of mitochondrial functions in healthy ageing explorations.

Could the transcription factor AtnN coordinating the aspercryptin secondary metabolite gene cluster in Aspergillus nidulans be a global regulator?

Products of dormant secondary metabolite gene clusters of fungal genomes can be exploited for medical purposes as bioactive agents. These clusters can be switched on under oxidative stress and may endow fungi with a versatile chemical armory in a competitive niche. In Aspergillus nidulans, the aspercryptin gene cluster, including the synthase [atnA (AN7884)] and its transcription factor (atnN), was activated under menadione sodium bisulfite (MSB) treatment. In this study, we generated and phenotypically examined the gene deletion and overexpression mutants of atnN and studied the secondary metabolite production of the mutants. Overexpression of atnN significantly reduced the colony growth of surface cultures compared to the control. The ΔatnN gene deletion strain showed higher sensitivity to tert-butyl hydroperoxide (tBOOH), while the atnNOE strain was more resistant to MSB, Congo Red, and sorbitol. Interestingly, deletion of atnN decreased cleistothecia formation of A. nidulans. Manipulation of atnN affected the synthesis of several secondary metabolites, for example, the siderophore production of A. nidulans. The extracellular triacetylfusarinine C (TAFC) production decreased, while the intracellular ferricrocin (FC) concentration of the cultures increased in the atnNOE mutant cultivating A. nidulans in a complex medium containing 1% mycological peptone and 2% maltose. In Czapek-Dox Broth medium, increased asperthecin production was observed in the ΔatnN mutant. The mycotoxin sterigmatocystin synthesis elevated in the ΔatnN mutant, while reduced in the atnNOE mutant on minimal medium. Our study supports previous observations that secondary metabolite production is coordinated in a complex way, and the linkage of stress response, sexual reproduction, and secondary metabolite production can be governed by several transcription factors.

High-throughput screening-based design of multifunctional natural polyphenol nano-vesicles to accelerate diabetic wound healing

Oxidative stress is a major pathological factor that impedes the diabetic wound healing process. Procyanidins (PC) form nanoparticle-vesicles (PPNs) through hydrogen bonding and exhibit good drug delivery capability; however, their application in diabetic wounds is unsatisfactory. To meet the antioxidant needs for treating, high-throughput screening in the natural product library (NPL) under in vitro oxidative stress conditions was conducted to enhance the antioxidant activity of PPNs. HUVECs treated with tert-Butyl Hydroperoxide (TBHP) were established as screening model in vitro. Baicalein (BAI) was identified from over 600 products in the library as the most effective one to combat oxidative stress. Further study showed that PC and BAI may react in equal proportions to synthesize new vesicles, named BAI-PC Polyphenolic nanovesicles (BPPNs), which possess reactive oxygen species (ROS) responsive and antioxidant effects. Network pharmacology indicated that in diabetic wounds, the target genes of PC are mainly enriched in the vascular endothelial growth factor (VEGF)-related pathways, while BAI primarily regulates tyrosine phosphorylation. The complementarity between the two has been validated in both in vitro and in vivo experiments. In summary, the antioxidant drug BAI, identified through high-throughput screening of NPL, could optimize the biological function of PPNs; the newly-synthesized BPPNs may accelerate diabetic wound healing through dual mechanisms of promoting angiogenesis and combating oxidative stress.Graphical abstract

Homogeneous catalytic oxidation of thymol with dinuclear Cu(II)-2-phenyl propionate-bipyridine complex

A carboxylate-bridged dinuclear copper(II) complex, [Cu2(μ2-η2:η1(ppa)2(μ2-η1:η1 (ppa)bpy)2]·ClO4·H2O (ppa (C9H9OO) = 2-phenyl propionate, bpy = 2,2′-bipyridine), was prepared and its structure was determined by X-ray diffraction analysis. The octacoordinated Cu(II) dimer complex exhibits an asymmetric conformation, with the metal centers linked by two distinct modes of the carboxylate group. These include an asymmetric chelating bridging bidentate involving two ppa ligands and a syn-syn bidentate bridging mode involving one ppa ligand. The complex was employed as a catalyst for the oxidation of thymol, demonstrating a high degree of quantitative conversion and selectivity with TBHP across a range of solvents at moderate temperatures. The homogeneous catalytic system, comprising Cu(II)-2-phenyl propionate-bipyridine, tert-butylhydroperoxide (TBHP) as oxidant, and a polar aprotic solvent (acetonitrile or acetone), demonstrated high turnover numbers (TOF) in the absence of any additives. The impact of temperature, solvent, the ratio of thymol to TBHP, different oxidants and the quantity of catalyst on the catalytic activity and product selectivity was examined. Under optimized conditions, the maximum conversion of thymol (100 %) was obtained with 100 % selectivity to thymoquinone with TBHP after 35 min at the thymol to catalyst mole ratio of 267 (TOF = 449 h−1) in acetonitrile (MeCN) at 55 °C. Based on the available evidence, this activity and selectivity to thymoquinone represent the highest reported level of performance achieved by a homogeneously copper-catalysed process.

PLGA/BK microspheres targeting the bradykinin signaling pathway as a therapeutic strategy to delay intervertebral disc degeneration

Intervertebral disc degeneration(IVDD) is a common spinal condition with limited effective treatments available. This study aims to investigate the impact of poly(lactic-co-glycolic acid)/Bradykinin (PLGA/BK) microspheres on IVDD and its underlying mechanisms. We collected nucleus pulposus samples from both healthy and degenerated human intervertebral disks and conducted immunohistochemical analyses, revealing reduced BK expression in degenerated tissues. Subsequently, we used BK to treat nucleus pulposus cells and conducted Bulk RNA sequencing (RNA-seq), identifying BK’s involvement in cellular senescence, extracellular matrix metabolism, and the PI3K signaling pathway. Further experiments using tert-butyl hydroperoxide (TBHP)-induced cell senescence showed that BK treatment reduced senescence, enhanced extracellular matrix synthesis, and inhibited degradation, along with activation of the PI3K pathway. These effects were mediated through B2R (BK receptor 2) and the downstream PI3K pathway. Following this, we developed sustained-release BK microspheres with an optimized manufacturing process. In vitro co-culture experiments showed no observable toxicity. We established an IVDD model in rat tail vertebrae through fine needle puncture, administering local injections of BK sustained-release microspheres. Using various experimental methods, including X-ray, MRI, histopathology, and immunohistochemistry, we found that these microspheres could slow the progression of IVDD. This study highlights the potential of injectable PLGA/BK microspheres to regulate cellular senescence and extracellular matrix metabolism via the B2R and PI3K pathways, ultimately delaying IVDD.

The Efficient and Environmentally Friendly Chlorination of Arene, Alcohol, Halobenzene, and Peroxide Catalyzed by Fe-Ba Binary Oxides Using Hydrochloric Acid as Chlorine Source and Aqueous H2O2 as Oxidant.

A series of Fe-Ba mixed oxides, including a pure Fe-containing sample as a reference, have been synthesized via a sol-gel process using Fe3+ or Fe2+ salts and BaSO4 as raw materials, with Pluronic P123 serving as a template. These oxides have been thoroughly characterized and subsequently utilized as catalysts for the chlorination of various organic molecules. Commercial hydrochloric acid, known for its relative safety, and environmentally friendly aqueous hydrogen peroxide were employed as the chlorine source and oxidant, respectively. The pure Fe-containing catalyst displays excellent thermal stability between 600 and 800 °C and exhibited moderate to high conversions in the chlorination of toluene, benzene, and tert-butyl hydroperoxide, with remarkable ortho-selectivity in chlorination of toluene. The combination of Fe3+ salt with BaSO4 in the sol-gel process results in a Fe-Ba mixed oxide catalyst composed of BaO2, BaFe4O7, and Fe2O3, significantly enhancing the chlorination activity compared to that displayed by the pure Fe catalyst. Notably, the chlorination of tert-butyl hydroperoxide (TBHP) does not require additional oxidants such as H2O2, and involves both electrophilic substitution and nucleophilic addition. Notably, the chlorination of bromobenzene yields chlorobenzene as the sole product, a transformation that has not been previously reported. Overall, this catalytic chlorination system holds promise for advancing the chlorination industry and enhancing pharmaceutical production.

Modulation of Urea Transport Attenuates TLR2-Mediated Microglial Activation and Upregulates Microglial Metabolism In Vitro.

Background: Alzheimer's disease (AD) is a neurodegenerative disorder traditionally characterised by the presence of amyloid beta (Aβ) plaques and neurofibrillary tau tangles in the brain. However, emerging research has highlighted additional metabolic hallmarks of AD pathology. These include the metabolic reprogramming of microglia in favour of glycolysis over oxidative phosphorylation. This shift is attributed to an 'M1'-like pro-inflammatory phenotype, which exacerbates neuroinflammation and contributes to neuronal damage. The urea cycle also presents as an altered metabolic pathway in AD, due to elevated urea levels and altered expression of urea cycle enzymes, metabolites, and transporters in the brain. However, to date, these changes remain largely unexplored. Methods: This study focuses on understanding the effects of extracellular urea and urea transporter-B (UT-B) inhibition on inflammatory changes in lipoteichoic acid (LTA)-stimulated BV2 microglia and on the viability of SH-SY5Y neuronal cells under oxidative stress and neurotoxic conditions. Results: In BV2 microglia, UT-B inhibition demonstrated a notable anti-inflammatory effect by reducing the formation of nitric oxide (NO) and the expression of tumour necrosis factor α (TNFα) and CCL2 in response to stimulation with the toll-like receptor (TLR)2 agonist, lipoteichoic acid (LTA). This was accompanied by a reduction in extracellular urea and upregulation of UT-B expression. The application of exogenous urea was also shown to mediate the inflammatory profile of BV2 cells in a similar manner but had only a modest impact on UT-B expression. While exposure to LTA alone did not alter the microglial metabolic profile, inhibition of UT-B upregulated the expression of genes associated with both glycolysis and fatty acid oxidation. Conversely, neither increased extracellular urea nor UT-B inhibition had a significant impact on cell viability or cytotoxicity in SH-SY5Y neurones exposed to oxidative stressors tert-butyl hydroperoxide (t-BHP) and 6-hydroxydopamine (6-OHDA). Conclusions: This study further highlights the involvement of urea transport in regulating the neuroinflammation associated with AD. Moreover, we reveal a novel role for UT-B in maintaining microglial metabolic homeostasis. Taken together, these findings contribute supporting evidence to the regulation of UT-B as a therapeutic target for intervention into neuroinflammatory and neurodegenerative disease.

Metal-Free Decarboxylative Cyanomethylation of β-Aryl/Heteroaryl Substituted α,β-Unsaturated Carboxylic Acids to γ-Ketonitriles.

A decarboxylative cyanomethylation of β-aryl/heteroaryl substituted α,β-unsaturated carboxylic acids has been accomplished via C(sp3)-H activation of alkyl nitriles to afford diverse γ-ketonitriles by making use of 1,8-diazabicyclo[5.4.0]undec-7-ene (DBU) and tert-butyl hydroperoxide (TBHP). The present report offers a metal-free approach and is featured with a broad substitution pattern and functional group compatibility.

Chorein deficiency promotes ferroptosis.

Ferroptosis is a type of programmed cell death owed to an intracellular accumulation of iron resulting in the generation reactive oxygen species, which in turn can cause peroxidation of plasma membrane lipids and ultimately result in cell death. We investigated the potential involvement of VPS13A deficiency in ferroptosis. The VPS13A gene encodes for chorein, and its deficiency is a molecular cause of chorea-acanthocytosis (ChAc), a Huntington-like disease with neurodegeneration in the striatum. In our previous study, we found male infertility characterized by increased malondialdehyde staining of the spermatozoa in the testes of the ChAc model mice. Thus, in this study we performed metabolome analysis of sperm extracted from the epididymis of the ChAc model mice, which revealed decreased cystine levels, suggesting an association between chorein deficiency and ferroptosis. We then investigated the role of chorein in ferroptosis using VPS13A knockdown (VPS13A-KD) HEK293 cells. We found that VPS13A-KD cells displayed a significantly diminished resistance to tert-Butyl hydroperoxide (tBHP)-induced lipid peroxidation and cell death compared to control cells, which could be rescued by treatment with ferrostatin-1. Moreover, VPS13A-KD cells showed Fe(II) accumulation, suggesting an impaired capacity for divalent iron removal. In the cytosolic fraction of VPS13A-KD cells, the protein level of glutathione peroxidase 4 (GPX4) was significantly reduced, suggesting that dysfunction of chorein impairs GPX4 transport, thereby facilitating ferroptosis. These results suggest that ferroptosis may contribute to neurodegeneration in ChAc caused by loss of chorein function.

Astaxanthin mediated repair of tBHP-Induced cellular injury in chondrocytes

ABSTRACT Objective This study investigates how astaxanthin (AST) counters tert-butyl hydroperoxide (tBHP)-induced cellular damage in C28/I2 chondrocytes, focusing on the circ-HP1BP3/miR-139-5p/SOD1 signaling pathway and its use in sustained-release microspheres for osteoarthritis treatment. Methods We employed a variety of techniques including real-time quantitative PCR, Western blot, ELISA, and dual-luciferase reporter gene assays to explore AST's molecular effects. Additionally, the efficacy of AST-loaded sustained-release microspheres was evaluated in vitro and in a mouse model of osteoarthritis. Results AST significantly enhanced SOD1 expression, reducing apoptosis and inflammation in damaged cells. The AST-loaded microspheres showed promising in vitro drug release, improved cell viability, and reduced oxidative stress. In the osteoarthritis mouse model, they effectively decreased joint inflammation and increased the expression of chondrocyte markers. Conclusion Astaxanthin effectively mitigates oxidative stress and inflammation in chondrocytes via the circ-HP1BP3/miR-139-5p/SOD1 pathway. The development of AST-loaded microspheres offers a novel and promising approach for osteoarthritis therapy, potentially extending to osteoarthritis treatment.

β-Hydroxybutyrate enhances chondrocyte mitophagy and reduces cartilage degeneration in osteoarthritis via the HCAR2/AMPK/PINK1/Parkin pathway.

Osteoarthritis (OA) is widely recognized as the prevailing joint disease associated with aging. The ketogenic diet (KD) has been postulated to impede the advancement of various inflammatory ailments. β-Hydroxybutyrate (βOHB), a prominent constituent of ketone bodies, has recently been proposed to possess crucial signaling capabilities. In this study, we propose to explore the role and mechanism of βOHB in OA. Tissue staining and inflammatory factor assay were employed to evaluate the impacts of KD and βOHB on OA rats. The oxidative stress conditions in chondrocytes were induced using tert-butyl hydroperoxide (TBHP). The mechanisms were determined using the siRNA of hydroxycarboxylic acid receptor 2 (HCAR2), the antagonist of adenosine monophosphate-activated protein kinase (AMPK), and the inhibitor of mitophagy. The administration of KD demonstrated a reduction in pathological damage to cartilage, as well as a decrease in plasma levels of inflammatory factors. Furthermore, it resulted in an increase in the concentration of βOHB in the blood and synovial fluid. Invitro experiments showed that βOHB facilitated mitophagy and adenosine triphosphate production. Besides, βOHB mitigated chondrocyte senescence, inflammatory factors secretion, extracellular matrix degradation, and apoptosis induced by TBHP. Subsequent investigations indicated that the protective effects of βOHB were no longer observed following the knockdown of HCAR2, the antagonist of AMPK, or the inhibitor of mitophagy. Moreover, invivo studies suggested that βOHB played a protective role by targeting the HCAR2-AMPK-PINK1 axis. In conclusion,βOHB enhanced chondrocyte mitophagy through the HCAR2/AMPK/PINK1/Parkin pathway, offering a potential therapeutic approach for the treatment of OA.

Tsa1 is the dominant peroxide scavenger and a source of H2O2-dependent GSSG production in yeast

Hydrogen peroxide (H2O2) is an important biological molecule, functioning both as a second messenger in cell signaling and, especially at higher concentrations, as a cause of cell damage. Cells harbor multiple enzymes that have peroxide reducing activity in vitro. However, the contribution of each of these enzymes towards peroxide scavenging in vivo is less clear. Therefore, to directly investigate in vivo peroxide scavenging, we used the genetically encoded peroxide sensors, roGFP2-Tsa2ΔCR and HyPer7, to systematically screen the peroxide scavenging capacity of baker’s yeast thiol and heme peroxidase mutants. We show that the 2-Cys peroxiredoxin Tsa1 alone is responsible for almost all exogenous H2O2 and tert-butyl hydroperoxide scavenging. Furthermore, Tsa1 can become an important source of H2O2-dependent cytosolic glutathione disulfide production. The two catalases and cytochrome c peroxidase only produce observable scavenging defects at higher H2O2 concentrations when these three heme peroxidases are deleted in combination. We also analyzed the reduction of Tsa1 in vitro, revealing that the enzyme is efficiently reduced by thioredoxin-1 with a rate constant of 2.8×106 M–1s–1 but not by glutaredoxin-2. Tsa1 reduction by reduced glutathione occurs nonenzymatically with a rate constant of 2.9 M–1s–1. Hence, the observed Tsa1-dependent glutathione disulfide production in yeast probably requires the oxidation of thioredoxins. Our findings clarify the importance of the various thiol and heme peroxidases for peroxide removal and suggest that most thiol peroxidases have alternative or specialized functions in specific subcellular compartments.

La1-xSrxFeO3-δ Perovskite Oxide Nanoparticles for Low-Temperature Aerobic Oxidation of Isobutane to tert-Butyl Alcohol.

The development of reusable solid catalysts based on naturally abundant metal elements for the liquid-phase selective oxidation of light alkanes under mild conditions to obtain desired oxygenated products, such as alcohols and carbonyl compounds, remains a challenge. In this study, various perovskite oxide nanoparticles were synthesized by a sol-gel method using aspartic acid, and the effects of A- and B-site metal cations on the liquid-phase oxidation of isobutane to tert-butyl alcohol with molecular oxygen as the sole oxidant were investigated. Iron-based perovskite oxides containing Fe4+ such as BaFeO3-δ, SrFeO3-δ, and La1-xSrxFeO3-δ exhibited catalytic performance superior to those of other Fe3+- and Fe2+-based iron oxides and Mn-, Ni-, and Co-based perovskite oxides. The partial substitution of Sr for La in LaFeO3 significantly enhanced the catalytic performance and durability. In particular, the La0.8Sr0.2FeO3-δ catalyst could be recovered by simple filtration and reused several times without an obvious loss of its high catalytic performance, whereas the recovered BaFeO3-δ and SrFeO3-δ catalysts were almost inactive. La0.8Sr0.2FeO3-δ promoted the selective oxidation of isobutane even under mild conditions (60 °C), and the catalytic activity was comparable to that of homogeneous systems, including halogenated metalloporphyrin complexes. On the basis of mechanistic studies, including the effect of Sr substitution in La1-xSrxFeO3-δ on surface redox reactions, the present oxidation proceeds via a radical-mediated oxidation mechanism, and the surface-mixed Fe3+/Fe4+ valence states of La1-xSrxFeO3-δ nanoparticles likely play an important role in promoting C-H activation of isobutane as well as decomposition of tert-butyl hydroperoxide.

SydR, a redox-sensing MarR-type regulator of Sinorhizobium meliloti, is crucial for symbiotic infection of Medicago truncatula roots.

Rhizobia associate with legumes and induce the formation of nitrogen-fixing nodules. The regulation of bacterial redox state plays a major role in symbiosis, and reactive oxygen species produced by the plant are known to activate signaling pathways. However, only a few redox-sensing transcriptional regulators (TRs) have been characterized in the microsymbiont. Here, we describe SydR, a novel redox-sensing TR of Sinorhizobium meliloti that is essential for the establishment of symbiosis with Medicago truncatula. SydR, a MarR-type TR, represses the expression of the adjacent gene SMa2023 in growing cultures, and this repression is alleviated by NaOCl, tert-butyl hydroperoxide, or H2O2 treatment. Transcriptional psydR-gfp and pSMa2023-gfp fusions, as well as gel shift assays, showed that SydR binds two independent sites of the sydR-SMa2023 intergenic region. This binding is redox-dependent, and site-directed mutagenesis demonstrated that the conserved C16 is essential for SydR redox sensing. The inactivation of sydR did not alter the sensitivity of S. meliloti to NaOCl, tert-butyl hydroperoxide, or H2O2, nor did it affect the response to oxidants of the roGFP2-Orp1 redox biosensor expressed within bacteria. However, in planta, ΔsydR mutation impaired the formation of root nodules. Microscopic observations and analyses of plant marker gene expression showed that the ΔsydR mutant is defective at an early stage of the bacterial infection process. Altogether, these results demonstrated that SydR is a redox-sensing MarR-type TR that plays a key role in the regulation of nitrogen-fixing symbiosis with M. truncatula.IMPORTANCEThe nitrogen-fixing symbiosis between rhizobia and legumes has an important ecological role in the nitrogen cycle, contributes to nitrogen enrichment of soils, and can improve plant growth in agriculture. This interaction is initiated in the rhizosphere by a molecular dialog between the two partners, resulting in plant root infection and the formation of root nodules, where bacteria reduce the atmospheric nitrogen into ammonium. This symbiosis involves modifications of the bacterial redox state in response to reactive oxygen species produced by the plant partner. Here, we show that SydR, a transcriptional regulator of the Medicago symbiont Sinorhizobium meliloti, acts as a redox-responsive repressor that is crucial for the development of root nodules and contributes to the regulation of bacterial infection in S. meliloti/Medicago truncatula symbiotic interaction.

GdVO4:Eu3+ and LaVO4:Eu3+ Nanoparticles Exacerbate Oxidative Stress in L929 Cells: Potential Implications for Cancer Therapy.

The therapeutic potential of redox-active nanoscale materials as antioxidant- or reactive oxygen species (ROS)-inducing agents was intensely studied. Herein, we demonstrate that the synthesized and characterized GdVO4:Eu3+ and LaVO4:Eu3+ nanoparticles, which have been already shown to have redox-active, anti-inflammatory, antibacterial, and wound healing properties, both in vitro and in vivo, worsen oxidative stress of L929 cells triggered by hydrogen peroxide or tert-butyl hydroperoxide (tBuOOH) at the concentrations that are safe for intact L929 cells. This effect was observed upon internalization of the investigated nanosized materials and is associated with the cleavage of caspase-3 and caspase-9 without recruitment of caspase-8. Such changes in the caspase cascade indicate activation of the intrinsic caspase-9-dependent mitochondrial but not the extrinsic death, receptor-mediated, and caspase-8-dependent apoptotic pathway. The GdVO4:Eu3+ and LaVO4:Eu3+ nanoparticle-induced apoptosis of oxidatively compromised L929 cells is mediated by ROS overgeneration, Ca2+ overload, endoplasmic reticulum stress-associated JNK (c-Jun N-terminal kinase), and DNA damage-inducible transcript 3 (DDIT3). Our findings demonstrate that GdVO4:Eu3+ and LaVO4:Eu3+ nanoparticles aggravate the oxidative stress-induced damage to L929 cells, indicating that they might potentially be applied as anti-cancer agents.

Nano Fe3O4 catalyzed selective, tandem, and oxidative conversion of alcohols, tetrahydropyranyl and trimethylsilyl ethers to oximes

Tandem and efficient conversion of alcohols, tetrahydropyranyl (THP) and trimethylsilyl (TMS) ethers as protected alcohols to oximes is described using a catalytic amount of nano Fe3O4 as a highly magnetic and nontoxic catalyst, tert-butyl hydroperoxide (TBHP) and hydroxylamine hydrochloride. The nanocatalyst is easily separated from the reaction medium using an external magnet and can be reused for several times without any considerable loss of its catalytic power. Also, it was found that it is possible to perform these oxidative conversions efficiently even in the presence of epoxides, carboxylic acids and esters, phenols, sulfides and pyridine rings with excellent chemoselectivity. The tandem and catalytic nature, catalyst reusability, high yields, and easy work up can be considered as the main advantages of the present environmentally friendly method.

Apparent kinetics study and efficient continuous-flow synthesis of tert-butyl hydroperoxide & tert-butyl peroxybenzoate in a microreaction system

This study advances the synthesis of tert-butyl hydroperoxide (TBHP) and tert-butyl peroxybenzoate (TBPB) using a continuous microreaction system, meticulously detailing kinetic behavior and optimization processes through over 1250 experimental data points. We have developed a platform capable of high-throughput kinetic experiments and precise reaction quenching, determining kinetic parameters and optimal conditions that significantly improve reaction efficiency and safety. Tailored microreaction strategies, including micro-mixers, plate microreactors, and micro-packed beds, were employed to manage exothermic reactions and enhance mass transfer for each peroxide. For TBHP, conditions were optimized to achieve a 99% conversion rate of tert-butanol and an 82% conversion of hydrogen peroxide, with product selectivity reaching 92%. For TBPB, under optimal conditions, benzoyl chloride conversion reached 99.5%, and TBHP conversion was 80%, with a product selectivity of 94%. The integration of the TBHP and TBPB synthesis processes into a single continuous-flow system demonstrates scalable, safe, and efficient production, highlighting significant potential for advancements in organic peroxide manufacturing.