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The field of coordination chemistry has evolved to intersect with organic chemistry and biochemistry, giving rise to the disciplines of organometallic and bioinorganic chemistry. Nuclear magnetic resonance (NMR) spectroscopy can be applied for characterizing transition metal complexes, spanning both diamagnetic and paramagnetic complexes prevalent in organometallic compounds and metalloproteins. This review offers a comprehensive overview of a wide variety of characterization techniques, ranging from basic 1H and 13C NMR spectroscopy to advanced methods such as heteronuclear experiments, polarization transfer techniques, relaxometry, and multidimensional NMR spectroscopy. The diverse array of NMR spectroscopic methods outlined here promises to enhance our comprehension of transition metal complexes, facilitating the development of innovative catalysts and therapeutics. This review covers the applications of nuclear magnetic resonance (NMR) spectroscopy in analyzing transition metal complexes in organometallic and bioinorganic chemistry, with some examples. Enhancing our grasp of NMR spectroscopy coupled with coordination chemistry will enable chemists to decipher the geometric and electronic properties of transition metal complexes.

This study develops a new type of C3-symmetric triphenylene triimide (TTI) bearing different oligo(ethylene glycol) side chains via imide linkages. By exploiting the unique TTI molecule as a building block, supramolecular polymerization is explored based on π–π stacking and hydrophilic/hydrophobic interactions in various solvents and the rates of heating/cooling process. The molecular chirality of the TTI unimer induces a preferential helicity formation in fibrous structures, while the achiral side chain allows the formation of linear nanofibers. The stacking type of supramolecular polymerization is highly dependent on the point chirality of the side chains, as indicated by the spectroscopic analyses, including ultraviolet–visible (UV/vis) and circular dichroism (CD) spectroscopy with atomic force microscopy (AFM), transmission electron microscopy (TEM), and wide-angle X-ray scattering (WAXS). Interestingly, the supramolecular polymerization does not occur in its monomeric state due to the generation of radical anions from the imide groups upon UV irradiation. In contrast, the fibrous structure in the assembled state is maintained, owing to the intermolecular interaction. This study provides a new direction in the phototriggered control of the supramolecular chiral assembly.

The progression of neurodegenerative disorders can lead to impaired neurotransmission; however, the role of pathogenic factors associated with these diseases and their impact on the structures and functions of neurotransmitters have not been clearly established. Here we report the discovery that conformational and functional changes of a native neuropeptide, somatostatin (SST), occur in the presence of copper ions, metal-free amyloid-β (Aβ) and metal-bound Aβ (metal–Aβ) found as pathological factors in the brains of patients with Alzheimer’s disease. These pathological elements induce the self-assembly of SST and, consequently, prevent it from binding to the receptor. In the reverse direction, SST notably modifies the aggregation profiles of Aβ species in the presence of metal ions, attenuating their cytotoxicity and interactions with cell membranes. Our work demonstrates a loss of normal function of SST as a neurotransmitter and a gain of its modulative function against metal–Aβ under pathological conditions.

Alzheimer’s disease (AD) is the most common form of dementia and is characterized by memory loss and cognitive decline. Approximately 50 million people worldwide are suffering from AD and related dementias. Very recently, the first new drug targeting amyloid-β (Aβ) aggregates has been approved by the United States Food and Drug Administration, but its efficacy against AD is still debatable. Other available treatments temporarily relieve the symptoms of AD. The difficulty in discovering effective therapeutics for AD originates from its complicated nature, which results from the interrelated pathogenic pathways led by multiple factors. Therefore, to develop potent disease-modifying drugs, multiple pathological features found in AD should be fully elucidated.

Amyloid‐β, metal ions, and reactive oxygen species are linked to the pathology of Alzheimer's disease (AD). To identify their roles in the pathology of AD and control their pathological reactivities, various chemical tools have been developed. The redox‐based strategy for designing small molecules with multiple reactivities toward pathogenic factors has recently received significant attention. This Accountbriefly illustrates our current understanding of diverse pathological elements associated with AD and their redox properties. Furthermore, we summarize some examples of redox‐active small molecules with multifunctionality that were constructed by tuning electronic properties through incorporating substituents onto the backbones. Multiple reactivities of small molecules with pathological factors, including amyloid‐β, metal ions, and reactive oxygen species, can be obtained by tuning their redox properties with basic structural frameworks.

Herein, we report a comprehensive coordination study of the previously reported ligands cyclam, CB-cyclam, TMC, DMC, and CB-DMCand of their C-functional analogues, cyclam-E, CB-cyclam-E, TMC-E, DMC-E, and CB-DMC-E. This group of ligands includes cyclam, cross-bridged cyclams, their di- or tetramethylated derivatives, and the analogues bearing an additional hydroxyethyl group on one β-N position of the ring. The Cu(II) and Zn(II) complexes of these macrocycles have been highlighted previously for the biological interest, but the details of their structures in the solid state and in solution remained largely unexplored. In particular, we analyzed the impact that adding noncoordinating N-methyl and C-hydroxyethyl functionalities has in the structures of the complexes. All the Cu(II) and Zn(II) complexes were synthesized and investigated using single crystal X-ray diffraction and NMR, electronic absorption, and EPR spectroscopies, along with DFT studies. Dissociation kinetics experiments in acidic conditions and electrochemical studies were also performed. Special attention was paid to analyze the different configurations present in solution and in the solid state, as well as the impact of the C-appended hydroxyethyl group on the coordination behavior. Various ratios of the trans-I, trans-III, and cis-V configurations have been observed depending on the degree of N-methylation and the presence of the ethylene cross-bridge.

We report a prodrug, Glu-DAPPD, to overcome the shortcomings of an anti-neuroinflammatory molecule, N,N′-diacetyl-p-phenylenediamine (DAPPD), in biological applicability for potential therapeutic applications. We suspect that Glu-DAPPDcan release DAPPDthrough endogenous enzymatic bioconversion. Consequently, Glu-DAPPDexhibits in vivo efficacies in alleviating neuroinflammation, reducing amyloid-β aggregate accumulation, and improving cognitive function in Alzheimer’s disease transgenic mice. Our studies demonstrate that the prodrug approach is suitable and effective toward developing drug candidates against neurodegeneration.

Aggregates of both metal‐free amyloid‐β (Aβ) and metal‐bound Aβ (metal–Aβ) are accumulated in the brain affected by Alzheimer's disease. To control metal‐free and metal‐bound Aβ species, chemical reagents capable of modulating their aggregation profiles have been developed. As an effort, the reactivity of natural products such as flavonoids with metal‐free Aβ and metal–Aβ has been investigated to identify their use as chemical reagents and structural features essential for such reactivity. This review illustrates the effects of flavonoids containing a catechol or pyrogallol group on metal‐free and metal‐mediated Aβ aggregation pathways. In addition, the studies regarding the structure–activity relationship of flavonoids against metal‐free Aβ or metal–Aβ are discussed. Reactivity of Flavonoids Containing a Catechol or Pyrogallol Moiety with Metal‐Free and Metal‐Associated Amyloid‐β

A functionalized metal–organic framework (MOF) catalyst applied to the sequential one-pot oxidation of alcohols to carboxylic acids controls the presence of a heterogeneous catalyst. The conversion of alcohols to aldehydes was acquired through aerobic oxidation using a well-known amino-oxy radical-functionalized MOF. In the same flask, a simple filtration of the radical MOF with mild heating of the solution completely altered the reaction media, providing radical scavenger-free conditions suitable for the autoxidation of the aldehydes formed in the first step to carboxylic acids. The mutually exclusive radical-catalyzed aerobic oxidation (the first step with MOF) and radical-inhibited autoxidation (the second step without MOF) are sequentially achieved in a one-pot manner. Overall, we demonstrate a powerful and efficient method for the sequential oxidation of alcohols to carboxylic acids by employing a readily functionalizable heterogeneous MOF. In addition, our MOF in-and-out method can be utilized in an environmentally friendly way for the oxidation of alcohols to carboxylic acids of industrial and economic value with broad functional group tolerance, including 2,5-furandicarboxylic acid and 1,4-benzenedicarboxylic acid, with good yield and reusability. Furthermore, MOF-TEMPO, as an antioxidative stabilizer, prevents the undesired oxidation of aldehydes, and the perfect “recoverability” of such a reactive MOF requires a re-evaluation of the advantages of MOFs from heterogeneity in catalytic and related applications.

Multiple pathogenic elements, including reactive oxygen species, amyloidogenic proteins, and metal ions, are associated with the development of neurodegenerative disorders. We report minimalistic redox-based principles for preparing compact aromatic compounds by derivatizing the phenylene moiety with various functional groups. These molecular agents display enhanced reactivities against multiple targets such as free radicals, metal-free amyloid-β (Aβ), and metal-bound Aβ that are implicated in the most common form of dementia, Alzheimer’s disease (AD). Mechanistic studies reveal that the redox properties of these reagents are essential for their function. Specifically, they engage in oxidative reactions with metal-free and metal-bound Aβ, leading to chemical modifications of the Aβ peptides to form covalent adducts that alter the aggregation of Aβ. Moreover, the administration of the most promising candidate significantly attenuates the amyloid pathology in the brains of AD transgenic mice and improves their cognitive defects. Our studies demonstrate an efficient and effective redox-based strategy for incorporating multiple functions into simple molecular reagents.

Aggregation of amyloid-β (Aβ) peptides is implicated in the development of Alzheimer’s disease (AD), the most common type of dementia. Thus, numerous efforts to identify chemical tactics to control the aggregation pathways of Aβ peptides have been made. Among them, transition metal complexes as a class of chemical modulators against Aβ aggregation have been designed and utilized. Transition metal complexes are able to carry out a variety of chemistry with Aβ peptides (e.g., coordination chemistry and oxidative and proteolytic reactions for peptide modifications) based on their tunable characteristics, including the oxidation state of and coordination geometry around the metal center. This Viewpoint illustrates three strategies employing transition metal complexes toward modulation of Aβ aggregation pathways (i.e., oxidation and hydrolysis of Aβ as well as coordination to Aβ), along with some examples of such transition metal complexes. In addition, proposed mechanisms for three reactivities of transition metal complexes with Aβ peptides are discussed. Our greater understanding of how transition metal complexes have been engineered and used for alteration of Aβ aggregation could provide insight into the new discovery of chemical reagents against Aβ peptides found in AD.

Recent research has questioned the conventional idea that amyloid-β (Aβ) primarily exits the brain across the blood–brain barrier. This has led to the emergence of alternative pathways for Aβ elimination from the brain, making a paradigm shift in our understanding of Aβ clearance mechanisms.The peripheral sink hypothesis posits that there is an equilibrium between soluble Aβ levels in the brain and peripheral fluids. Thus, reducing Aβ amounts in the periphery can impact Aβ levels in the brain. This concept has sparked research into the identification of proteins capable of binding to Aβ in peripheral fluids, with the aim of sequestering and removing Aβ from both the brain and peripheral fluids.The ongoing debate surrounding drug development for Alzheimer’s disease underscores the importance of expanding therapeutic targets to encompass Aβ interactions with other peripheral proteins.

Complex amyloid aggregation of amyloid-β (1–40) (Aβ1–40) in terms of monomer structures has not been fully understood. Herein, we report the microscopic mechanism and pathways of Aβ1–40aggregation with macroscopic viewpoints through tuning its initial structure and solubility. Partial helical structures of Aβ1–40induced by low solvent polarity accelerated cytotoxic Aβ1–40amyloid fibrillation, while predominantly helical folds did not aggregate. Changes in the solvent polarity caused a rapid formation of β-structure-rich protofibrils or oligomers viaaggregation-prone helical structures. Modulation of the pH and salt concentration transformed oligomers to protofibrils, which proceeded to amyloid formation. We reveal diverse molecular mechanisms underlying Aβ1–40aggregation with conceptual energy diagrams and propose that aggregation-prone partial helical structures are key to inducing amyloidogenesis. We demonstrate that context-dependent protein aggregation is comprehensively understood using the macroscopic phase diagram, which provides general insights into differentiation of amyloid formation and phase separation from unfolded and folded structures.

Both amyloid-β (Aβ) and metal ions are implicated in the pathology of Alzheimer’s disease (AD). Research efforts elucidating the pathogenic roles of these two biological components denote a connection between them. This highlight review presents the current understanding of Aβ and metal ions in AD and their relationship prompting a hybrid concept: metal-bound Aβ (metal–Aβ).Both amyloid-β (Aβ) and metal ions are implicated in the pathology of Alzheimer’s disease (AD). Research efforts elucidating the pathogenic roles of these two biological components denote a connection between them. This highlight review presents the current understanding of Aβ and metal ions in AD and their relationship prompting a hybrid concept: metal-bound Aβ (metal–Aβ).

A fluorescence chemosensor HBC((E)‐3‐((2‐hydroxybenzylidene)amino)benzofuran‐2‐carboxamide) for detection of Zn2+was designed by the condensation combination of 3‐aminobenzofuran‐2‐carboxamide and salicylaldehyde. Sensor HBCshowed an excellent selective “off–on” fluorescent response toward Zn2+. Detection limit (1.08 μM) for Zn2+was much lower than the WHO standard (76.0 μM). Importantly, HBCcould recognize and quantify Zn2+in real samples and live cells. Detection process of HBCfor Zn2+was explained by ESI‐mass, Job plot, UV–Vis and 1H NMR titrations, and theoretical calculations.

Although there has been extensive effort to develop chemical regulators, progress has been static, in part because of these regulators’ unclear mechanisms. Here, we report using advanced electron paramagnetic resonance (EPR) spectroscopy to obtain the first molecular-level structural information regarding a ternary complex of CuII–amyloid-β (Aβ) with a chemical regulator that can specifically modulate Cu-induced Aβ aggregation. Our advanced EPR spectroscopic results revealed that a chemical regulator (1) for CuII–Aβ1–16disrupted the coordination environment of CuIIin Aβ, resulting in the detachment of the primary amine at the N-terminal and a carbonyl group between Asp1 and Ala2 from the CuIIcenter and the subsequent formation of a ternary complex, chemical regulator–CuII–Aβ1–16. Therefore, our results demonstrate how a chemical regulator interacts with metal–Aβ at the molecular level. These findings provide novel insight into working mechanisms and thereby contribute to the establishment of a rational design for chemical regulators of metal–Aβ complexes.

The complexity of Alzheimer’s disease (AD) stems from the inter-relation of multiple pathological factors upon initiation and progression of the disease. To identify the involvement of metal-bound amyloid-β (metal-Aβ) aggregation in AD pathology, among the pathogenic features found in the AD-affected brain, small molecules as chemical tools capable of controlling metal–Aβ aggregation were developed. Herein, we report a new class of 2,2′-bipyridine (bpy) derivatives (1–4) rationally designed to be chemical modulators toward metal–Aβ aggregation over metal-free Aβ analogue. The bpyderivatives were constructed through a rational design strategy employing straightforward structural variations onto the backbone of a metal chelator, bpy: (i) incorporation of an Aβ interacting moiety; (ii) introduction of a methyl group at different positions. The newly prepared bpyderivatives were observed to bind to metal ions [i.e., Cu(II) and Zn(II)] and interact with metal–Aβ over metal-free Aβ to varying degrees. Distinguishable from bpy, the bpyderivatives (1–3) were indicated to noticeably modulate the aggregation pathways of Cu(II)–Aβ and Zn(II)–Aβ over metal-free Aβ. Overall, our studies of the bpyderivatives demonstrate that the alteration of metal binding properties as well as the installation of an Aβ interacting capability onto a metal chelating framework, devised via the rational structure-based design, were able to achieve evident modulating reactivity against metal–Aβ aggregation. Obviating the need for complicated structures, our design approach, presented in this work, could be appropriately utilized for inventing small molecules as chemical tools for studying desired metal-related targets in biological systems.

Bilirubin (BR) is a de novosynthesized metabolite of human cells. However, subcellular localization of BR in the different organelles of human cells has been largely unknown. Here, utilizing UnaG as a genetically encoded fluorescent BR sensor, we report the existence of relatively BR-enriched and BR-depleted microspaces in various cellular organelles of live cells. Our studies indicate that (i) the cytoplasmic facing membrane of the endoplasmic reticulum (ER) and the nucleus are relatively BR-enriched spaces and (ii) mitochondrial intermembrane space and the ER lumen are relatively BR-depleted spaces. Thus, we demonstrate a relationship between such asymmetrical BR distribution in the ER membrane and the BR metabolic pathway. Furthermore, our results suggest plausible BR-transport and BR-regulating machineries in other cellular compartments, including the nucleus and mitochondria.

The complex and multifaceted pathology of Alzheimer’s disease (AD) continues to present a formidable challenge to the establishment of long-term treatment strategies. Multifunctional compounds able to modulate the reactivities of various pathological features, such as amyloid-β (Aβ) aggregation, metal ion dyshomeostasis, and oxidative stress, have emerged as a useful tactic. Recently, an incorporation approach to the rational design of multipurpose small molecules has been validated through the production of a multifunctional ligand (ML) as a potential chemical tool for AD. In order to further the development of more diverse and improved multifunctional reagents, essential pharmacophores must be identified. Herein, we report a series of aminoquinoline derivatives (AQ1–4, AQP1–4, and AQDA1–3) based on ML’s framework, prepared to gain a structure–reactivity understanding of ML’s multifunctionality in addition to tuning its metal binding affinity. Our structure–reactivity investigations have implicated the dimethylamino group as a key component for supplying the antiamyloidogenic characteristics of MLin both the absence and presence of metal ions. Two-dimensional NMR studies indicate that structural variations of MLcould tune its interaction sites along the Aβ sequence. In addition, mass spectrometric analyses suggest that the ability of our aminoquinoline derivatives to regulate metal-induced Aβ aggregation may be influenced by their metal binding properties. Moreover, structural modifications to MLwere also observed to noticeably change its metal binding affinities and metal-to-ligand stoichiometries that were shown to be linked to their antiamyloidogenic and antioxidant activities. Overall, our studies provide new insights into rational design strategies for multifunctional ligands directed at regulating metal ions, Aβ, and oxidative stress in AD and could advance the development of improved next-generation multifunctional reagents.

A newborn with a vascular ring exhibiting a right-dominant double aortic arch (DAA), a left-side patent ductus arteriosus (PDA), and esophageal atresia with a tracheoesophageal fistula (TEF), was admitted to our neonatal intensive care unit. Although very rare, TEF and DAA may co-occur early in development. We recommend that, first, the fistula should be repaired and the esophageal anastomosis should be performed after division of the DAA. When an AA abnormality (including a DAA) is evident, the approach to the AA and the direction of the thoracotomy incision should be reversed to render surgery relatively easy.

Protein misfolding and metal ion dyshomeostasis are believed to underlie numerous neurodegenerative diseases, including Alzheimer’s disease (AD). The pathological hallmark of AD is accumulation of misfolded amyloid-β (Aβ) peptides and hyperphosphorylated tau (ptau) proteins in the brain. Since AD etiology remains unclear, several hypotheses have emerged to elucidate its pathological pathways. The amyloid cascade hypothesis, a leading hypothesis for AD development, advocates Aβ as the principal culprit. Additionally, evidence suggests that tau may contribute to AD pathology. Aβ and tau have also been shown to impact each other’s pathology either directly or indirectly. Furthermore, metal ion dyshomeostasis is associated with these misfolded proteins. Metal interactions with Aβ and tau/ptau also influence their aggregation properties and neurotoxicity. Herein, we present current understanding on the roles of Aβ, tau, and metal ions, placing equal emphasis on each of these proposed features, as well as their inter-relationships in AD pathogenesis.

An FeIVO group meets with H2O2!Reaction of high‐valent iron with the reactive oxygen species (ROS) hydrogen peroxide (H2O2) is in general reserved for heme centers. Employing a biomimetic metal complex, the direct reaction of a mononuclear nonheme oxoiron(IV) species with H2O2was observed and studied mechanistically, offering a new perspective for the chemistry between ROS and high‐valent oxometal complexes.

FeIVO trifft H2O2!Die Reaktion von hochvalentem Eisen mit Wasserstoffperoxid (H2O2) ist allgemein dem Häm‐Zentrum vorbehalten. Die direkte Umsetzung einer biomimetischen einkernigen Nichthäm‐Oxoeisen(IV)‐Spezies mit H2O2wurde beobachtet und mechanistisch untersucht, was neue Einblicke in die Reaktionen zwischen reaktiven Sauerstoffspezies (ROS) und hochvalenten Oxometallkomplexen bietet.

Circularly polarized light (CPL) is an inherently chiral entity and is considered one of the possible deterministic signals that led to the evolution of homochirality. While accumulating examples indicate that chirality beyond the molecular level can be induced by CPL, not much is yet known about circumstances where the spin angular momentum of light competes with existing molecular chiral information during the chirality induction and amplification processes. Here we present a light-triggered supramolecular polymerization system where chiral information can both be transmitted and nonlinearly amplified in a “sergeants-and-soldiers” manner. While matching handedness with CPL resulted in further amplification, we determined that opposite handedness could override molecular information at the supramolecular level when the enantiomeric excess was low. The presence of a critical chiral bias suggests a bifurcation point in the homochirality evolution under random external chiral perturbation. Our results also highlight opportunities for the orthogonal control of supramolecular chirality decoupled from molecular chirality preexisting in the system.

Developing chemical methodologies to directly modify harmful biomolecules affords the mitigation of their toxicity by persistent changes in their properties and structures. Here we report compact photosensitizers composed of the anthraquinone (AQ) backbone that undergo excited-state intramolecular hydrogen transfer, effectively oxidize amyloidogenic peptides, and, subsequently, alter their aggregation pathways. Density functional theory calculations showed that the appropriate position of the hydroxyl groups in the AQbackbone and the consequent intramolecular hydrogen transfer can facilitate the energy transfer to triplet oxygen. Biochemical and biophysical investigations confirmed that these photoactive chemical reagents can oxidatively vary both metal-free amyloid-β (Aβ) and metal-bound Aβ, thereby redirecting their on-pathway aggregation into off-pathway as well as disassembling their preformed aggregates. Moreover, the in vivo histochemical analysis of Aβ species produced upon photoactivation of the most promising candidate demonstrated that they do not aggregate into oligomeric or fibrillar aggregates in the brain. Overall, our combined computational and experimental studies validate a light-based approach for designing small molecules, with minimum structural complexity, as chemical reagents targeting and controlling amyloidogenic peptides associated with neurodegenerative disorders.

The reaction of [Mn(TF4TMAP)](CF3SO3)5(TF4TMAP=meso‐tetrakis(2,3,5,6‐tetrafluoro‐N,N,N‐trimethyl‐4‐aniliniumyl)porphinato dianion) with H2O2(2 equiv) at pH 10.5 and 0 °C yielded an oxomanganese(V) porphyrin complex 1in aqueous solution, whereas an oxomanganese(IV) porphyrin complex 2was generated in the reactions of tert‐alkyl hydroperoxides such as tert‐butyl hydroperoxide and 2‐methyl‐1‐phenyl‐2‐propyl hydroperoxide. Complex 1was capable of epoxidizing olefins and exchanging its oxygen with H218O, whereas 2did not epoxidize olefins. From the reactions of [Mn(TF4TMAP)]5+with various oxidants in the pH range 3–11, the O−O bond cleavage of hydroperoxides was found to be sensitive to the hydroperoxide substituent and the pH of the reaction solution. Whereas the O−O bond of hydroperoxides containing an electron‐donating tert‐alkyl group is cleaved homolytically, an electron‐withdrawing substituent such as an acyl group in m‐chloroperoxybenzoic acid (m‐CPBA) facilitates O−O bond heterolysis. The mechanism of the O−O bond cleavage of H2O2depends on the pH of the reaction solution: O−O bond homolysis prevails at low pH and O−O bond heterolysis becomes a predominant pathway at high pH. The effect of pH on 18O incorporation from H218O into oxygenated products was examined over a wide pH range, by carrying out the epoxidation of carbamazepine (CBZ) with [Mn(TF4TMAP)]5+and KHSO5in buffered H218O solutions. A high proportion of 18O was incorporated into the CBZ‐10,11‐oxide product at all pH values but this proportion was not affected significantly by the pH of the reaction solution.

The catalytic hydroxylation of aliphatic hydrocarbons by m-chloroperbenzoic acid (MCPBA) has been studied in the presence of elecrtron-deficient iron(III) porphyrin complexes. High yields of alcohol products were obtained with small amounts of ketone formation under mild reaction conditions. The stereospecificity and regioselectivity of the iron porphyrin complexes have been investigated in hydroxylation reactions as well. The hydroxylation of alkanes has been performed in the presence of isotopically 18O-labeled water, H218O, in order to understand the effects of the electronic nature of iron porphyrin complexes, the concentration of H218O, the C–H bond strength of alkanes, and the reaction temperature on the 18O-incorporation from the labeled water into alcohols. We found that the amounts of 18O incorporated into the alcohol products varied in the reactions; these results were interpreted with that the reaction of oxygen atom transfer from a high-valent iron oxoporphyrin complex to alkanes competes with that of oxygen atom exchange between the intermediate and labeled water that leads to 18O-incorporation from H218O into the alcohol products. Deuterium kinetic isotope effects (KIEs) in the alkane hydroxylations by the iron porphyrin complexes and MCPBA have been studied with a mixture of cyclohexane and cyclohexane-d12. The KIE values obtained in the reactions were found to depend significantly on the nature to the iron porphyrin complexes. The temperature dependence of kH/kDwas also studied from -40 to 25 °C and the parameters of Arrhenius equation (i.e., the pre-exponential factor ratio, AH/AD, and the isotopic difference of C–H and C–D bond activation energies, Ea(D)–Ea(H)) were determined.

Treatment of mononuclear nonheme ironii complexes bearing two cis-labile sites with perbenzoic acids results in the self-hydroxylation of the aromatic ring to form the corresponding ironiii–salicylate complexes through an intramolecular oxo-transfer process.

No Abstract

The crystal structure of the title compound, [Fe(C44H20F8N4)(CH3O)], has been determined. The Fe atom lies 0.485 (1) Å out of the plane of the four N atoms to which it is coordinated and from the inversion centre at the origin of the unit cell. The methoxy group is axially coordinated to the Fe atom with O—Fe—N angles of 106.3 (2) and 102.4 (2)°, a C—O—Fe angle of 128.3 (5)° and an Fe—O distance of 1.788 (5) Å. Di­fluoro­phenyl rings are tilted from the porphyrin (por) plane with torsion angles of −68.1 (6) and 77.7 (5)° across the two Cpor—­C—C—Carsystems.

An electron-deficient iron porphyrin complex catalyzes the epoxidation of olefins by tert-alkyl hydroperoxides via radical-free oxidation reactions in aprotic solvent; the epoxidation reactions were markedly influenced by reaction temperature and high yields of epoxide products were obtained with retention of stereospecificity at low temperature.

Review: 104 refs.

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ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.