Intraligand Charge Transfer Enables Visible-Light-Mediated Nickel-Catalyzed Cross-Coupling Reactions.

We demonstrate that several visible-light-mediated carbon-heteroatom cross-coupling reactions can be carried out using a photoactive Ni precatalyst that forms in situ from a nickel salt and a bipyridine ligand decorated with two carbazole groups (Ni(Czbpy)Cl ). The activation of this precatalyst towards cross-coupling reactions follows a hitherto undisclosed mechanism that is different from previously reported light-responsive nickel complexes that undergo metal-to-ligand charge transfer. Theoretical and spectroscopic investigations revealed that irradiation of Ni(Czbpy)Cl with visible light causes an initial intraligand charge transfer event that triggers productive catalysis.

Benzylic Fluorination Induced by a Charge-Transfer Complex with a Solvent-Dependent Selectivity Switch.

We present a divergent strategy for the fluorination of phenylacetic acid derivatives that is induced by a charge-transfer complex between Selectfluor and 4-(dimethylamino)pyridine. A comprehensive investigation of the conditions revealed a critical role of the solvent on the reaction outcome. In the presence of water, decarboxylative fluorination through a single-electron oxidation is dominant.

Simultaneous Recovery of Matrix and Fiber in Carbon Reinforced Composites through a Diels-Alder Solvolysis Process.

Efficient and comprehensive recycling of fiber-reinforced thermosets is particularly challenging, since the irreversible degradation of the matrix component is necessary in order to separate the fiber component in high purity. In this work, a new approach to fully recyclable thermoset composites is presented, based on the thermal reversibility of an epoxy-based polymer network, crosslinked through Diels-Alder (DA) chemistry. Carbon fiber composites, fabricated by compression molding, were efficiently recycled through a simple solvolysis procedure in common solvents, under mild conditions, with no catalysts.

Magnesium, calcium and cancer.

Magnesium ion (Mg(2+)) and calcium ion (Ca(2+)) control a diverse and important range of cellular processes, such as gene transcription, cell proliferation, neoplastic transformation, immune response and therapeutic treatment. Their characteristic biologic antagonism makes it important to treat the most important aspects of that competitive behavior together. This synopsis aims to be a useful means of promoting further research on the relationship between both cations and human health affected by environmental conditions.

The paradoxical immuno-response of adenosine triphosphate effects.

The actual research on the paradoxical effects of ATP to obtain to optimal conditions of the immune response against certain pathologies. The ATP Paradox, after its interaction with iron or aluminum, which have shown important effects on carcinogenesis, suggests its implication in pathological systems in which overcalcification may play a role.

Aluminum, calcium ion and radiofrequency synergism in acceleration of lymphomagenesis.

This study that was done on lymphomagene-bearing mice indicates a synergism aluminum-radiofrequency which induces an early increase in mortality that is in concomitance with lymphoid elements proliferation and infiltration of spleen and liver. These two last phenomena were assessed by determination of the hypertrophic index (Growth Index) which is the organ weight to to the body weight ratio, as well as by the histopathological examination of the organ tissue. The importance of this synergism appears to be determined by the ionization at the physiological pH of the used aluminum complexes: much higher with lactate complex than with the citrate one.

Iron-radiofrequency synergism in lymphomagenesis.

The parenteral iron administration effects on the acceleration of lymphomagenesis by radiofrequency exposure were investigated using an animal model that develops spontaneous lymphomas with ageing. Complementary studies of the in vivo uptake of 59Fe-labeled ferric gluconate and ferric-ATP complex showed differences ob absorption and excretion between both iron compounds. In vitro assays of their effects on calcium cellular uptake using a cell model and tissues homogenates showed a molecular structure-dependence.

Evaluation of health risks caused by radio frequency accelerated carcinogenesis: the importance of processes driven by the calcium ion signal.

The acceleration of carcinogenesis, which was induced either by radio frequency radiation from a cellular telephone or by the ferric-ATP complex, was similar in a mouse strain characterized by age-determined carcinogenesis of lymphoid tissues. Organ hypertrophy, the presence of lymphoid blood and ascites, the development of solid tumours, and mortality were very different to those found in control animals. These results emphasize the role of calcium ion signal influx in the activation of oncogenes and the failure of thymus-determined immune defences.

Role of iron-ATP complex in lymphocyte proliferation and infiltration.

The roles of sodium-ATP (NaATP) and ferric-ATP complex (FeATP) on the proliferation and infiltration of lymphocytes have been studied by evaluation of the hypertrophy and histopathologic examination of spleen and liver, as well of the modifications in the elemental balance of iron, calcium, magnesium, and phosphorus. The results showed that in the implicated biochemical processes, calcium and magnesium have a principal role. An in vitro study on a cell model has permited one to evaluate the effects of deferoxamine, a known iron chelator and inhibitor of human lymphocyte proliferation, on FeATP-modified cellular calcium fluxes.

Radiofrequency-induced carcinogenesis: cellular calcium homeostasis changes as a triggering factor.

The aim was to study the effects of radiofrequency (Rf) in a mice strain characterized by age-determined carcinogenesis of lymphatic tissues. Mice were treated with a 1?h/week Rf exposure for 4 months. A group submitted to sham exposure was used as control animals.

Molecular exchange of metal ions and tissular calcium overload.

In vitro and in vivo, mouse tissues assayed for 45Ca2+ uptake have shown that ATP increases the Ca2+ take-up in the presence of lactates of iron and aluminum, but this effect is absent with the citrates. The in vitro metal ion exchange with ATP has been demonstrated by electrophoresis and by chromatography. It is considered the cause of the increased capacity of ATP to modify the cellular effects of lactates.

Toxic and carcinogenic effects of parenteral and percutaneous ATP and its iron complex.

The long term effects of percutaneous, subcutaneous and intraperitoneal administration of sodium-ATP (NaATP) and ferric iron-ATP (FeATP) were studied on an animal model. Both compounds induce a generalized lymphoadenitis which in the case of FeATP led to lymphomas. The analytical study of the involved target tissues showed intracellular composition changes that result from the impairment of the cell membrane permeability.

Cellular calcium homeostasis changes in lymphoma-induction by ATP iron complex.

An in vivo comparative study of 45Ca-uptake and lipid peroxidation in tissues of mice treated with ATP complex of iron and sodium salt of ATP shows that only the iron complex produces a sustained increase of intracellular calcium on the organs susceptibles to develop lymphomas. A paralled study of 59Fe-uptake from 59Fe-iron complex of ATP presents a coincidental increase of iron uptake in those organs. To prove the involvement of the calcium homeostasis change in lymphoma-induction we have studied it with the lanthanum complex of ATP.

Role of iron in lymphoma-induction by ATP.

Iron complexed by ATP induces lymphomas in mouse organs other than the specific targets of the lympho-adenitis provoked by sodium ATP: lymph nodes, spleen and liver. The reduction of life spans and the production of substantial volumes of ascites, that are lacking in the case of sodium ATP, are an index of the degree of malignancy of the induced lymphomas. On the basis of the known characteristics of iron-ATP complex of cellular calcium homeostasis alteration, the mechanism of these phenomena is discussed.

Iron- and aluminum-induced carcinogenesis.

Ferric and aluminum complexes with ATP have shown the induction of tumors in the site of subcutaneous injection, whereas sodium ATP has not. A concomitant but apparently independent phenomenon was a severe lymphoadenitis. The tumor calcium concentration showed an inverse relationship with the tumor growth rate.

Natural polyphenols-iron interaction: its biological importance.

The iron-binding capacity of different fractions of natural polyphenols extracts was determined by chromatographic and electrophoretic methods. Their effects on iron-induced calcium homeostasis changes in liver tissue suspension showed that mate tea and green tea extracts provoke a very significant inhibition of the iron effects, whereas it is much less significant with red wine extract. The biological importance of this phenomenon is discussed.

Iron-ethanol synergism and pathological liver transformation.

The synergistic effects of iron overload and ethanol on the liver of mice were studied over a period of 46 weeks. The determination of several parameters (iron, calcium, magnesium, alpha-hydroxyproline, lipid peroxidation, hepatomegalic and splenomegalic indexes) showed that ferrous and ferric lactates provoke an increase of calcium in the liver, higher than that of ethanol in the control animals. The relationship between liver calcium homeostasis modification and the increase of collagen and lipid peroxidation is discussed.

ATP in iron overload-induced intracellular calcium changes.

The cellular iron uptake from low molecular weight iron complexes (ferric citrate, ferric lactate and ferric ATP complex) is concentration-dependent, and only a small part of the iron penetrates the cell as shown by deferoxamine treatment. A threshold of iron concentration in the cell must be reached for the iron complex-induced increase of cellular Ca2+-uptake. ATP seems to play a key role in an iron translocation that enhances the effects of the iron complexes.

Effects of low-molecular-weight aluminum complexes on brain tissue calcium homeostasis.

The in vitro effects of low-molecular-weight aluminum complexes (citrate, lactate, and ATP complex) on the Ca2+ uptake and aluminum-induced lipid peroxidation of brain tissue show that the modification of the calcium homeostasis is determined by the nature of the ligand and that there is no correlation between the aluminum-induced lipid peroxidation and the Ca2+ uptake. The same characteristics have been shown by a similar study performed with Ehrlich carcinoma cells. The electrophoretic analyses of the aluminum lactate-albumin and aluminum lactate-ATP interactions indicate an aluminum transfer from the lactate to the albumin and ATP ligands.

ATP in cellular calcium-overload by trivalent metal ions.

Extracellular Ca2+-influx induced by trivalent metal ions (Fe3+, Al3+, Cr3+, In3+, Ga3+, and La3+) in Ehrlich carcinoma cells is enhanced by ATP. This action seems to be related to the high coordination capacity of the ATP ligand that inhibits the polymerization of the solvated cations taking place at physiological pH, and consequently permits their biological activity. A general relationship between induced lipid peroxidation and increased calcium uptake was not found.

Non-transferrin-bound iron and tumor cells.

The study of iron uptake from low molecular weight complexes by Ehrlich carcinoma cells shows concentration-dependence, and ATP increases the iron uptake from citrate and lactate complexes. Blood proteins can act as inhibitors, and deferoxamine chelation of cell-bound iron complex indicates that the percentage of iron penetrating the cell is about the same for a wide range of iron complex concentrations in the incubation medium (about 5% for ferric lactate). Ascorbic acid increases iron uptake and simultaneously decreases lipid peroxidation.

Effects of iron complexes on brain calcium homeostasis.

The effects of two physiological low molecular weight iron complexes, ferric lactate and ferric adenosine triphosphate (ATP) on brain Ca2+ homeostasis modification, have been studied in vitro and in vivo. In vitro ferric ATP complex shows a higher efficiency as modifier of Ca2+ homeostasis. This higher reactivity and the in vivo observed effect of increased brain uptake of iron from ferric lactate provoked by the presence of ATP, corroborate in vitro results showing an iron transfer from ferric lactate to ATP, as well as the mediator role of ATP in the iron-induced cellular Ca2+ homeostasis modification process.

Role of lipid peroxidation in iron-induced cellular calcium overload.

Calcium overload is the common pathway leading to cell injury. The role of iron-induced lipid peroxidation in the modification of Ehrlich carcinoma cells calcium homeostasis has been studied. There is a lack of correlation between that modification and the value of lipid peroxidation.

Iron, intracellular calcium ion, lipid peroxidation and carcino-genesis.

The evaluation of the accumulated experimental results on the action of complexed iron on cells indicates that the provoked cell injury is rather the consequence of an inhibition of the cytosolic Ca2+ concentration regulatory system than an effect of iron-induced lipid peroxidation. The role of the consequent intracellular ionic environment change in the preneoplastic and neoplastic transformation of the cell is discussed.

Cardiotoxicity of parenterally administered iron complexes.

The role of cell calcium overload in the cardiotoxicity of low molecular weight iron complexes has been studied using 45Ca(2+)-uptake determinations in mice intraperitoneally injected with ferric lactate and ferric-ATP complex. Heart tissue shows a very high increase of 45Ca(2+)-uptake which appears to corroborate the hypothesis of cardiotoxicity by calcium overload. ATP seems to play a role in the degree of iron complex efficiency as cell calcium homeostasis modifier.