No abstract

Ca2AlMnO5+δ with a brownmillerite‐type structure can topotactically store/release a large amount of excess oxygen (about 3.0 wt.%) depending on temperature and the surrounding atmosphere in a highly reversible manner.

Hepatotoxicity of diclofenac has been known in experimental animals and humans but its mechanism has not been fully understood. The present study examined the role of mitochondrial permeability transition (MPT) in the pathogenesis of diclofenac-induced hepatocyte injury by using isolated mitochondria and primary culture hepatocytes from rats. Incubation of energized mitochondria with succinate in the presence of Ca 2؉ and diclofenac resulted in mitochondrial swelling, leakage of accumulated Ca 2؉ , membrane depolarization, and oxidation of nicotinamide adenine dinucleotide phosphate and protein thiol. All of these phenomena were suppressed by coincubation of the mitochondria with cyclosporin A, a typical inhibitor of MPT, showing that diclofenac opened the MPT pore. It was also suggested that reactive oxygen species probably generated during mitochondrial respiration and/or voltage-dependent mechanism was involved in MPT, which are proposed as mecha D iclofenac is a nonsteroidal anti-inflammatory drug (NSAID) widely used clinically. Hepatotoxicity is one of the side effects associated with the drug. Various mechanisms for the diclofenac-induced liver injury were proposed, but have not been fully understood. The diclofenac liver toxicity in humans is idiosyncratic, 1 and immunologic and metabolic idiosyncrasies have been suggested. 2,3 Thus, metabolic activation of this drug has been a focus, 4-6 and several reactive metabolites were proposed as candidates to contribute to the toxicity in experimental animals and humans. [7][8][9][10] On the other hand, we currently obtained the following evidence that diclofenac rather than its metabolite was responsible for the toxicity. Diclofenac toxicity to rat hepatocytes was not prevented by inhibiting its oxidation of conjugative metabolism. 11 NSAIDs including diclofenac that have a common chemical structure have hepatocyte toxicity, and these toxic NSAIDs depleted cellular adenosine triphosphate (ATP) before the enzyme leakage. 11 The toxic NSAIDs have been shown to be uncouplers of mitochondrial oxidative phosphorylation, which results in impairment of ATP synthesis. 12 Furthermore, rescue of hepatocytes from depletion of ATP conferred protection against hepatocyte injury induced by diclofenac. 13 It was thus concluded that the uncoupling property of diclofenac plays a crucial role in its hepatotoxicity, whereas an additional and/or alternative step is necessary to explain the mechanism for clinically observed idiosyncratic liver injury.Mitochondrial permeability transition (MPT) is recently focused as a mechanism for drug-induced hepatocyte necrosis and apoptosis. [14][15][16] The MPT represents an abrupt increase in permeability of the mitochondrial inner membrane to allow solutes with a molecular weight less than 1,500. 17 The MPT is promoted by the accumulation of excessive Ca 2ϩ and stimulated by various compounds and conditions. It leads to dissipation of membrane potential (⌬⌿), uncoupling, loss of preaccumulated Ca 2ϩ , and expansion of the matrix volume. Uncou...

Here, we report the remarkable oxygen intake/release capability of a double perovskite BaYMn 2 O 5þδ . This oxide rapidly stores/releases a large amount of oxygen (>3.7 wt %) at moderate temperatures in a perfectly reversible manner. The oxygen intake/release behaviors of BaYMn 2 O 5þδ are clearly beyond those of any conventional oxides in terms of the magnitude and sharpness of the processes. It also appeared that this oxide exhibits a significant catalytic activity for flameless combustions of hydrocarbons, presumably owing to its oxygen-storage ability.

Here we report the magnetic properties of the layered cobalt oxide system, Li x CoO 2 , in the whole range of Li composition, 0 Յ x Յ 1. Based on dc-magnetic-susceptibility data, combined with results of 59 Co nuclear magnetic resonance ͑NMR͒ and nuclear quadrupole resonance ͑NQR͒ observations, the electronic phase diagram of Li x CoO 2 has been established. As in the related material Na x CoO 2 , a magnetic critical point is found to exist between x = 0.35 and 0.40, which separates the Pauli-paramagnetic and Curie-Weiss metals. In the Pauli-paramagnetic regime ͑x Յ 0.35͒, the antiferromagnetic spin correlations systematically increase with decreasing x. Nevertheless, CoO 2 , the x = 0 end member is a noncorrelated metal in the whole temperature range studied. In the Curie-Weiss regime ͑x Ն 0.40͒, on the other hand, various phase transitions are observed. For x = 0.40, a susceptibility hump is seen at 30 K, suggesting the onset of static antiferromagnetic order. A magnetic jump, which is likely to be triggered by charge ordering, is clearly observed at T t Ϸ 175 K in samples with x = 0.50 ͑=1 / 2͒ and 0.67 ͑=2 / 3͒, while only a tiny kink appears at T Ϸ 210 K in the sample with an intermediate Li composition, x = 0.60. Thus, the phase diagram of the Li x CoO 2 system is complex and the electronic properties are sensitively influenced by the Li content ͑x͒.