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Leber's hereditary optic atrophy: further evidence for a defect of cyanide metabolism?
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We studied one patient with Leber's optic atrophy (LOA) in the acute stage and 12 at the chronic stage of the disease, and measured the activity of rhodanese in white blood cells and the level of cyanide in whole blood. In the patient with acute disease the blood cyanide level was significantly
Role of the orbitally degenerate Mn(III) ions in the single-molecule magnet behavior of the cyanide cluster ([MnII(tmphen)2]3[Mn(III)(CN)6]2) (tmphen = 3,4,7,8-tetramethyl-1,10-phenanthroline).
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We report a new theoretical model that accounts for the unusual magnetic properties of the cyanide cluster ([MnII(tmphen)2]3[MnIII(CN)6]2) (tmphen = 3,4,7,8-tetramethyl-1,10-phenanthroline). The model takes into account (1) the spin-orbit interaction, (2) the trigonal component of the crystal field
SKELETAL MANIFESTATIONS IN LEBER'S HEREDITARY OPTIC ATROPHY. A POSSIBLE DISORDER OF CYANIDE METABOLISM.
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[Leber's optic atrophy: a disorder of cyanide metabolism?].
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Leber's hereditary optic atrophy: a possible defect of cyanide metabolism.
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Altered myoplasmic Ca(2+) handling in rat fast-twitch skeletal muscle fibres during disuse atrophy.
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Calcium-dependent signalling pathways are believed to play an important role in skeletal muscle atrophy, but whether intracellular Ca(2+) homeostasis is affected in that situation remains obscure. We show here that there is a 20% atrophy of the fast-type flexor digitorum brevis (FDB) muscle in rats
Clinical and biochemical findings in Leber's hereditary optic atrophy.
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Clinical findings in Leber's hereditary optic atrophy (LHOA) are reviewed and the results given of treatment with a regimen based on the hypothesis that the disease is a manifestation of cyanide toxicity. Recent biochemical investigations confirm disturbed cyanide metabolism and suggest that zinc
Inhibitors of lipid peroxidation protect cultured neurons against cyanide-induced injury.
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We tested the 21-aminosteroid U-74500A and the 2-methylaminochroman U-83836E, two potent inhibitors of lipid peroxidation, for their protective efficacy against cyanide- or Fe2+/Fe(3+)-induced damage of cultured neurons from chick embryo telencephalon. U-74500A (0.1-10 microM) as well as U-83836E
Spontaneous resolution of extensive descemet membrane detachment caused by sodium cyanide injury to the eye.
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OBJECTIVE
To describe the clinical course, ultrasonographic and confocal microscopic findings in a patient who developed a large Descemet membrane (DM) detachment that resolved spontaneously after ocular sodium cyanide injury.
METHODS
Case report.
RESULTS
The patient presented with severe corneal
Differential susceptibility of brain areas to cyanide involves different modes of cell death.
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We have demonstrated that cyanide (KCN) induces selective degeneration of dopaminergic neurons in mice and apoptotic cell death in cultured neurons. In the present study the mode of cyanide-induced cell death was determined in the susceptible brain areas. Mice were treated with KCN (6 mg/kg ip) or
Clinical and pathological effects of short-term cyanide repeated dosing to goats.
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The purpose of this work is to determine and describe the effects of subacute cyanide toxicity to goats. Eight female goats were divided into two groups. The first group of five animals was treated with 8.0 mg KCN kg(-1) body weight day(-1) for seven consecutive days. The second group of three
A single-molecule magnet based on heptacyanomolybdate with the highest energy barrier for a cyanide compound.
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Three trinuclear Mn2Mo molecules based on the orbitally degenerate [Mo(CN)7](4-) anion were prepared, one of which is the first single-molecule magnet (SMM) based on heptacyanomolybdate. The blocking temperature and the energy barrier (U = 40.5 cm(-1)) are records for a cyanide-based SMM. Wide
Decreased thiosulfate sulfur transferase (rhodanese) in Leber's hereditary optic atrophy.
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In mammals the major portion of cyanide is converted to thiocyanate by the liver enzyme thiosulfate sulfur transferase (TST) (rhodanese). We have found a much reduced activity of this enzyme in liver biopsies from two affected males of a family with Leber's hereditary optic atrophy and in two
Isoform-specific effects of transforming growth factors-beta on degeneration of primary neuronal cultures induced by cytotoxic hypoxia or glutamate.
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The transforming growth factors-beta (TGFs-beta) are multifunctional peptide growth factors that have been localized in neuronal and glial cells of the CNS of mice, rats, and chick embryos. We tested the TGF-beta isoforms 1, 2, and 3 for their protective effects against neuronal degeneration caused
Characterization of inorganic fraction of spent potliners: evaluation of the cyanides and fluorides content.
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Spent potliner (SPL) is a solid waste generated by the aluminum industry during the manufacture of aluminum metal in electrolytic cells. Initially the electrolityc cell liners comprise of graphite and carbonaceous materials, but after several years of operation, the liner materials deteriorate and
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