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Bladzijde 1 van 23 resultaten
Menadione-induced cell degeneration is related to lipid peroxidation in human cancer cells.
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The role of lipid peroxidation, intracellular glutathione and Ca2+ concentration in menadione-mediated toxicity was investigated in human hepatoma cell lines, Hep G2 and Hep 3B, and in human leukemia cell lines, CCRF-CEM and MOLT-3. Incubation of these cells with 80 microM menadione at 37 degrees C
Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment.
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Feulgen and actin-phalloidin staining as well as gel electrophoresis have been employed in conjunction with cell ultrastructure to describe the effects of 1-, 2-, and 4-hr ascorbate (VC), menadione (VK(3)), and ascorbate:menadione (VC:VK(3)) treatments on the T24 human bladder carcinoma cell line.
Cellular thiols as a determinant of responsiveness to menadione in cardiomyocytes.
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The role of intracellular thiols in menadione-mediated toxicity was studied in neonatal rat cardiomyocytes. The sensitivity of cardiomyocytes to menadione was greater than that of skeletal muscle cells and 3T3 fibroblasts. Before cell degeneration, menadione induced marked depletion of intracellular
The role of lipid peroxidation in menadione-mediated toxicity in cardiomyocytes.
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The role of lipid peroxidation in menadione-mediated toxicity was studied in neonatal rat cardiomyocytes. Incubation of cardiomyocytes with menadione resulted in depleted cellular glutathione levels, increased intracellular Ca2+ and increased lipid peroxidation which all occurred prior to cell
Differences in gene expression profiles in dermal fibroblasts from control and patients with age-related macular degeneration elicited by oxidative injury.
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The pathogenesis of age-related macular degeneration (AMD) is still unknown but there is growing evidence that a combination of both oxidative injury and genetic factors may play a role. One particle hypothesis proposes that dysregulation of multiple genes in response to an oxidative injury could
Cardiac and renal toxicity of menadione in rat.
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Menadione induced oxidative stress in cells. The acute and cumulative toxic effects of menadione were evaluated by intravenous injection of the drug in Wistar rats. For evaluation of acute toxicity, single bolus doses of 25, 50, 100 and 150 mg/kg menadione were used. For evaluation of cumulative
Menadione-induced cardiotoxicity is associated with alteration in intracellular Ca2+ homeostasis.
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Cardiotoxicity of menadione was elucidated in neonatal rat cardiomyocytes. When incubated with menadione, contraction of myocytes initially slowed down and eventually stopped. Later blebs appeared on the cell surface, leading to cell degeneration. During the time of diminished cellular contraction,
Sulforaphane ameliorates serum starvation-induced muscle atrophy via activation of the Nrf2 pathway in cultured C2C12 cells.
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Oxidative stress, an imbalance of redox homeostasis, contributes to the pathogenesis and progress of muscle atrophy. However, it is debated whether oxidative stress is a cause or consequence of muscle atrophy. In this study, we investigated the relationship between menadione-induced oxidative stress
Menadione-Induced DNA Damage Leads to Mitochondrial Dysfunction and Fragmentation During Rosette Formation in Fuchs Endothelial Corneal Dystrophy.
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Fuchs endothelial corneal dystrophy (FECD), a leading cause of age-related corneal edema requiring transplantation, is characterized by rosette formation of corneal endothelium with ensuing apoptosis. We sought to determine whether excess of mitochondrial reactive oxygen species leads to chronic
[Reducing body myopathy--a case report].
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A 2-year-old girl with reducing body myopathy was reported. She had no family history of neuromuscular disease. She developed normally with no delay in milestones during infancy. She had no muscle weakness or hypotonia up to 2 years of age when she received mumps vaccination. Three days after the
AROMATIC-INDUCED PREVENTION OF FETAL TOXICITY OF 7,12-DIMETHYLBENZ(ALPHA)ANTHRACENE.
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Large doses of 7,12-dimethylbenz[a]anthracene (7,12-DMBA) caused the death of rats within 1 day. A small amount of any of 5 polynuclear aromatic hydrocarbons or of an aromatic amine given before the highly toxic dose of 7,12-DMBA resulted in survival for more than 2 months and the specific atrophy
Distinct subtypes of type I fibers of human skeletal muscle.
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We have identified two distinct and consistent type I fiber subtypes in histochemically normal biopsies (vastus lateralis or biceps brachialis) from 12 healthy persons, both sexes, ages 15 to 42. The type I fibers were uniformly light with the regular ATPase (9.4) and uniformly dark with the
Neuroprotective effects of nicergoline in immortalized neurons.
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We studied the potential neuroprotective action of nicergoline in immortalized hypothalamic GT1-7 cells exposed to agents which deplete levels of reduced glutathione, thus causing oxidative stress and cell death. Treatment with diethylmaleate (1 mM), buthionine sulfoximine (500 microM) or menadione
Familial reducing body myopathy.
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Reducing body myopathy (RBM) is a rare pathologically defined myopathy characterized by the presence of inclusion bodies which are abnormally stained by menadione-nitroblue-tetrazolium. The clinical symptoms vary widely as to the age of onset, disease progression and severity. Among the many
FHL1 mutants that cause clinically distinct human myopathies form protein aggregates and impair myoblast differentiation.
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FHL1 mutations cause several clinically heterogeneous myopathies, including reducing body myopathy (RBM), scapuloperoneal myopathy (SPM) and X-linked myopathy with postural muscle atrophy (XMPMA). The molecular mechanisms underlying the pathogenesis of FHL1 myopathies are unknown. Protein
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