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13 hasil
Time and dose dependent effects of oxidative stress induced by cumene hydroperoxide in neuronal excitability of rat motor cortex neurons.
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It has been claimed that oxidative stress and the production of reactive oxygen radicals can contribute to neuron degeneration and might be one factor in the development of different neurological diseases. In our study, we have attempted to clarify how oxidative damage induces dose dependent changes
Iron-accelerated cumene hydroperoxide decomposition in hexadecane and trilaurin emulsions.
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Free radicals arising from lipid peroxides accelerate the oxidative deterioration of foods. To elucidate how lipid peroxides impact oxidative reactions in food emulsions, the stability of cumene hydroperoxide was studied in hexadecane or trilaurin emulsions stabilized by anionic (sodium dodecyl
Prevention of cumene hydroperoxide induced oxidative stress in cultured neonatal rat myocytes by scavengers and enzyme inhibitors.
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Oxidative stress induced by cumene hydroperoxide was studied in cultured neonatal rat myocytes. A progressive increase of irreversible cell injury as determined by leakage of the cytoplastic enzyme alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) from the cells was noted at concentrations ranging
Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo.
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The occurrence of oxidative stress has been proposed as a pathogenetic mechanism for melanocyte degeneration in vitiligo. In order to evaluate this possible correlation we focused on the lipid component of cell membranes. We observed in vitiligo melanocytes, through FACS methods, an increased median
Toxicity induced by cumene hydroperoxide in PC12 cells: protective role of thiol donors.
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Oxidative shock and production of reactive oxygen species are known to play a major role in situations leading to neuron degeneration, but the precise mechanisms responsible for cell degeneration remain uncertain. In the present article, we have studied in PC 12 cells the effect of cumene
Oxidative stress induced by cumene hydroperoxide produces synaptic depression and transient hyperexcitability in rat primary motor cortex neurons.
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Pyramidal neurons of the motor cortex are selectively degenerated in Amyotrophic Lateral Sclerosis (ALS). The mechanisms underlying neuronal death in ALS are not well established. In the absence of useful biomarkers, the early increased neuronal excitability seems to be the unique characteristic of
p-Bromophenacyl bromide prevents cumene hydroperoxide-induced mitochondrial permeability transition by inhibiting pyridine nucleotide oxidation.
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Mitochondrial permeability transition is commonly characterized as a Ca2+ -dependent non-specific increase in inner membrane permeability that results in swelling of mitochondria and their de-energization. In the present study, the effect of different inhibitors of phospholipase A2--p-bromophenacyl
alpha-Tocopherol protects against radical-induced injury in cultured neurons.
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The effect of alpha-tocopherol on neurons in protecting against radical-induced injuries caused by cumene hydroperoxide was assessed using a culture system. Structural and biochemical deteriorations in both clonal neuroblastoma cells and primary cultured neurons were induced by cumene hydroperoxide.
Oxygen radical injury in the immature isolated rabbit heart.
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We speculated that the increased vulnerability of the immature rabbit heart to global ischemia might be due to an increased susceptibility to free radical injury. To evaluate this, we exposed newborn (age 2.4 +/- 0.3 days, n = 20) (mean +/- SEM), juvenile (2 to 3 weeks, mean 16.6 +/- 0.5 days, n =
Comparative inhalation toxicity of ethyltoluene isomers in rats and mice.
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The C9 alkylbenzenes, composed mostly of ethyltoluenes and trimethylbenzenes, comprise 75-90% of the naphtha fraction of crude oil. Occupational and environmental exposure to C9 alkylbenzenes occur via inhalation. We conducted short-term inhalation studies on the ethyltoluene isomers (2-, 3- or 4-)
Cytotoxic effects of an oxidative stress on neuronal-like pheochromocytoma cells (PC12).
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Although the generation of oxygen derivatives during ischemia and reperfusion is generally held as a major event in the process leading to neuronal death, the biochemical mechanisms responsible for cell degeneration remain poorly understood. To better understand the toxicity induced by oxidative
Increased sensitivity to peroxidative agents as a possible pathogenic factor of melanocyte damage in vitiligo.
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To examine the sensitivity of vitiligo melanocytes to external oxidative stress, we studied enzymatic and non-enzymatic anti-oxidants in cultured melanocytes of normal subjects (n = 20) and melanocytes from apparently normal skin of vitiligo patients (n = 10). The activity of superoxide dismutase
An inducible form of Nrf2 confers enhanced protection against acute oxidative stresses in RPE cells.
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Increasing evidence suggests that overt oxidative stress within the retina plays an important role in the progression of age-related retinal decline, and in particular, in the disease age-related macular degeneration (AMD). Nuclear factor erythroid 2-like 2 (Nrf2) is a master transcription factor
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