Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition. - Wikidata - awgldk - TriplyDB

Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition.

Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition.

http://www.wikidata.org/entity/Q50691799

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Biomechanical effects of environmental and engineered particles on human airway smooth muscle cells Custom-designed nanomaterial libraries for testing metal oxide toxicity Comparison of the mechanism of toxicity of zinc oxide and cerium oxide nanoparticles based on dissolution and oxidative stress properties The effect of zinc and the role of p53 in copper-induced cellular stress responses.Effects of dietary supplementation of carnosine on mitochondrial dysfunction, amyloid pathology, and cognitive deficits in 3xTg-AD mice.Coupling of semiconductor nanowires with neurons and their interfacial structure Reactive gamma-ketoaldehydes formed via the isoprostane pathway disrupt mitochondrial respiration and calcium homeostasis.Anti-Inflammatory and Neuroprotective Effects of Constituents Isolated from Rhodiola rosea Zinc: indications in brain disorders.Role of H2O2 in the oxidative effects of zinc exposure in human airway epithelial cells.Mechanisms of rapid reactive oxygen species generation in response to cytosolic Ca2+ or Zn2+ loads in cortical neurons.Mechanism(s) of Toxic Action of Zn and Selenite: A Study on AS-30D Hepatoma Cells and Isolated Mitochondria The neurophysiology and pathology of brain zinc.ZnO nanoparticles impose a panmetabolic toxic effect along with strong necrosis, inducing activation of the envelope stress response in Salmonella enterica serovar Enteritidis Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.Zinc Modulates Nanosilver-Induced Toxicity in Primary Neuronal Cultures.Quantitative imaging of mitochondrial and cytosolic free zinc levels in an in vitro model of ischemia/reperfusion.Intracellular Zn2+ accumulation contributes to synaptic failure, mitochondrial depolarization, and cell death in an acute slice oxygen-glucose deprivation model of ischemia.Intracellular Zn2+ increases contribute to the progression of excitotoxic Ca2+ increases in apical dendrites of CA1 pyramidal neurons Nitric oxide in health and disease of the nervous system.A comparison of Zn2+- and Ca2+-triggered depolarization of liver mitochondria reveals no evidence of Zn2+-induced permeability transition Labile Low-Molecular-Mass Metal Complexes in Mitochondria: Trials and Tribulations of a Burgeoning Field Differential Vulnerability of CA1 versus CA3 Pyramidal Neurons After Ischemia: Possible Relationship to Sources of Zn2+ Accumulation and Its Entry into and Prolonged Effects on Mitochondria.Non-phenolic radical-trapping antioxidants.Early and Late Pathomechanisms in Alzheimer's Disease: From Zinc to Amyloid-β Neurotoxicity Zinc: new clues to diverse roles in brain ischemia.Zinc homeostasis and signaling in glia.Zinc and insulin in pancreatic beta-cells.Differences in intracellular mobile zinc levels affect susceptibility to plasma-activated medium-induced cytotoxicity.Mechanistic studies of the toxicity of zinc gluconate in the olfactory neuronal cell line Odora.In vitro protection by pyruvate against cadmium-induced cytotoxicity in hippocampal HT-22 cells.Intracellular shunting of O2(-) contributes to charge compensation and preservation of neutrophil respiratory burst in the absence of voltage-gated proton channel activity.Water induced protonation of amine-terminated micelles for direct syntheses of ZnO quantum dots and their cytotoxicity towards cancer.Intramitochondrial Zn2+ accumulation via the Ca2+ uniporter contributes to acute ischemic neurodegeneration.Intracellular zinc distribution in mitochondria, ER and the Golgi apparatus.Different in vitro exposure regimens of murine primary macrophages to silver nanoparticles induce different fates of nanoparticles and different toxicological and functional consequences.Cross talk between increased intracellular zinc (Zn2+) and accumulation of reactive oxygen species in chemical ischemia.Zinc oxide nanoparticles interfere with zinc ion homeostasis to cause cytotoxicity.Mitochondrial permeability transition induced by different concentrations of zinc.Rising zinc: a significant cause of ischemic neuronal death in the CA1 region of rat hippocampus.

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P2860

Zinc irreversibly damages major enzymes of energy production and antioxidant defense prior to mitochondrial permeability transition.

http://www.wikidata.org/entity/Q50691799

description

2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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Zinc irreversibly damages majo ...... drial permeability transition.

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Zinc irreversibly damages majo ...... drial permeability transition.

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Zinc irreversibly damages majo ...... drial permeability transition.

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Zinc irreversibly damages majo ...... drial permeability transition.

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Zinc irreversibly damages majo ...... drial permeability transition.

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Journal of Biological Chemistry

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Zinc irreversibly damages majo ...... drial permeability transition.

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Abraham M Brown

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Bruce S Kristal

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Inna P Krasinskaya

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P2860

Structure and mechanism of mammalian thioredoxin reductase: the active site is a redox-active selenolthiol/selenenylsulfide formed from the conserved cysteine-selenocysteine sequence

A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis

Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology.

Study of PTPC composition during apoptosis for identification of viral protein target.

The permeability transition pore complex: another view.

Modulation of mitochondrial function by endogenous Zn2+ pools.

Zinc and excitotoxic brain injury: a new model.

Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain

Ca2+ ions, an allosteric activator of calcium uptake in rat liver mitochondria.

On the interactions of Ca2+ and cyclosporin A with a mitochondrial inner membrane pore: a study using cobaltammine complex inhibitors of the Ca2+ uniporter.

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