cytochrome c/hypoxia

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Broadband NIRS Cerebral Cytochrome-C-Oxidase Response to Anoxia Before and After Hypoxic-Ischaemic Injury in Piglets.

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Perinatal hypoxic ischaemic (HI) encephalopathy is associated with severe neurodevelopment problems and mortality. This study uses broadband continuous-wave near-infrared spectroscopy (NIRS) to assess the early changes in cerebral oxygenation and metabolism after HI injury in an animal model using

Chronic hypoxia and developmental regulation of cytochrome c expression in rats.

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OBJECTIVE To test the hypothesis that chronic hypoxia upregulates cytochrome c expression in heart, brain, and liver of fetal and maternal rats. METHODS Time-dated pregnant Sprague-Dawley rats were divided into normoxic and hypoxic (48 hours of 10.5% oxygen from days 19 to 21) groups, and were

[Cytochrome C release and apoptosis in neonatal rat cerebral hypoxia-ischemia].

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OBJECTIVE To study the relation of cytochrome C release from mitochondria to cytosol and neuronal apoptosis after cerebral hypoxia-ischemia (HI) in neonatal rats. METHODS Hypoxia-ischemia was induced in 7-day-old rat pups by ligation of left carotid artery and 7.7% oxygen was inhaled for 55 min. The

Cytochrome C is released from mitochondria into the cytosol after cerebral anoxia or ischemia.

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Mitochondrial dysfunction may underlie both acute and delayed neuronal cell death resulting from cerebral ischemia. Specifically, postischemic release of mitochondrial constituents such as the pro-apoptotic respiratory chain component cytochrome c could contribute acutely to further mitochondrial

Anoxia-reoxygenation-induced cytochrome c and cardiolipin release from rat brain mitochondria.

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Rat brain mitochondria were successively submitted to anoxia and reoxygenation. The main mitochondrial functions were assessed at different reoxygenation times. Although the respiratory control ratio decreased, the activity for each one of the enzymes participating in the respiratory chain was not

[Effect of opening of mitochondrial ATP-sensitive K⁺ channel on the distribution of cytochrome C and on proliferation of human pulmonary arterial smooth muscle cells in hypoxia].

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The objective of this paper was to investigate the contribution of mitochondrial ATP-sensitive K+ channel (mitoK(ATP)) and mitochondrial membrane potential (Deltapsim) to the distribution of cytochrome C in human pulmonary arterial smooth muscle cells (HPASMCs) and to the proliferation of HPASMCs

Intracellular delivery of cytochrome C using hypoxia-responsive polypeptide micelles for efficient cancer therapy

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To begin with, it is important to note that biodegradable polypeptides have been extensively applied as drug delivery carriers due to their excellent bioavailability, neglectful toxicity, good encapsulation and controlled release. Thus, a biodegradable and hypoxia-responsive polypeptide is a benefit

Azoreductase and Target Simultaneously Activated Fluorescent Monitoring for Cytochrome c Release under Hypoxia.

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Hypoxia-induced cell apoptosis is closely related to degenerative diseases, autoimmune disorders, and tumor disease. In the process of apoptosis, the release of cytochrome c (Cyt c) is deemed to be a critical factor of the intrinsic pathway. Strategies for tracking Cyt c release in living cells

Hypoxia/reoxygenation of isolated rat heart mitochondria causes cytochrome c release and oxidative stress; evidence for involvement of mitochondrial nitric oxide synthase.

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The objective of the present study was to delineate the molecular mechanisms for mitochondrial contribution to oxidative stress induced by hypoxia and reoxygenation in the heart. The present study introduces a novel model allowing real-time study of mitochondria under hypoxia and reoxygenation, and

[Correlation between intermittent hypoxia-induced apoptosis of human umbilical vein endothelial cells and release of cytochrome C from mitochondria].

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OBJECTIVE To explore the correlation between intermittent hypoxia (IH)-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and release of cytochrome C (cytC) from mitochondria. METHODS HUVECs in IH groups were exposed to repetitive cycles (1% O2 5 min alternating with 21% O2 5 min,

Serine protease inhibitors suppress cytochrome c-mediatedcaspase-9 activation and apoptosis during hypoxia-reoxygenation.

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We have shown that reoxygenation of hypoxic rat kidney proximaltubule cells leads to apoptosis. This is mediated by translocation ofBax from the cytosol to mitochondria, accompanied by release ofmitochondrial cytochrome c (cyt.c). The present studyhas examined the proteolytic mechanisms responsible

Hypoxia induces apoptosis by caspase activation accompanying cytochrome C release from mitochondria in MC3T3E1 osteoblasts. p38 MAPK is related in hypoxia-induced apoptosis.

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The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3E1 osteoblasts. MC3T3E1 osteoblasts under hypoxic conditions (2% oxygen) resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay and nuclear morphologystained with

Hypoxia induces apoptosis in human neuroblastoma SK-N-MC cells by caspase activation accompanying cytochrome c release from mitochondria.

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We have attempted to elucidate the mechanism of apoptotic cell death induced by hypoxia (very low oxygen conditions) in neuronal cells. Human neuroblastoma SK-N-MC cells under hypoxic conditions resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay and nuclear

PI3K inhibition in neonatal rat brain slices during and after hypoxia reduces phospho-Akt and increases cytosolic cytochrome c and apoptosis.

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Acute hypoxia can deplete ATP and induce mitochondrial release of cytochrome c (cyt c) to initiate or enhance apoptosis, a process delayed or overcome with sufficient ATP and phosphorylation (activation) of survival factors such as Akt (also known as Protein Kinase B). We used an ex vivo brain slice

Caspase activation and mitochondrial cytochrome C release during hypoxia-mediated apoptosis of adult ventricular myocytes.

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Oxygen deprivation for prolonged periods leads to cardiac cell death and ventricular dysfunction. The ability to prevent myocardial cell death would be of significant therapeutic value in maintaining cardiac function after injury. While caspases have been suggested to play a critical role in

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