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benzoquinone/hypoxia
Врската е зачувана во таблата со исечоци
Страница 1 од 22 резултати
Conjugation of para-benzoquinone of Cigarette Smoke with Human Hemoglobin Leads to Unstable Tetramer and Reduced Cooperative Oxygen Binding.
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Besides multiple life-threatening diseases like lung cancer and cardiovascular disease, cigarette smoking is known to produce hypoxia, a state of inadequate oxygen supply to tissues. Hypoxia plays a pivotal role in the development of chronic obstructive pulmonary disease. Smoking during pregnancy
Interaction of p-benzoquinone with hemoglobin in smoker's blood causes alteration of structure and loss of oxygen binding capacity.
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Cigarette smoke (CS) is an important source of morbidity and early mortality worldwide. Besides causing various life-threatening diseases, CS is also known to cause hypoxia. Chronic hypoxia would induce early aging and premature death. Continuation of smoking during pregnancy is a known risk for the
[A comparative study of the activity of antihypoxic agents in hemic hypoxia].
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Amino derivatives of ortho-benzoquinone (OBQ) were demonstrated to have a protective action in acute toxic hemic hypoxia induced by sodium nitrite given to laboratory animals. This action of OBQ was due to its capacity to activate the recovery of blood oxygen transport function by accelerating the
Geldanamycin inhibits migration of glioma cells in vitro: a potential role for hypoxia-inducible factor (HIF-1alpha) in glioma cell invasion.
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Focal adhesion kinase (FAK) and hypoxia-inducible factor (HIF-1alpha) are both up-regulated in glioblastoma multiforme (GBMs), particularly in invasive zones. Because FAK may play an important role in the invasion of glioma cells into the surrounding brain, we sought an agent that causes
Indolequinone antitumor agents: reductive activation and elimination from (5-methoxy-1-methyl-4,7-dioxoindol-3-yl)methyl derivatives and hypoxia-selective cytotoxicity in vitro.
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A series of indolequinones bearing a variety of leaving groups at the (indol-3-yl)methyl position was synthesized by functionalization of the corresponding 3-(hydroxymethyl)indolequinone, and the resulting compounds were evaluated in vitro as bioreductively activated cytotoxins. The elimination of a
Geldanamycin induces degradation of hypoxia-inducible factor 1alpha protein via the proteosome pathway in prostate cancer cells.
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Hypoxia-inducible factor 1 (HIF-1) is a heterodimeric transcription factor composed of alpha and beta subunits. HIF-1 is critically involved in cellular responses to hypoxia, glycolysis, and angiogenesis. Here, we show that treatment of prostate cancer PC-3 and LNCaP cells with the benzoquinone
The importance of DT-diaphorase and hypoxia in the cytotoxicity of RH1 in human breast and non-small cell lung cancer cell lines.
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The diaziridiny/benzoquinone RH1 is shortly to enter a phase I clinical trial. The drug was originally designed as a substrate for the enzyme DT-diaphorase (DTD) such that metabolic activation of the drug would lead to toxicity. To evaluate this, we have measured the toxicity of RH1 in a pair of
Synthesis and antitumour activity of the Primin (2-methoxy-6-n-pentyl-1,4-benzoquinone) and analogues.
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Cancer is a serious worldwide health threat, killing almost seven million people per year. Quinones are an important class of antitumour agents that are activated by tumour hypoxia. Primin (2-methoxy-6-n-pentyl-1,4-benzo-quinone), a naturally-occurring product obtained from Primula obconica
Overexpression of HIF-1a could partially protect K562 cells from 1,4-benzoquinone induced toxicity by inhibiting ROS, apoptosis and enhancing glycolysis.
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Benzene is an environmental contaminant which causes hematological diseases. Previously, hypoxia inducible factor-1a (HIF-1a) was found to be involved in benzene-induced hematotoxicity. This study aims to explore whether overexpression of HIF-1a in K562 cell line could influence the toxicity caused
Quinone-enhanced ascorbate reduction of nitric oxide: role of quinone redox potential.
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The quinones 1,4-naphthoquinone (NQ), methyl-1,4-naphthoquinone (MNQ), trimethyl-1,4-benzoquinone (TMQ) and 2,3-dimethoxy-5-methyl-1,4-benzoquinone (UQ-0) enhance the rate of nitric oxide (NO) reduction by ascorbate in nitrogen-saturated phosphate buffer (pH 7.4). The observed rate constants for
Hydrogen production in Chlamydomonas: photosystem II-dependent and -independent pathways differ in their requirement for starch metabolism.
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Under sulfur deprivation conditions, the green alga Chlamydomonas reinhardtii produces hydrogen in the light in a sustainable manner thanks to the contribution of two pathways, direct and indirect. In the direct pathway, photosystem II (PSII) supplies electrons to hydrogenase through the
Characterization of the NAD(P)H oxidase and metronidazole reductase activities of the RdxA nitroreductase of Helicobacter pylori.
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Metronidazole (MTZ) is widely used in combination therapies against the human gastric pathogen Helicobacter pylori. Resistance to this drug is common among clinical isolates and results from loss-of-function mutations in rdxA, which encodes an oxygen-insensitive nitroreductase. The RdxA-associated
Inducers of hypoxic response: marine sesquiterpene quinones activate HIF-1.
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The hypoxia-inducible factor-1 (HIF-1) transcription factor regulates cellular oxygen homeostasis. Agents that activate HIF-1 and downstream HIF targets represent potential drug leads for the prevention and/or treatment of ischemic disorders. In a search for small-molecule HIF-1 activators, 1936
Effects of geldanamycin on HIF-1alpha mediated angiogenesis and invasion in prostate cancer cells.
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Geldanamycin (GA), a benzoquinone ansamycin, is a naturally occurring inhibitor of heat shock protein (Hsp90), which regulates the transcription activity of hypoxia-inducible factor 1 (HIF-1alpha). Under hypoxia, HIF-1alpha is activated in tumor cells, and induces the transcription of vascular
Effects of geldanamycin on signaling through activator-protein 1 in hypoxic HT29 human colon adenocarcinoma cells.
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One of the characteristic responses of HT29 human colon adenocarcinoma cells to hypoxic stress is the induction of c-jun expression and binding to the activator-protein 1 (AP-1) element. To study the mechanism of c-jun activation during hypoxia, inhibitors of signaling pathways leading to the
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