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phenylalanine/hypoxie
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Investigation of cobalt(iii)-phenylalanine complexes for hypoxia-activated drug delivery
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Four cobalt(iii)-phenylalanine complexes, [Co(Phe)(py2en)](ClO4)2·H2O (1), [Co(Phe)(TPA)](ClO4)2·H2O (2), [Co(Phe)(py2enMe2)](ClO4)2·H2O (3) and [Co(bipy)2(Phe)](ClO4)2·H2O (4), were investigated as prototype models for hypoxia-activated delivery of melphalan - a phenylalanine derivative anticancer
Influence of anoxia on the induction of mutations by phenylalanine radicals during gamma-irradiation of plasmid DNA in aqueous solution.
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When DNA is irradiated in aqueous solution, most of the damage is inflicted by water-derived radicals. This is called the indirect effect of ionizing radiation. However in whole cells not only the primary formed water radicals play a role, because some cellular compounds form secondary radicals
Extensin and Phenylalanine Ammonia-Lyase Gene Expression Altered in Potato Tubers in Response to Wounding, Hypoxia, and Erwinia carotovora Infection.
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Potato (Solanum tuberosum L.) tubers are susceptible to infection by Erwinia carotovora, causal agent of bacterial soft rot, when wounded and subjected to wet, hypoxic environments. The expression of two putative plant defense genes, extensin and phenylalanine ammonia-lyase (PAL), was examined by
Hypoxia in fetal lambs: a study with (1)H-MNR spectroscopy of cerebrospinal fluid.
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In fetal lambs, severe hypoxia (SH) will lead to brain damage. Mild hypoxia (MH) is thought to be relatively safe for the fetal brain because compensating mechanisms are activated. We questioned whether MH, leading to mild acidosis, induces changes in cerebral metabolism. Metabolites in
Radioprotective Activity and Preliminary Mechanisms of N-oxalyl-d-phenylalanine (NOFD) In Vitro.
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The radiation-induced damage to the human body is primarily caused by excessive reactive oxygen species (ROS) production after irradiation. Therefore, the removal of the increase of ROS caused by ionizing radiation (IR) has been the focus of research on radiation damage protective agents. Hypoxia
Cytotoxic response of sinusoidal endothelial cells to polymorphonuclear leukocytes and its potential implication in hypoxia-reoxygenation injury.
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OBJECTIVE
Interactions between polymorphonuclear leukocytes (PMN) and sinusoidal endothelial cells (SEC) may contribute to ischemia-reperfusion injury. The aim of the study was to determine the influence of PMN hypoxia-reoxygenation and degranulation, on SEC toxic response.
METHODS
PMNs collected
Hypoxemia regulates effect of lipopolysaccharide on polymorphonuclear leukocyte CD11b/CD18 expression.
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Expression of the receptor CD11b/CD18 on the polymorphonuclear leukocyte (PMN) surface is important for several aspects of PMN function during endotoxemia. The mechanisms underlying regulation of CD11b/CD18 expression during hypoxemia and endotoxemia, however, are less clear. We investigated the
Decreased total ventricular and mitochondrial protein synthesis during extended anoxia in turtle heart.
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The turtle heart provides a model system to study the effects of anoxia on protein synthesis without the potentially confounding factor of contractile failure and decreased ATP levels. Protein synthesis, as measured by 3H-labeled phenylalanine incorporation, was studied under conditions of normoxia
Pharmacological characterization of 3-azabicyclo[3,2,1] octane-1-yl-l-leucyl-d-tryptophanyl-d-4-Cl-phenylalanine: A novel ET(A) receptor-selective antagonist.
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OBJECTIVE
Pulmonary hypertension is a kind of disease associated with a very high rate of mortality. There are not many effective drugs for the treatment of pulmonary hypertension. Treatment with ET-1 receptor antagonists was proved to be effective in the treatment of pulmonary hypertension. Aiming
Studies on hypoxia: XII. Detrimental effects of synthetic polyribonucleotides on epiphyseal plates of rats exposed to hypoxia.
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The effect of different doses of polyadenylic and polyuridylic acids (poly A:U) was studied in control rats and in rats exposed to hypoxia. In the control rats, administration of different doses of poly A:U did not change the thickness of the epiphyseal plate or increase the incorporation of
Alterations in jejunal transport and (Na+-K+)-ATPase in an experimental model of hypoxia in rats.
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Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0
Effect of hypoxia and hypercapnia on ACE activity in the cerebral microcirculation of anesthetized dogs.
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Angiotensin-converting enzyme (ACE) activity of the cerebral microcirculation of anesthetized dogs was measured from cerebral venous outflow curves after bolus injection of a synthetic ACE substrate, [3H]benzoyl-phenylalanyl-alanylproline ([3H]BPAP), into a common carotid artery. Cerebral BPAP
Blood-brain amino acid transport and content during anoxia and reoxygenation.
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The isolated dog brain preparation was used to investigate the dynamics of cerebral amino acid metabolism during perfusion with anoxic blood (PO2 less than 10 mmHg). Significant uptake of histidine and lysine, as determined by arteriovenous (A-V) differences in whole blood samples, was observed
Profile of plasma amino Acid levels in rats exposed to acute hypoxic hypoxia.
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The effect of acute hypoxic hypoxia on the profile of plasma amino acids in rats was studied and compared to that resulting from acute liver injury induced by giving carbon tetrachloride. In hypoxic rats exposed to 45% air in N(2) for 5 h, the concentrations of branched chain amino acids, including
Transcerebral exchange kinetics of large neutral amino acids during acute inspiratory hypoxia in humans.
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Hypoxaemia is present in many critically ill patients, and may contribute to encephalopathy. Changes in the passage of large neutral amino acids (LNAAs) across the blood-brain barrier (BBB) with an increased cerebral influx of aromatic amino acids into the brain may concurrently be present and also
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