The blood and plasma kinetics of intravenously administered 3H-labelled PAF-acether were determined in seven rabbits. PAF-acether was rapidly distributed and slowly eliminated. Individual variations were very small. The main route of metabolism involves deacetylation of the PAF-acether into lyso-PAF-acether, leading to an equilibrium between the two molecules (10%/90%). This equilibrium, observed within 30 minutes, was still the same after 6 hours suggesting in vivo reacetylation of lyso-PAF-acether into PAF-acether. However, this could not be verified. After intravenous administration of lyso-PAF-acether in two rabbits, PAF-acether could not be found in any blood sample. The pharmacokinetic behaviour of both PAF-acether and lyso-PAF-acether can be described by a three-compartment model.
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http://dx.doi.org/10.1007/BF01966786 | DOI Listing |
Chin Med J (Engl)
September 2007
Department of Pathophysiology, Kunming Medical College, Kunming 650031, China.
Background: It has been known that platelet activating factor receptors (PAFR) may mediate many acute pathological responses and that PAFR antagonist Ginkgolide B (GB) possesses multiple effects, but the actions of GB on PAFR affinity and mitochondrial respiration in the ischemic neuron were unclear until now. This study explored the possible effects of GB on PAFR and the mitochondrial respiration of the neuron in the ischemic microenvironment.
Methods: Thrombotic cerebral ischemia in tree shrews was induced by a photochemical reaction; changes in the regional cerebral blood flow (rCBF, using (99m)Tc tracer technique), the brain water content (specific gravimetric method), PAFR (3H-labelled PAF assay), the respiratory control rate (RCR), the phosphorus-oxygen (P/O) ratio of mitochondrial respiration (Clark oxygen electrode), mitochondrial permeability transition (MPT) pore, and the mitochondrial ultrastructure in the ischemic neurons were also observed.
Eur J Biochem
December 1997
Laboratoire de Pharmacologie Moléculaire, Faculté de Pharmacie, Université de Rennes I, France.
1-O-Alkylglycerols (alkyl-Gro), naturally occurring compounds abundant in shark liver oil, protect patients from radiotherapy side-effects. However, the protection mechanism is not well understood. It might be mediated by alkyl-Gro incorporation into pools of platelet-activating factor (PAF) precursor and subsequent modification of PAF biosynthesis.
View Article and Find Full Text PDFBiochem J
May 1992
Haemobiology Research Department, Sanofi Recherche, Toulouse, France.
Binding of 3H-labelled platelet-activating factor ([3H]PAF) to guinea-pig tracheal epithelial cells was time-dependent, reversible and saturable. Scatchard analysis of the saturation-binding data indicated that [3H]PAF bound to one class of specific binding sites with high affinity (KD = 4.3 +/- 0.
View Article and Find Full Text PDFThe distribution of liposomes prepared from total mouse liver lipids and containing (3H)-labelled platelet activation factor in mouse organs was studied. It was shown that the majority of intraperitoneally injected liposomes prepared from total mouse liver lipids were transported to mouse liver and spleen. The interaction of liposomes with spleen cells in vitro revealed that the affinity of liposomes prepared from total spleen macrophage or total spleen lymphocyte lipids for mouse spleen cells was much higher than that of liposomes prepared from a model lipid mixture.
View Article and Find Full Text PDFEur J Biochem
February 1990
Department of Biochemistry, University of Fribourg, Switzerland.
Horse eosinophils preincubated with 3H-labelled acetate and stimulated with the Ca2+ ionophores ionomycin or A23187 form a radioactive compound, which we have shown to be 1-O-alkyl-2-[3H]acetyl-sn-glycero-3-phosphocholine (platelet-activating factor). We could detect no 1-O-acyl-2-[3H]acetyl-glycero-3-phosphocholine in the radioactive fraction. The formation of platelet-activating factor was strongly correlated to the generation of leukotriene C4, the main arachidonate metabolite in horse eosinophils, suggesting that platelet-activating factor and leukotriene C4 have a common precursor pool (1-O-alkyl-2-arachidonyl-glycero-3-phosphocholine) and a common regulation of synthesis.
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