PubMed Health⌕ Search

Biomedical subjects

F F Sun

Publications and source records attributed to F F Sun.

At least 91 records · Page 5Linked to original sources
PubMed1978

Prostacyclin biosynthesis in activated, stimulated and normal mouse peritoneal cell populations.

Nonspecific resistance to infectious and neoplastic disease can be enhanced by administration of "immunomodulators". The levels of enhancement can be monitored by following in vitro function of cells of the lympho-reticuloendothelial system. To gain a better understanding of the physiological and biochemical nature of this enhancement, the metabolism of prostaglandin endoperoxide PGH2 was followed in mouse peritoneal cells (PCs). Homogenates of PCs from normal, unstimulated mice yielded primarily prostacyclin (PGI2) when incubated with PGH2. Homogenates of PCs from mice injected with the immunomodulators C. parvum, levamisole HCl, pyran copolymer, or thioglycollate yielded less PGI2. Reductions ranged from 73% for C. parvum to 32% for levamisole. A statistically significant inverse correlation existed between the level of macrophage "activation" and ability of cellular homogenates to produce prostacyclin. The results suggest that prostacyclin may be involved in modulation of nonspecific resistance.

Animals↗
PubMed1978

Metabolism of cis-delta4-15(S)-15-methylprostaglandin F1alpha methyl ester in the rat.

The metabolic transformation and excretion of tritium-labeled cis-delta4-15(S)-15-methylprostaglandin F1alpha methyl ester (1) have been investigated in rats after chronic and single dose oral administration. Three metabolites have been identified from a partially purified urinary extract. They were the cis-delta4-15-methylprostaglandin F1alpha (2), 15-methyl-2,3-dinorprostaglandin F1alpha (3), and 15-methyl-2,3,4,5-tetranorprostaglandin F1alpha (4). The excretion of the drug-related species was significantly slower than that of the natural prostaglandin F2alpha. The slow excretion rate and the presence of unchanged cis-delta4-15-methylprostaglandin F1alpha in urine suggested that the metabolically protected prostaglandin could persist in the body and, therefore, exhibit longer duration of action.

Animals↗
PubMed1978

Preparation and spectral properties of 12-hydroxyl eicosatetraenoic acid (HETE).

A convenient method for the biosynthesis of 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) from archidonic acid with human platelets was developed, and milligram quantities were made for biological and spectroscopic characterization. This compound has only weak activity in two of five biological prostaglandin assays and no activity in the other three. The 13C and 1H NMR spectra of HETE were obtained and the signal due to each carbon atom was assigned.

Arachidonic Acids↗
PubMed1977

Prostaglandins H1 and H2. Convenient biochemical synthesis and isolation. Further biological and spectroscopic characterization.

An easy biochemical preparation of the prostaglandin endoperoxides, PGH1 and PGH2, is described. Both of the endoperoxides are potent contractors of isolated gerbil colon smooth muscle. Contracture with PGH2 is about equal to that caused by the standard, PGE1, while contracture with PGH1 is about half of that caused by PGE1. PGH1 was found to inhibit platelet aggregation induced by PGH2 and is about 1/10 as potent a stimulator of cAMP accumulation as is PGE1. The mass spectra of the methyl esters of both PGH1 and PGH2 were obtained, as were the infrared spectra of the two compounds. The nuclear magnetic resonance spectrum of PGH2 is characterized by signals at 4.58 delta and 4.47 delta for the C-9 and C-11 protons, respectively.

Animals↗
PubMed1977

Inhibition of human platelet thromboxane synthetase by 9,11-azoprosta-5,13-dienoic acid.

The synthetic prostaglandin analog 9,11-azoprosta-5,13-dienoic acid (azo analog I) has been found to be a potent inhibitor of human platelet thromboxane synthetase by three independent analytical methods: electron-capture gas chromatography, radioisotopic thin-layer chromatography, and radioimmunoassay. In the presence of azo analog I, human platelet aggregation induced by either the prostaglandin endoperoxide PGH2 or arachidonic acid was antagonized. The addition of azo analog I shifted the transformation of endoperoxides away from thromboxane synthesis and toward prostaglandin E2 synthesis. The specificity of azo analog I is demonstrated by its selective inhibition of the second wave of either ADP- or epinephrine-induced platelet aggregation. These data indicate that PGH2 must be converted to thromboxane A2 in order to induce human platelet aggregation.

Arachidonic Acids↗
PubMed1976

The chemical structure of prostaglandin X (prostacyclin).

The chemical structure of prostaglandin X, the anti-aggregatory substance derived from prostaglandin endoperoxides, is 9-deoxy-6, 6alpha-epoxy-delta5-PGF1alpha. The stable compound formed when prostaglandin X undergoes a chemical transformation in biological systems in 6-keto-PGF1alpha. Prostaglandin X is stabilized in aqueous preparations by raising the pH to 8.5 or higher. The trivial name prostacyclin is proposed for 9-deoxy-6, 9alpha-epoxy-delta5-PGF1alpha.

Animals↗
PubMed1975

Interactions between prostaglandin analogues and a receptor in bovine Corpora lutea. Correlation of dissociation constants with luteolytic potencies in hamsters.

The dissociation constants for the interactions between some prostaglandin analogues and a prostaglandin F2 receptor in bovine corpora lutea were determined. These values were compared to the antifertility potencies of these compounds in hamsters and the rates of metabolism by 15-hydro-syprostaglandin dehydrogenase. The most active analogues with regard to both affinity for the receptor and luteolytic potency were 17-phenyl-18, 19, 20-trinorprostaglandin F2alpha and 15-methylprostaglandin F2alpha. The alkyl side chain of prostaglandins could be modified considerably without altering the affinity for the receptor. In this way metabolism by 15-hydroxyprostaglandin dehydrogenase could be blocked. Some of these compounds -ad greatly increased luteolytic effects. Substitution of a phenyl group for the 3 terminal carbon units of the alkyl side chain of prostaglandins increased both the affinity for the receptor and the luteolytic activity in vivo. 7-oxa-13-prostynoic acid, an antagonist of the luteolytic effect of prostaglandin F2alpha in vivo was a weak competitive inhibitor of the interation between prostaglandin F2alpha and the receptor.

Animals↗
PubMed1975

Preparation and quantitation of urinary metabolites of prostaglandin F2alpha by radioimmunoassay.

Radioimmunoassay systems are described which have been developed to quantitate two principle urinary metabolites of PGF2alpha; 9alpha,11alpha-dihydroxy-15-oxo-2,3,4,5-tetranorprostanoic acid (I) and 9alpha,11alpha-dihydroxy-15-oxo-2,3,4,5-tetranorprosta-1,20-dioic acid (II). Preparation of the required metabolites was achieved by total synthesis (I) or by bioconversion (isolation from urine of animals treated with 15-keto-PGF2alpha, II). These metabolites were used to prepare conjugates for immunization. Labelled metabolites, suitable as binding markers, were prepared by metabolism of 3-H-PGF2alpha in vitro (I) or in vivo (II). Specificity of the resulting antibodies was compared to an antibody to PGF2alpha and to 13,14-dihydro-15-keto PGF2alpha. Antisera of II had little or no affinity for 20-carbon precursors (PGF2alpha or 13,14-dihydro-15-keto PGF2alpha), but had nearly equal affinity for metabolite I. Antisera of I, however, had little or no affinity for antigen of II. Therefore, analysis of samples by both assay systems enables quantitation of these excretion products of PGF2alpha. Other assay parameters (binding, affinity, recovery, precision and the repeatability of the assays) were similar to those previously described for other RIA systems, and were considered satisfactory for quantitation of compounds in biological fluids. Quantitation of 24 hour urinary excretion of di-acid metabolite in humans was in close agreement with previously published values determined by physical-chemical means. Greater quantity of di-acid metabolite was excreted by human males (42.0 mug/24 hr) than by females sampled either during the follicular (20.0) or luteal phase (21.2) of the menstrual cycle. The total quantity of C-16 metabolites (as approximated by system II) excreted/kg body weight by the rhesus monkey was similar to that excreted by the human. However, the ratio of di-acid to monoacid was much nearer unity in the monkey than the human.

Animals↗