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Biomedical subjects

K Satouchi

Publications and source records attributed to K Satouchi.

At least 19 recordsLinked to original sources

Mitochondrial changes in phospholipid molecular species during the increased oxidative phosphorylation after hepatectomy.

The changes in liver mitochondrial and microsomal phospholipid molecular species were analyzed during the period of remarkably increased oxidative phosphorylation following partial hepatectomy in rabbits. At 24 hours after hepatectomy, phosphorylative activity increased significantly from 69.7 +/- 5.5 to 118.5 +/- 5.7 nmol of ATP synthesized/min/mg protein, compared to the sham operated group. The ratio of phosphatidylethanolamine to phosphatidylcholine (PE/PC) in mitochondria increased significantly in the hepatectomy group compared with the sham operated group. Remarkable changes in molecular species were observed in mitochondrial phosphatidylethanolamine. 1-Stearoyl-2-arachidonoyl species decreased in the hepatectomy group. On the other hand, microsomal phospholipids hardly changed compared with mitochondrial ones. The change in content of 1-stearoyl-2-arachidonyl phosphatidylethanolamine in mitochondria tended to return to normal levels concomitant with the normalization of phosphorylative activity. The changes in content of mitochondrial phospholipids, especially phosphatidylethanolamine, might also be related to enhancement of phosphorylative activity.

Animals

Evidence of platelet-activating factor in nasal polyps.

Platelet-activating factor (PAF) was measured in human nasal polyps obtained from patients with chronic sinusitis. PAF was quantitated by platelet-aggregating activity and was found to be 7.8 +/- 1.8 pg/micrograms phosphorus of polyp phospholipid (mean +/- SE; n = 23). In the polyps, phosphatidylcholine constituted 30% of the total phospholipids, of which 8.5% was the ether-linked type. Incubations of replicates of the fresh polyps in Tyrode's solution in the presence of calcium ionophore A23187 and antihuman immunoglobulin E resulted in 295 and 65% increases in the amount of PAF, respectively. Thus, nasal polyps in humans with chronic sinusitis possess PAF and have the potential to produce PAF upon stimulation. The participation of PAF in nasal polyp formation is discussed.

Adolescent

Effect of dietary alpha-linolenate on platelet-activating factor production in rat peritoneal polymorphonuclear leukocytes.

The effects of dietary alpha-linolenate (18:3, n-3) and linoleate (18:2, n-6) on platelet-activating factor (PAF) production were examined. Rats were fed an alpha-linolenic acid-rich (perilla oil) diet or a linoleic acid-rich (safflower oil) diet for 6 wk, and polymorphonuclear leukocytes (PMN) were elicited by peritoneal injection of casein. The overall phospholipid content and composition as well as the subclass distribution of choline and ethanolamine glycerophospholipids in PMN were not altered by these diets. However, with the perilla oil diet their content of a putative precursor of PAF, 1-alkyl-2-arachidonoyl-sn-glycero-3-phosphocholine was approximately 50% of that with safflower oil diet. On exposure to various concentrations of FMLP, PAF formation by PMN in the perilla oil group was less than 50% of that by PMN in the safflower oil group. A larger difference in PAF productions by PMN in the two dietary groups was observed on their stimulation with calcium ionophore A23187. These results demonstrate that PAF production is modulated in some as yet unknown way by changing the alpha-linolenate/linoleate balance of the diet.

Animals

Platelet-activating factor detected in bronchoalveolar lavage fluids from an asthmatic patient.

It recently has been recognized that platelet-activating factor (PAF) may be a mediator of asthma exacerbation. We had the opportunity to analyze bronchoalveolar lavage fluids from an asthmatic infant, which were characterized by neutrophil infiltration. The patient's lungs were washed on three occasions with saline during asthmatic attacks. PAF was found in each case on the basis of its ability to cause the immediate aggregation of washed rabbit platelets. The PAF detected was equivalent to 1-1.4 pmol of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine, three quarters of which were recovered in cell-associated form. By contrast, we did not detect PAF in bronchoalveolar exudates from patients with laryngeal stenosis or with respiratory distress syndrome. LysoPAF, the direct precursor as well as initial metabolite of PAF, was also analyzed after being converted to PAF by acetylation. There was a wide variation in the amount of lysoPAF present in individual patients, suggesting that lysoPAF levels cannot be taken as an indicator for the presence of PAF.

Asthma

Molecular heterogeneity of platelet-activating factor (PAF) in rat glandular stomach determined by gas chromatography/mass spectrometry. PAF molecular species changes upon water-immersion stress.

The molecular heterogeneity of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (alkylacetyl-GPC) and 1-acyl-2-acetyl-sn-glycero-3-phosphocholine (acylacetyl-GPC) in normal rat glandular stomach was studied by gas chromatography/mass spectrometry (GC/MS) and tandem mass spectrometry. The percentage compositions of the molecular species of 1-alkyl-2-acetyl-GPC and 1-acyl-2-acetyl-GPC in the antrum were, respectively, 1-alkyl [16:0 (34%) and 18:0 (66%)]-2-acetyl-GPC and 1-acyl [16:0 (60%), 18:0 (14%) and 18:1 (26%)]-2-acetyl-GPC. The alkyl chain composition of 1-alkyl-2-acetyl-GPC was quite different from that of 1-alkyl-2-acyl-GPC in both the antrum and corpus, demonstrating a high degree of selectivity of alkyl chain utilization in PAF biosynthesis. The amount of 1-acyl-2-acetyl-GPC was much greater than that of 1-alkyl-2-acetyl-GPC. The molecular heterogeneity of 1-alkyl-2-acetyl-GPC and 1-acyl-2-acetyl-GPC in the corpus was similar to that in the antrum. Water-immersion stress affected not only the amount of 1-alkyl-2-acetyl-GPC and 1-acyl-2-acetyl-GPC, but also their molecular heterogeneity in the antrum and corpus. Whereas the amounts of 1-hexadecyl-2-acetyl-GPC and 1-acyl [16:0, 18:0 and 18:1]-2-acetyl-GPC decreased markedly (to less than one-fifth) in the antrum after such stress for 1 hr, the amount of 1-octadecyl-2-acetyl-GPC increased markedly (up to 4-fold) in the corpus and severe lesions were observed after stress for 7 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Production of platelet-activating factor in slugs.

The land slug, Incilaria bilineata, was shown to contain a large amount of 1-O-alkyl-2-acyl (long chain)-sn-glycero-3-phosphocholine, which accounts for as much as 47% of the choline glycerophospholipid fraction. Since this unique either phospholipid has been regarded as a stored precursor form of platelet-activating factor (PAF) in mammalian inflammatory cells, we examined the possibility of the presence of PAF in this animal. We obtained the evidence for the occurrence of significant amounts of PAF in two species of slugs, Incilaria bilineta and Incilaria fruhstorferi. Gas chromatography-mass spectrometry analysis revealed that the alkyl fatty chain of PAF principally consists of 16:0. We confirmed the presence of both enzyme activities catalyzing the formation of PAF, one for the remodeling pathway and the other for the de novo pathway. We also found the occurrence of other enzyme activities involved in PAF metabolism: acetylhydrolase activity which inactivates PAF and phospholipase A2 activity toward alkylacylglycerophosphocholine. However, we failed to detect cofactor-independent transacylation activity in this animal. The amounts of PAF in slugs were markedly increased when slugs were administered several treatments which are considered to induce shock, such as the injection of dimethyl sulfoxide or injuries. These results suggest that PAF is produced and may have certain physiological and pathological roles in the land slug, as in the case of mammals.

Acetyltransferases

The presence of platelet-activating factor associated with eosinophil and/or neutrophil accumulations in the pleural fluids.

Platelet-activating factor (PAF) has been reported to play a role in the inflammatory reaction, but the mechanism of PAF in humans is still unclear. We examined the presence of PAF in pleural fluids from 23 patients with pleural effusion and in all cases detected PAF associated with eosinophil and/or neutrophil infiltrations. The amounts of PAF in pleural fluids were, respectively, 340, 50 to 170, and 1,250 to 2,130 fmol/ml for a patient with eosinophilic pneumonia, those with pneumothorax (n = 9), and empyema (n = 3). In contrast, patients with tuberculous pleuritis (n = 2), lung edema (n = 3), or malignant disease (n = 5) had no detectable amounts of pleural fluid PAF (less than or equal to 10 fmol/ml). The amount of PAF showed a close correlation with the numbers of eosinophils and neutrophils in the pleural fluids. Furthermore, PAF was mostly detected in the cellular fractions, and the molecular species of PAF from the patients with empyema were almost consistent with those of PAF generated by human blood neutrophils. These results indicate that neutrophils and, presumably, eosinophils were the cellular source of PAF in the pleural fluids in the pathologic state of inflammation.

Adult

Changes in phospholipid composition of the mitochondrial membrane after orthotopic liver transplantation.

Changes in phospholipids and their fatty acid composition in liver mitochondria obtained from allogenic rats with orthotopic liver transplants were measured with and without immunosuppressive treatment. In untreated allogenic rats, mitochondrial phosphorylation activity was severely deteriorated at 8 days after transplantation. A significant change was also found in the amount of cardiolipin compared with other classes of phospholipids. Namely, cardiolipin decreased, and lysodiphosphatidylglycerol and phosphatidylglycerol increased concomitantly. Furthermore, the percentage of linoleic acid in cardiolipin decreased dramatically. Decrease in cardiolipin and changes in its fatty acid composition may be attributed to the deterioration of mitochondrial function upon acute rejection.

Animals

1-O-hexadec-1'-enyl-2-acetyl-sn-glycero-3-phosphocholine and its biological activity.

1-O-Alk-1'-enyl analog of platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine, alkylacetyl-GPC) was prepared semi-synthetically from choline plasmalogens of beef heart muscle. The main compound was identified mass spectrometrically as 1-hexadec-1'-enyl-2-acetyl-sn-glycero-3-phosphocholine (16:O alk-1'-enylacetyl-GPC, 16:O vinyl form of PAF) and its platelet aggregation activity was about one-fifth of that of the corresponding 16:O alkylacetyl-GPC. The irreversible platelet aggregation activity induced by 5X10(-10) M 16:O alk-1'-enylacetyl-GPC was completely inhibited by 5X10(-7) M CV-3988 and 1X10(-7) M L-652, 731, specific PAF antagonists, and more than 99% of the activity was also lost by acid treatment. The hydrogenated product, alkylacetyl analog, showed quite same activity as that of authentic 16:O alkylacetyl-GPC. The platelets desensitized with 16:O alkylacetyl-GPC and with 16:O alk-1'-enylacetyl-GPC were not aggregated with 5X10(-10) M 16:O alk-1'-enylacetyl-GPC, suggesting that alk-1'-enylacetyl-GPC occupied the same receptor site of alkylacetyl-GPC.

Animals

Acyl type platelet-activating factor in normal rat uterus determined by gas chromatography mass spectrometry.

1-Fatty acyl-2-acetyl-sn-glycero-3-phosphocholine (1-fatty acyl-2-acetyl GPC, acyl type platelet-activating factor (PAF) was found in normal rat uterus without addition of any exogenous stimuli and identified as 1-palmitoyl, 1-oleoyl and 1-stearoyl species by gas chromatography/mass spectrometry coupled with selected ion monitoring (SIM). The main species was the 1-palmitoyl species. The ions used for SIM were chosen on the basis of the acetyl and fatty acyl moieties and molecular weight. The amount of 1-fatty acyl-2-acetyl GPC was significantly more than that of PAF (1-fatty alkyl-2-acetyl GPC, AGEPC), and the ratio of 1-palmitoyl-2-acetyl GPC to 1-0-hexadecyl-2-acetyl GPC was about 4.5:1 in normal rat uterus.

Animals

Endogenous platelet-activating factor and anti-platelet-activating factor in patients with renovascular hypertension.

Renovascular hypertension is relieved by percutaneous transluminal renal angioplasty. In four patients with renovascular hypertension, platelet-activating factor (PAF) was found to be released into the ipsilateral renal venous blood after percutaneous transluminal renal angioplasty, but was not found in the contralateral renal venous blood following this procedure. Anti-platelet-activating factor with a lipid-like property was also found, and its polarity was slightly lower than that of PAF judging by its behavior on thin layer chromatography. Anti-platelet-activating factor completely blocked the aggregation of rabbit platelets induced by PAF, ADP or arachidonic acid. These results indicate that PAF and anti-platelet-activating factor are released into renal venous blood following percutaneous transluminal renal angioplasty in patients with renovascular hypertension.

Adenosine Diphosphate

1-Acyl-2-acetyl-sn-glycero-3-phosphocholine from stimulated human polymorphonuclear leukocytes.

1-Acyl-2-acetyl-sn-glycero-3-phosphocholine (1-acyl-2-acetyl GPC) was found in the fraction of platelet-activating factor obtained from stimulated human polymorphonuclear leukocytes (PMN). The amount of 1-acyl-2-acetyl GPC obtained from 1 X 10(7) PMN stimulated with ionophore A23187 at 37 C for 15 min ranged from 8 to 56 pmol (32 +/- 10 pmol, mean +/- standard error; n = 4). The main species was 16:0 palmitoyl (17 +/- 5 pmol), followed by 18:0 stearoyl (8 +/- 3 pmol) and 18:1 oleoyl (7 +/- 3 pmol). Although the physiological significance is unknown, 1-acyl-2-acetyl GPC was always detected when 1-alkyl-2-acetyl GPC was detected.

Animals

Platelet-activating factor in normal rat uterus.

Platelet-activating factor (PAF) was found in normal rat uterus and identified as 1-0-hexadecyl/octadecenyl-2-acetyl-sn-glycero-3-phosphocholine. PAF was purified by several successive chromatographic procedures. It showed platelet aggregating activity, which was inhibited by CV 3988, and had no effect on platelets desensitized with 1-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine. The tert-butyldimethyl-silylderivative of 1-0-alkyl-2-acetyl-sn-glycerol, which was obtained by hydrolysis of uterine PAF with phospholipase C, was analyzed by gas chromatography-mass spectrometry. One rat uterus contained approximately 21.3 ng of 1-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine. This is the first report of the occurrence of a significant amount of PAF in a normal animal tissue.

Animals

Polymorphonuclear leukocyte-platelet interactions: acetylglyceryl ether phosphocholine-induced platelet activation under stimulation with chemotactic peptide.

A mixture of rabbit polymorphonuclear leukocytes (PMNs) and platelets at concentrations of 5 X 10(6) PMN and 3.5 X 10(8) platelets/ml Tyrode's solution was stimulated with the chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (FMLP). A micromolar concentration of FMLP elicited an immediate weak aggregation, followed by a strong aggregation with a time lag of about 1 min. Microscopic examination showed that the immediate aggregation was due to PMNs and the delayed one was more complex and involved platelets. The delayed aggregation was dependent upon the concentrations of both the PMNs and FMLP. The delayed aggregation was completely blocked by pretreatment of the PMN-platelet mixture with 8 microM CV-3988, a specific receptor antagonist of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC), or by the application of platelets desensitized to AGEPC. The time course of AGEPC production by PMNs was well matched to that of the biphasic aggregation response. Furthermore, nordihydroguaiaretic acid inhibited both the AGEPC production by PMNs and the delayed aggregation in a similar dose-dependent manner. These result demonstrate that AGEPC, newly-generated by PMNs under FMLP-stimulation, is of primary importance in platelet aggregation in a PMN-platelet mixed system.

Animals

Evidence for production of 1-acyl-2-acetyl-sn-glyceryl-3-phosphorylcholine concomitantly with platelet-activating factor.

The presence of 1-acyl-2-acetyl-sn-glyceryl-3-phosphorylcholine in a sample of platelet-activating factor from stimulated rabbit neutrophils was demonstrated by a gas-liquid chromatography/mass spectrometry technique coupled with selected ion monitoring. The ions chosen for identification were those of acetyl and long-chain acyl moieties and molecular weight. Species containing palmitic, oleic and stearic acids were detected. A good correlation was observed between the productions of 1-acyl-2-acetyl-sn-glyceryl-3-phosphorylcholine and 1-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine by neutrophils stimulated with ionophore A23187.

Animals

Generation of acetyl glyceryl ether phosphorylcholine from the rat skin and muscle tissues stimulated by moxibustion.

Platelet-activating factor was obtained from the rat skin and muscle tissues which were stimulated by moxibustion. It showed a typical aggregation pattern on interaction with washed rabbit platelets but when it was treated with phospholipases A2 and C, and CV 3988 the aggregation activity was lost. Platelet-activating factor was hydrolysed with phospholipase C and the resulting lipid product was converted to the tert-butyldimethylsilyl derivative. After purification by thin layer chromatography, the ether type of derivative was analysed by a selected ion monitoring technique of gas chromatography-mass spectrometry. 1-0-Hexadecyl-2-acetyl-sn-glyceryl-3-phosphorylcholine only was identified.

Animals