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Biomedical subjects

F Taki

Publications and source records attributed to F Taki.

43 records · Page 3Linked to original sources
PubMed1986

Neutrophils biosynthesize leukotoxin, 9, 10-epoxy-12-octadecenoate.

An epoxy derivative of linoleate, 9,10-epoxy-12-octadecenoate, was demonstrated to be biosynthesized by neutrophils from various sources such as canine and human blood, and guinea-pig peritonea. It was nominated as leukotoxin from its 'toxic' activity onto mitochondrial respiration. From the reaction mixture of leukocytes with linoleate, an isomer of leukotoxin, 12,13-epoxy-9-octadecenoate, and a 'non-toxic' hydroxy derivative of linoleate, 9-hydroxy-12-octadecenoate, were detected. Such a cascade reaction of linoleate by leukocytes was discussed. Biosynthesis of leukotoxin by neutrophils was substantially enhanced by the presence of calcium ion and calcium-ionophore, A23187. Neutrophils contained leukotoxin, ca. 7 f moles/cell, which was extractable by 60% ethanol, but little of the isomer.

Animals↗
PubMed1986

Biosynthesis of leukotoxin, 9,10-epoxy-12 octadecenoate, by leukocytes in lung lavages of rat after exposure to hyperoxia.

In lung lavages of rat after pure oxygen breathing, a toxic linoleate peroxide, 9,10-epoxy-12-octadecenoate, and its isomer, 12,13-epoxy-9-octadecenoate were detected by HPLC analyses. The epoxide(s) was demonstrated to be biosynthesized by incubating linoleate with leukocytes collected from lung lavages, thus nominated to be leukotoxin. The chemical structures of leukotoxin and its isomer were determined by gas-chromatography/mass spectrometry and nuclear magnetic resonance measurements. Leukotoxin showed a potent uncoupling activity to rat liver mitochondrial respiration and a dose-dependent relaxation of rat stomach smooth muscle. These findings were discussed with 'oxygen toxicity' on the lung.

Animals↗
PubMed1986

The role of phospholipase in reduced beta-adrenergic responsiveness in experimental asthma.

This investigation was designed to elucidate the role of phospholipase (PLase) in relation to reduced beta-adrenergic responsiveness in guinea pigs subjected to experimental asthma. In the in vivo experiment, guinea pigs that had developed asthma-like symptoms after exposure to an aerosol of 2% ovalbumin for 7 to 8 min for 10 successive days were used as the experimental asthma group. The control group was exposed to saline. The endogenous PLase activity was determined by high performance liquid chromatography using ditridecanoyl phosphatidylcholine as a substrate. PLase activity of lung membranes in the experimental asthma group was significantly elevated by 50% compared with that in the control group. Phospholipid content of lung membranes in the experimental asthma group was decreased by 11% compared with that in the control group. The experimental asthma group showed a 37% decrease in the number of beta-adrenoceptors in lung membranes and a 54% decrease in isoproterenol-stimulated adenylate cyclase activity in lung membranes compared with the control group. Although forskolin-stimulated adenylate cyclase activity was also reduced by 24%, decreases in forskolin-stimulated activity were less than decreases in isoproterenol-stimulated activity. In the in vitro experiment phospholipids in lung membranes were degraded by pretreatment with 0.1 U of PLase A2. After pretreatment of lung membranes with PLase A2, the number of beta-adrenoceptors was reduced by 25% compared with that in the control group, and adenylate cyclase activity stimulated by isoproterenol and forskolin were also reduced by 67 and 28%, respectively. PLase A2 had a minor effect on forskolin-stimulated activity as compared with isoproterenol-stimulated activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

The role of leukotriene B4 in the genesis of oxygen toxicity in the lung.

Leukotriene B4 (LTB4) is a metabolite of arachidonic acid that has potent chemotactic activity for polymorphonuclear leukocytes (PMN). Pulmonary oxygen toxicity is considered to be a good model of an acute inflammatory lung injury, and an increase in the number of PMN is found in the lungs acutely injured by hyperoxia. In order to estimate the role of LTB4 responsible for this influx of PMN, we measured the LTB4 by radioimmunoassay in lung lavages of rats exposed to hyperoxia for 60 h. We found that the level of LTB4 in lung lavages in rats exposed to hyperoxia for 60 h increased significantly compared with that in normoxic control rats. At the same time, the marked increase in the number of PMN in lung lavages and the decrease in the activity of NADPH-cytochrome c reductase in lung microsomes were also observed. The administration of AA861, a 5-lipoxygenase inhibitor, reduced not only the increase in LTB4 but also the increase in the number of PMN in lung lavages of rats exposed to hyperoxia for 60 h. Furthermore, treatment with AA861 also protected the decrease in the activity of NADPH-cytochrome c reductase. The effects of AA861 on these parameters were observed in a dose-dependent fashion. In addition, there is a good correlation between the level of LTB4 and the number of PMN in the lavage of rats exposed to hyperoxia for 60 h with or without AA861 administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Biochemical changes in airways after antigen inhalation.

These results suggest that activation of phospholipase A2 after antigen exposure triggers an increase in leukotriene synthesis resulting in inflammatory cell influx into the airway and contraction of bronchial smooth muscle. That is, it was demonstrated that inhaled antigen concerns with IgE-mast cell system, but, on the other hand it might act as non specific stimuli.

Administration, Oral↗
PubMedDate not supplied

Effects of sodium channel blockers on electrical field stimulation-induced guinea-pig tracheal smooth muscle contraction.

The effects of sodium channel blockers, a conventional one: tetrodotoxin, and clinically available ones: cibenzoline, flecainide and SUN 1165 [N-(2,6-dimethylphenyl)-8-pyrrolizidine-acetamide hydrochloride hemihydrate] on electrical field stimulation-induced and carbachol-induced guinea-pig tracheal smooth muscle contraction were investigated. Electrical field stimulation was performed at 50 V with 20 Hz and 0.8 msec square pulse duration. Carbachol (5 x 10(-8) M) was used for induction of tracheal contractions. All agents were administered before electrical field stimulation or carbachol administration. Electrical field stimulation-induced tracheal smooth muscle contraction was dose-dependently reduced by all sodium channel blockers used. The effects of sodium channel blockers on electrical field stimulation-induced contraction were greater than those on carbachol-induced contractions, except for SUN 1165 which reduced similarly both electrical field stimulation- and carbachol-induced contractions. These results indicate that the sodium influx is closely related to the acetylcholine release, resulting in smooth muscle contraction. Since the parasympathetic nervous system may be involved in the genesis of various pathological conditions, such as bronchial asthma, sodium channel blockers could contribute to the management of these conditions.

Animals↗