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Biomedical subjects

K Takeshige

Publications and source records attributed to K Takeshige.

At least 127 records · Page 7Linked to original sources
PubMed1984

Diacylglycerol, 1-oleoyl-2-acetyl-glycerol, stimulates superoxide-generation from human neutrophils.

1-Oleoyl-2-acetyl-glycerol which activates Ca2+-activated phospholipid-dependent protein kinase, induced the superoxide-production of human neutrophils, while other diacylglycerols did not. The induction was independent of extracellular calcium and did not accompany the increase of the intracellular free calcium. The superoxide-release by the diacylglycerol was inhibited by retinal, the inhibitor of the protein kinase. The diacylglycerol stimulated the phosphorylation of at least 4 proteins in intact neutrophils, the phosphorylation of which was stimulated by phorbol 12-myristate 13-acetate, the activator of the protein kinase. These observations indicate the possible involvement of the kinase in the induction process.

Diglycerides↗
PubMed1984

Superoxide production of human polymorphonuclear leukocytes stimulated by leukotriene B4.

Leukotriene B4 stimulated a transient production of superoxide anions (O2-) by human polymorphonuclear leukocytes which continued for only about 1 min. The production was dependent on Ca2+ in the suspending medium and no production was observed without the addition of calcium. The concentrations of leukotriene B4 and calcium for the half-maximal production were about 1 microM and 200 microM, respectively. 8-(N,N,-Diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8), an intracellular calcium antagonist, did not inhibit the O2- production stimulated by leukotriene B4 in the presence of calcium, while N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), a calmodulin inhibitor, did. When leukotriene B4 was added to the cells treated with cytochalasin B, the production of O2- was biphasic: an initial rapid phase, followed by a slow one. The slow phase was also dependent on Ca2+ concentrations but it could be induced even without the addition of Ca2+ to the medium. The cells treated with both cytochalasin B and TMB-8 in Ca2+-free medium showed a negligible production of superoxide on addition of leukotriene B4, but the production appeared upon addition of CaCl2. These findings suggest that the superoxide production stimulated by leukotriene B4 is associated with the influx of Ca2+.

Animals↗
PubMed1984

NADPH-dependent reduction of ubiquinone-1 associated with the superoxide-forming oxidase of pig polymorphonuclear leucocytes.

NADPH-dependent ubiquinone-1 reductase activity was present in the phagocytic vesicles of pig polymorphonuclear leucocytes. The apparent Km-value of the reductase for NADPH was 29 microM which is similar to that of the NADPH-dependent superoxide formation. Increase of the quinone-reductase activity by increasing the concentrations of ubiquinone-1 was associated with the decrease of the superoxide forming activity, the rate of the NADPH oxidation being constant independent of the quinone concentration. p-Chloromercuribenzoate inhibited both superoxide formation and reduction of the quinone, whereas low concentrations of cetyltrimethylammonium bromide which inhibit the superoxide formation did not inhibit the reduction of the quinone. The reduction of 2,6-dichlorophenolindophenol which has been shown not to be inhibited by both inhibitors. The quinone-reductase activity could be extracted with a mixture of deoxycholate and Tween 20 which extracts the superoxide forming activity. The observations indicate that a region of the superoxide-forming NADPH oxidase between a mercurial-sensitive site and a site sensitive to the cationic detergent is responsible for the reduction of ubiquinone.

Animals↗
PubMed1984

Phosphorylation of myosin light chain in intact pig leukocytes stimulated by phorbol 12-myristate 13-acetate.

Phosphorylation of myosin light chain was investigated in intact pig polymorphonuclear leukocytes. The labeling of the myosin light chain (Mr = 21000) was increased by exposure of the cells to phorbol 12-myristate 13-acetate. Two-dimensional gel electrophoresis revealed three forms of Mr = 21000 light chain, of which two were phosphorylated. The phosphorylation of the myosin light chain was inhibited by neither N-(6-aminohexyl)-5-chloro-1-naphthalene sufonamide nor trifluoperazine, suggesting that calmodulin is not involved in the phosphorylation.

Animals↗
PubMed1984

Endoscope assisted surgery for the treatment of bleeding esophageal varices.

In attempts to obtain complete control of bleeding esophageal varices, terminal esophago-proximal gastrectomy (TEPG) and its modification proximal gastric transection (PGT) were performed, under endoscopic assistance, in 42 patients with cirrhotic portal hypertension. Complete disappearance of varices was confirmed in all patients at surgery and 4 weeks after surgery, and this condition was maintained for up to 60 months in 15 patients of TEPG and 16 of PGT. Recurrent varices in 3 (17 per cent) TEPG and 8 (34 per cent) PGT were attributed to the advance in the liver cirrhosis in 7, hepatoma in 3 and portal vein thrombosis in 1. In 8 of 11 recurrences, type C variceal blood circulation drained into the cervical veins. Endoscopic assistance during surgical treatment for bleeding esophageal varices plays a decisive role.

Adult↗
PubMed1984

Oxygen metabolism of human colostral macrophages: comparison with monocytes and polymorphonuclear leukocytes.

Human colostral macrophages stimulated by opsonized zymosan or phorbol myristate acetate (PMA) released superoxide anions (O2-) and hydrogen peroxide (H2O2) with activities comparable to those of monocytes and about one-fourth of those of polymorphonuclear leukocytes (PMNL) of blood. The O2- -forming oxidase in the macrophages stimulated by PMA was dependent on NADPH as an electron donor with an apparent Km value for NADPH of 27.6 +/- 4.0 microM, which is comparable to those obtained for the stimulated monocytes and PMNL of blood. The Vmax was 1.86 +/- 0.33 nmol O2/min/10(6) cells, which is essentially the same as that of monocytes and about half of that of PMNL. p-Chloromercuribenzoate or cetyltrimethylammonium bromide completely inhibited oxidases of all three types of phagocytes. A b-type cytochrome was identified in the macrophages but the concentrations in the macrophages and monocytes were less than half of that in PMNL. These results suggest that the differences in the O2- -forming activities of the three types of phagocytes are quantitative rather than qualitative. The macrophages and monocytes showed very low activities of myeloperoxidase [EC 1.11.1.7] in contrast to PMNL. The activity of beta-glucuronidase [EC 3.2.1.31] in the macrophages was much higher than those of the monocytes and PMNL, but little difference was observed in the activities of lysozyme [EC 3.2.1.17], catalase [EC 1.11.1.6] and superoxide dismutase [EC 1.15.1.1] among the three types of phagocytes examined. Electron micrographs of the macrophages showed little increase of vacuoles upon exposure to PMA, in contrast to the cases of monocytes and PMNL.

Catalase↗
PubMed1983

NADPH-dependent reduction of 2,6-dichlorophenol-indophenol by the phagocytic vesicles of pig polymorphonuclear leucocytes.

NADPH-dependent 2,6-dichlorophenol-indophenol (DCIP) reductase activity in the homogenate of phagocytosing pig polymorphonuclear leucocytes was twice that of the resting cells and the activity in the phagocytic vesicles corresponded to the activity increment due to phagocytosis. The apparent Km value of the reductase activity in the vesicles for NADPH was 30 microM, which is similar to that of the NADPH-dependent superoxide (O2-) formation. Increasing the DCIP reductase activity by increasing the DCIP concentration caused a decrease in the O2- -forming activity, the NADPH oxidation rate being constant and independent of the dye concentration. p-Chloromercuribenzoate and cetyltrimethylammonium bromide at low concentrations inhibited the O2- -forming activity of the vesicles without inhibiting the DCIP reductase. Quinacrine inhibited both O2- formation and DCIP reduction. The DCIP reductase activity could be extracted with a mixture of deoxycholate and Tween-20, which extracts the O2- -forming activity. The reductase activity in the extract was enhanced 2-fold by the addition of FAD, and its apparent Km was 0.085 microM. These results indicate that the NADPH-dependent DCIP reductase activity of the phagocytic vesicles is catalysed by a flavin-containing component of the O2- -forming system.

2,6-Dichloroindophenol↗
PubMed1983

Kinetics of superoxide formation by respiratory chain NADH- dehydrogenase of bovine heart mitochondria.

Formation of superoxide anions (O2-) by bovine heart NADH-dehydrogenase preparation (Complex I) supported by an NADH- or NADPH-generating system was studied kinetically. Both NADH- and NADPH-dependent superoxide-forming activities of Complex I were biphasic in double reciprocal plots. The NADH-dependent reaction had two sets of kinetic parameters: One Km value for NADH was 10 times higher than the other one, and the Vmax of the reaction with high Km was about 4 times higher than that of the reaction with low Km. Similar Vmax values were obtained for the NADPH-dependent reactions but the Km values were a thousand times higher than those of the NADH-dependent reactions. The plots of the NADH-dependent activity of rotenone-treated submitochondrial particles were also biphasic. The double reciprocal plots of NADH- and NADPH-dependent 2,6-dichlorophenolindophenol (DCIP) reductase activities of Complex I were linear and the plots of the superoxide-forming activities against the DCIP reductase activities were biphasic. These results indicate that the biphasic double reciprocal plots of the superoxide-forming activities against reduced coenzymes are not caused by interaction between reduced coenzymes and the NADH-dehydrogenase but are due to the presence of at least two superoxide-forming sites in the respiratory chain NADH-dehydrogenase.

Animals↗
PubMed1982

Superoxide-forming NADPH oxidase preparation of pig polymorphonuclear leucocyte.

A phagocytic vesicle fraction with high NADPH-dependent superoxide-forming activity was obtained in large quantity from pig blood polymorphonuclear leucocytes, phagocytosing oil droplets in the presence of cyanide. The activity of the homogenate of the phagocytosing cells was 40 times that of the resting cells, and 70% of the activity in the homogenate was recovered in the phagocytic vesicle fraction. Essentially all of the superoxide-forming activity was extracted by repeated extraction with a mixture containing deoxycholate and Tween 20. The extract had a superoxide-forming activity of 1 mumol/min per mg of protein with NADPH, and one-fifth of this with NADH, Km values being similar to those of the vesicle fraction (40 microM for NADPH and 400 microM for NADH). A stoichiometric relationship of 1:2 for NADPH oxidation and superoxide formation was obtained, in agreement with the reaction NADPH +2O2 leads to NADP+ + 2O2 -. + H+. The activity of the extract was enhanced 2-fold by the addition of FAD, suggesting that the flavin is a component of the enzyme system. The Km value for FAD was 0.077 microM. The activities in both vesicle fraction and extract were labile even on refrigeration, but could be kept for several months at -70 degrees C.

Animals↗
PubMed1982

Alteration of inner-membrane components and damage to electron-transfer activities of bovine heart submitochondrial particles induced by NADPH-dependent lipid peroxidation.

We investigated the changes of the inner-membrane components and the electron-transfer activities of bovine heart submitochondrial particles induced by the lipid peroxidation supported by NADPH in the presence of ADP-Fe3+. Most of the polyunsaturated fatty acids were lost as a result of the peroxidation, and phospholipids were changed to polar species. Ubiquinone was also modified to polar substances as the peroxidation proceeded. Sodium dodecyl sulphate/polyacrylamide-gel electrophoresis showed the disappearance of 27000-Mr and 30000-Mr proteins and the appearance of highly polymerized substances. Flavins and cytochromes were not diminished, but the respiratory activity was lost. The reactions of NADH oxidase and NADH-cytochrome c reductase were most sensitive to the peroxidation, followed by those of succinate oxidase and succinate-cytochrome c reductase. Succinate dehydrogenase and duroquinol-cytochrome c reductase were inactivated by more extensive peroxidation, but cytochrome c oxidase was only partially inactivated. NADH-ferricyanide reductase was not inactivated. The pattern of the inactivation indicated that the lipid peroxidation affected the electron transport intensively between NADH dehydrogenase and ubiquinone, and moderately at the succinate dehydrogenase step and between ubiquinone and cytochrome c.

Animals↗
PubMed1982

Release of the membrane-calcium and its relation to the superoxide formation by polymorphonuclear leukocytes.

The relationship between the intracellular translocation of calcium from the storage pool and the oxidative metabolism was studied. An intracellular calcium-antagonist, TMB-8, inhibited the release of superoxide induced by a calcium ionophore A23187 and the inhibition was relieved by the addition of calcium ions. The release induced by cytochalasin D or by the ingestion of bacteria was similarly inhibited by TMB-8. The mobilization of intracellular divalent cations of leukocytes was monitored by a fluorescent probe, CTC. When the CTC-loaded cells were stimulated with cytochalasin D or E. coli, a fluorescence change ascribable to the release of calcium from the intracellular hydrophobic environment was observed. The dose-response curve of the fluorescence change and that of the superoxide release of th cells were very similar. TMB-8 inhibited both metabolic and fluorescence changes in parallel. The results support the hypothesis that an intracellular translocation of calcium is stimulated the oxidative metabolism of leukocytes.

Calcimycin↗
PubMed1982

Case report of a pancreatic pseudocyst ruptured into the splenic vein causing extrahepatic portal hypertension.

In a 42 year old female, a fistula developed between the splenic vein and the pancreatic duct through the cavity of a pseudocyst in the tail of the pancreas and resulted in an extrahepatic portal hypertension. The fistula was visualized by endoscopic retrograde cholangiopancreatography and percutaneous transhepatic portography, then was successfully resected by surgery. The possible etiology of extended obstruction of both splenic and portal veins in chronic pancreatitis with pseudocyst was discussed.

Adult↗