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T Watabe

Publications and source records attributed to T Watabe.

At least 73 records · Page 4Linked to original sources
PubMed1988

[A case of multiple superficial temporal artery pseudoaneurysms following craniotomy].

A case of multiple superficial temporal artery (STA) pseudoaneurysms following craniotomy is reported and a review of the literature is made. The patient was a 17-year-old male who was hospitalized as he developed right hemiparesis 4 hours after golf ball injury to the left temporal region. He had been diagnosed as hemophilia A one year prior to the injury. CT scan showed right parietal intracranial hematoma with mass effect when he was submitted to emergency craniotomy. At surgery a linear scalp incision was made over the left temporal area after high factor VIII concentrates (con-VIII), 2,000 units, were administered. His postoperative course was uneventful and hemiparesis improved substantially, however two pulsatile masses along the incision scar over the scalp were noticed some 40 days after the hematoma removal. There was another pulsating mass in the left wrist where an arterial cannulation was made at the time of craniotomy. Selective angiograms showed two left STA pseudoaneurysms and left radial pseudoaneurysm was also demonstrated. The left STA was embolized with Gelfoam pieces through catheterization after administration of con-VIII, and the radial artery aneurysm was surgically resected. There was no evidence of recurrence of these lesions during the follow-up period of eight months. Among over 130 cases of STA pseudoaneurysms reported, there was no case with hemophilia and also no such a case described which developed after craniotomy on reviewing the literature. And it was proved that con-VIII has enabled a patient to tolerate embolization procedure through catheterization.

Adolescent↗
PubMed1987

Diurnal rhythm of plasma immunoreactive corticotropin-releasing factor in normal subjects.

Plasma corticotropin-releasing factor (CRF), corticotropin (ACTH) and cortisol levels were simultaneously determined by radioimmunoassays at 0600 h, 1200 h, 1800 h and 2200 h in six normal subjects, in order to examine whether the diurnal rhythm in plasma CRF exists and how it correlates to the diurnal rhythm in plasma ACTH and cortisol concentration. The highest CRF level was observed at 0600 h (7.0 +/- 1.2 pg/ml) and significantly lower levels (p less than 0.01) at 1800 h (1.7 +/- 0.2 pg/ml) and 2200 h (1.9 +/- 0.4 pg/ml). A clear diurnal rhythm was demonstrated in plasma ACTH and cortisol levels, with the highest values at 0600 h (44.6 +/- 8.1 pg/ml and 15.9 +/- 2.0 micrograms/dl, respectively) and the lowest at 2200 h (12.3 +/- 2.8 pg/ml and 4.6 +/- 1.0 micrograms/ml, respectively). These results suggest that the diurnal rhythm in ACTH and cortisol is under the regulation, at least in part, of the diurnal rhythm in CRF secretion.

Adrenocorticotropic Hormone↗
PubMed1987

Long-chained 1-mercapto-n-alkanes as potent inhibitors toward liver alcohol dehydrogenase.

Long-chained 1-mercapto-n-alkanes showed potent inhibitory effects on horse liver alcohol dehydrogenase (HLADH). The inhibitory effect of the thiols was enhanced by increasing the number of the alkyl carbon atoms up to 10-12 and steeply lowered by further increase in the carbon number. The HLADH activity was almost completely inhibited in competitive manner by an equivalent concentration of 1-mercapto-n-decane or -n-dodecane to that of the subunit of the dimeric zinc enzyme; inhibition constant Ki was 0.55 nM for the former. The present study strongly suggests that the thiols interact simultaneously with at least two sites of HLADH; the primary one could be the zinc atom in the active site of the enzyme, interacting with the sulfhydryl groups, and the other a hydrophobic binding site for the their alkyl carbons.

Alcohol Dehydrogenase↗
PubMed1987

Inversion of enantioselectivity in glutathione conjugation of 9,10-dihydrobenzo[a]pyrene 7,8-oxide in hepatic cytosol of rats following induction of hepatic hyperplastic nodules by chemical carcinogens.

Enantiomers of 9,10-dihydrobenzo[a]pyrene 7,8-oxide (DBPO) were stereoselectivity conjugated with glutathione (GSH) specifically at benzylic carbon (C7) in normal Sprague--Dawley (SD) rat liver cytosol: (7R,8S)-(+)- greater than (7S,8R)-(-)-DBPOs. In contrast, in liver cytosol of SD rats bearing hepatic hyperplastic nodules induced with chemical carcinogens, (7S,8R)-(-)-DBPO was preferentially conjugated with GSH to (7R,8S)-(+)-DBPO. GSH S-transferases (GSTs) having sub-unit protein 4 were strongly suggested to play an important role in the preferential conjugation of (7R,8S)-(+)-DBPO in the normal rat liver cytosol, while the preferential conjugation of (7S,8R)-(-)-DBPO in the liver cytosol of the rat bearing hepatic hyperplastic nodules, was most likely to be attributable to GST 7-7, a characteristically induced protein in the hepatic hyperplastic nodules.

Animals↗
PubMed1987

Sulphotransferase-mediated covalent binding of the carcinogen 7,12-dihydroxymethylbenz[a]anthracene to calf thymus DNA and its inhibition by glutathione transferase.

The carcinogen, 7,12-dihydroxymethylbenz[a]anthracene (DHBA), bound covalently through its 7-methylene carbon to calf thymus DNA via DHBA 7-sulphate, a regiospecifically formed, reactive metabolite, when incubated with rat liver cytosol in the presence of 3'-phosphoadenosine 5'-phosphosulphate (PAPS). The hydroxysteroid sulphotransferase inhibitor, dehydroepiandrosterone sulphate, strongly retarded the covalent binding of DHBA to DNA as well as the DHBA 7-sulphate formation from DHBA in the biological system, while pentachlorophenol and dichloronitrophenol showed little effect on these reactions. DHBA 7-sulphate was a good substrate for rat liver cytosolic glutathione (GSH) transferases, so that the PAPS-dependent covalent binding of DHBA to DNA could be markedly retarded in the presence of GSH with concomitant formation of a significant amount of the stable conjugate, S-(12-hydroxymethylbenz[a]anthracen-7-yl)methylglutathione. From DNA, incubated with DHBA in the presence of the hepatic cytosol and PAPS as well as with DHBA 7-sulphate alone, two purine base adducts were isolated after hydrolysis. The purine base adducts accounted for 70% of the total covalent binding of the carcinogen or its 7-sulphate to the nucleic acid and were identified with synthetic specimens as N6-(12-hydroxymethylbenz[a]anthracen-7-yl)-methyladenine and N2-12-hydroxymethylbenz[a]anthracen-7-yl)-methylguanine. The ratio of the adenine to guanine adducts was 1:2.5 with DNA, incubated with DHBA in the presence of hepatic cytosol and PAPS as well as with various concentrations of DHBA 7-sulphate.

Animals↗
PubMed1987

Hormonal responses to insulin-induced hypoglycemia in man.

Insulin-induced hypoglycemia is a potent stress stimulating ACTH release, but the factors responsible for this ACTH secretion are not known. In this study, several ACTH-stimulating factors, such as CRH, arginine vasopressin (AVP), epinephrine (E), norepinephrine (NE), and dopamine, in addition to ACTH, cortisol, and glucose, were simultaneously measured in plasma before and 15, 30, 60, 90, and 120 min after iv administration of 0.1 U/kg BW regular insulin to seven normal subjects. Insulin administration resulted in significant rises in the mean plasma ACTH level from 4.6 +/- 1.1 (+/- SEM) to 21.6 +/- 4.8 pmol/L at 30 min (P less than 0.01) and in plasma cortisol from 330 +/- 60 to 720 +/- 50 nmol/L at 60 min (P less than 0.01). These increases were preceded by a 41.0 +/- 1.9% (P less than 0.001) fall in blood glucose levels. The mean plasma CRH level rose significantly from 1.0 +/- 0.1 to 1.2 +/- 0.1 pmol/L (P less than 0.01) at 30 min and remained elevated until 120 min. In addition, concomitant and significant rises in plasma AVP levels (basal, 1.5 +/- 0.01; peak, 4.5 +/- 1.1 pmol/L at 30 min; P less than 0.01), E (basal, less than 50; peak, 640 +/- 130 pmol/L at 30 min; P less than 0.01), and NE (basal, 0.07 +/- 0.01; peak, 0.17 +/- 0.03 nmol/L at 60 min; P less than 0.05), but not dopamine, also occurred. These results suggest that multiple ACTH-releasing factors, such as CRH, AVP, E, and NE, are involved in ACTH secretion induced by insulin-induced hypoglycemia in man.

Adrenocorticotropic Hormone↗
PubMed1986

Hepatic microsomal cholesterol epoxide hydrolase: selective inhibition by detergents and separation from xenobiotic epoxide hydrolase.

Cholesterol epoxide hydrolase (CEHase) activities of mouse liver microsomes were completely inhibited by Emulgen 108 and Lubrol PX and approximately half by cholate, Triton WR-1339, and Tween 80 when preincubated with 0.1% of these detergents, while their xenobiotic epoxide hydrolase (XEHase) activities were markedly enhanced under the same preincubation conditions. The CEHase and XEHase activities were separately eluted from a gel column applied with mouse liver microsomes which were solubilized in a phosphate buffer containing cholate, glycerol, urea, dithiothreitol, and EDTA.

Animals↗
PubMed1986

Covalent binding of a mercaptan S-sulfate to hepatic cytosolic proteins and its inhibition by glutathione.

4-Nitrobenzyl mercaptan (NBM) S-sulfate, a new type of the sulfate conjugate enzymatically formed from NBM in the presence of 3'-phosphoadenosine 5'-phosphosulfate in rat liver cytosol, bound covalently to rat liver cytosolic proteins at pH 7.4. The protein binding of NBM S-sulfate was strongly retarded by GSH. GSH not only played a role as a scavenger for NBM S-sulfate with formation of NBM and GSSG via S-(4-nitrobenzyl)thioglutathione, but also cleaved the covalent bonds, possibly disulfides formed from NBM S-sulfate and sulfhydryl groups of the cytosolic proteins. Thus, evidence was provided that NBM S-sulfate be a new type of the reactive metabolite.

Animals↗
PubMed1986

Epoxidation of androsta-5,16-dien-3 beta-ol by hepatic microsomal lipid peroxidation.

Male rat liver microsomes oxidized androsta-5,16-dien-3 beta-ol (delta 16-ANDO) to delta 16-ANDO-5,6 alpha-, -5,6 beta-, -16,17 alpha-, and -16,17 beta-epoxides and delta 16-ANDO-5 alpha,6 beta-, -16 alpha,17 beta-, and -16 beta,17 alpha-glycols in the presence of an NADPH-generating system and the microsomal lipid peroxidation accelerator, Fe2+-ADP. The hepatic microsomes hydrolyzed all the delta 16-ANDO epoxides to the glycols. delta 16-ANDO-5 alpha,6 beta-glycol was the sole metabolite from both 5,6 alpha- and 5,6 beta-epoxides. Microsomal epoxide hydrolase also hydrolyzed delta 16-ANDO-16,17 alpha-epoxide specifically to the 16 beta,17 alpha-glycol and the isomeric 16,17 beta-epoxide to the 16 alpha,17 beta- and 16 beta,17 alpha-glycols approximately in the equal ratio. The delta 5-epoxidation of delta 16-ANDO by microsomes occurred only under the conditions that lipid peroxidation took place. Direct evidence was obtained for the participation of microsomal lipid hydroperoxides in the epoxidation of delta 16-ANDO by using photochemically prepared hydroperoxides of phospholipids separated from the hepatic microsomes. The hydroperoxides generated active oxygens, tentatively assigned as alk(ylper)oxy radicals, by the action of ferrous ion and epoxidized delta 16-ANDO to afford the 5,6- and 16,17-epoxides. The Fe2+-ADP-mediated epoxidation of delta 16-ANDO by the phospholipid hydroperoxides occurred preferentially at delta 5 to delta 16 and afforded the 5,6 beta-epoxide in a higher ratio than the 5,6 alpha-epoxide, similar to the Fe2+-ADP-mediated microsomal epoxidation, while the alpha-epoxide was preferentially formed to the beta-epoxide for delta 16 in the epoxidation by both systems.

Androstenols↗
PubMed1986

Regioselective glutathione conjugation of the carcinogen, 7, 12-dihydroxymethylbenz[a]anthracene, via reactive 7-hydroxymethyl sulfate ester in rat liver cytosol.

Potent mutagenicity of 7,12-dihydroxymethylbenz[a]anthracene (DHBA) toward Salmonella typhimurium TA 98 in the presence of rat liver cytosol fortified with 3'-phosphoadenosine 5'-phosphosulfate (PAPS) was completely retarded by the addition of glutathione (GSH). The reactive and intrinsically mutagenic metabolite, DHBA 7-sulfate, formed by hepatic cytosolic sulfotransferase disappeared from the incubation mixture by the addition of GSH. Non-mutagenic S-(12-hydroxymethylbenz[a]anthracen-7-yl)methylglutathione was isolated from the incubation mixture consisting of the hepatic cytosol, DHBA, PAPS, and GSH and proved to be formed by GSH S-transferase directly from DHBA 7-sulfate as an obligatory intermediate.

Animals↗
PubMed1986

A 7-hydroxymethyl sulphate ester as an active metabolite of the carcinogen, 7-hydroxymethylbenz[a]anthracene.

7-Hydroxymethylbenz[a]anthracene (7-HBA) showed potent mutagenicity towards Salmonella typhimurium TA 98 in the presence of untreated rat liver cytosol fortified with the PAPS-generating system, sodium sulphate and ATP. No mutagenic activity was observed either when the cytosol was boiled or when sodium sulphate or ATP was omitted from the assay medium. A highly reactive sulphate ester of 7-HBA was isolated and identified from the medium. It had a half-life of 3.5 min at 37 degrees C and pH 7.4 in water and showed potent, intrinsic mutagenicity towards TA 98. The mutagenicity of 7-HBA sulphate was almost completely retarded in the presence of the cytosol and glutathione. From the biological systems containing glutathione a non-mutagenic and stable glutathione conjugate was isolated that was assigned as S-(benz[a]anthracen-7-yl)methylglutathione. 7-HBA sulphate covalently bound to calf thymus DNA and cytosolic proteins. A fluorospectroscopic study indicated that the carcinogen bound to the biomacromolecules through its 7-methylene group with loss of a sulphate anion as a leaving group.

Animals↗