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T Endoh

Publications and source records attributed to T Endoh.

At least 73 records · Page 4Linked to original sources
PubMed1995

Effects of oxidative stress induced by redox-enzyme modulation on rat hepatocarcinogenesis.

Inducibility of oxidative stress by menadione-associated redox cycling activation under redox-enzyme modulated conditions was examined in F344 male rat liver, by monitoring 8-hydroxydeoxyguanosine (8-OHdG) levels in DNA and hepatocyte injury. Further, the treatment-associated liver tumor-initiating, -promoting and -progressing potentials were assessed in terms of development of enzyme-altered preneoplastic foci, neoplastic nodules and hepatocellular carcinomas. With or without menadione, redox-enzyme modulation consisting of increased cytochrome P450 reductase by phenobarbital (PB), depletion of glutathione by phorone, inhibition of DT-diaphorase by dicumarol, with or without further supplement of iron, caused both 8-OHdG production and hepatocyte necrosis. Thus-induced oxidative stress exerted liver tumor promoting-activity in N-nitrosodiethylamine (DENA)-initiated rats, but neither initiating activity when promoted by 0.05% PB diet for 64 weeks, nor progressing activity when the oxidative stress was given for 33 weeks to preneoplastic nodule-bearing rats which was induced by DENA.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Initiation of hepatocarcinogenesis by endogenously formed N-nitrosobis(2-hydroxypropyl)amine, N-nitrosodiethanolamine and N-nitroso-2,6-dimethylmorpholine in rats.

Initiation activities of endogenously formed N-nitrosobis(2-hydroxypropyl)amine (NBHPA), N-nitrosodiethanolamine (NDELA) and N-nitroso-2,6-dimethylmorpholine (NDMM) were investigated in a modified short-term assay for rat hepatocarcinogenesis. Male Wistar rats were fed 1% bis(2-hydroxypropyl)amine, 0.5% diethanolamine or 0.25% 2,6-dimethylmorpholine in the diet plus 0.3% sodium nitrite in the drinking water. Two weeks after starting the experimental regimen they underwent 2/3 partial hepatectomy and were then maintained on the respective diets for a further week. Following a 2 week recovery period on basal diet rats were subjected to a resistant hepatocyte regimen consisting of 0.02% 2-acetylaminofluorene in the diet for 2 weeks and 1 mg carbon tetrachloride/kg body wt by gavage at the midpoint. Initiation activity was assayed by measuring hepatic foci positive for gamma-glutamyltranspeptidase. Numbers of such foci per cm2 were significantly increased in the groups given the secondary amines together with nitrite compared with values for groups given each precursor or nitrite alone. Further, the numbers of lesions were essentially similar to those found in rats given carcinogenic doses of NBHPA, NDELA and NDMM. The results clearly of demonstrate hepatocyte initiation activities of endogenously formed carcinogens, presumably NBHPA, NDELA and NDMM.

Animals↗
PubMed1995

Viability of partial liver graft from living donor in pigs.

For evaluation of the viability of partial liver graft from a living donor, we investigated energy production of mitochondria and radical scavenging enzyme activities in partial and whole liver transplantation in pigs. The values of adenosine triphosphate (ATP) and total adenine nucleotide (TAN) of the partial liver graft were higher than those of the whole liver graft, whereas the hypoxanthine of the partial liver graft was lower than that of the whole liver graft. There was no statistical difference in the radical scavenging enzyme activities between the two groups. The values of respiratory control ratio (RCR) in both groups were above 3.0 and there was no statistical difference. The survival rates of pigs received partial liver and whole liver graft with 2 to 3 hr cold preservation was 71% and 91%, respectively and there was no statistical difference between two groups. These results suggest that viabilities of the partial liver graft from the living donor are satisfactory enough, compared with those of whole liver graft from a cadaver.

Adenine Nucleotides↗
PubMed1995

[Free radical generation in electron transport system of mitochondria after cold preservation in UW solution].

UNLABELLED: In the liver transplantation one of the causes of primary graft nonfunction is likely associated with lipid peroxidation at reperfusion after cold preservation. In this study, we investigated whether free radicals produced in mitochondrial electron transport system would result in lipid peroxidation after cold preservation in UW solution. MATERIALS AND METHODS: Under anesthesia, the liver of male Wistar rat was flushed via the portal vein with cold Ringer lactate, and then placed in 4 degrees C UW solution for 24 hr. After cold preservation, we examined mitochondrial respiratory control ratio (RCR), free radicals (O2-) from mitochondrial electron transport system by MCLA induced chemiluminescence, and lipid peroxidation by chemiluminescence (CL) after reoxygenation. RESULTS: RCR gradually decreased up to 24 hr preservation. O2- generation from mitochondrial electron transport system was not recognized at any length of the time after cold preservation up to 24 hr. At 6 hr, CL values were slightly higher than those of the control, but significantly decreased at 24 hr. CONCLUSION: O2(-)-generated in electron transport system of mitochondria did not increase with cold preservation up to 24 hr, therefore, the radical from mitochondria did not cause a lipid peroxidation at reperfusion injury.

Adenosine↗
PubMed1995

The effects of delta-opioid receptor agonists on synaptic transmission in hamster submandibular ganglion.

The effects of agonists for delta-opioid receptors on synaptic transmission in hamster submandibular ganglion were studied in vitro, using an intracellular recording technique. [Met5]enkephalinamide (17 microM), [D-Ser2¿Leu-enkephalin-Thr (14 microM) and [D-Pen2, D-Pen5]enkephalin (10 microM), delta selective agonists caused reversible depression of the fast EPSP amplitude in 10 of 30 cells tested. The inhibitory actions of [D-Pen2, D-Pen5]enkephalin were antagonized by ICI 174,864, a delta selective antagonist. Naloxon a non-selective antagonist and ICI 174,864 both also potentiated the fast EPSP amplitude in 5 of 11 cells tested.

Animals↗
PubMed1994

Selective 8-hydroxyguanine formation in pancreatic DNA due to a single intravenous administration of 4-hydroxyaminoquinoline 1-oxide in rats.

8-Hydroxyguanine (8-OHG) formation, a possible initiating event, was determined in pancreatic and liver DNA and compared with the genesis of acinar cell and hepatocyte necrosis in male Wistar rats given a single intravenous administration of 4-hydroxyaminoquinoline 1-oxide (4-HAQO). At the non-necrotic but tumorigenic dose of 7.0 mg/kg body weight, 8-OHG was selectively generated in pancreatic DNA, in the absence of acinar cell necrosis, at the 6 and 24 h time points and repaired by the 48 h time point. When rats were exposed to 4-HAQO at a necrotic dose of 14.0 mg/kg body weight, 8-OHG was also selectively formed in pancreatic DNA with the same time-dependence of generation and repair, while acinar cell necrosis became evident at the 24 h time point and progressed thereafter. Whereas no hepatocyte necrosis was detected in any rats, 8-OHG values for liver DNA merely expressed slight increases only at the 24 and 48 h time points in rats given 14.0 mg/kg body weight of 4-HAQO. The present data suggest that formation of oxidative DNA damage, assayed by 8-OHG, in pancreatic DNA is independent from toxicity and may be involved, along with quinoline adducts, in mutational events underlying 4-HAQO-induced rat acinar cell carcinogenesis.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1994

Inhibitory effects of 2-O-octadecylascorbic acid and other vitamin C and E derivatives on the induction of enzyme-altered putative preneoplastic lesions in the livers of rats fed a choline-deficient, L-amino acid-defined diet.

Effects of a lipophilic derivative of vitamin C, 2-O-octadecylascorbic acid (CV-3611), as well as its parent L-ascorbic acid (AscA), DL-alpha-tocopherol (alpha-T) and its hydrophilic derivative, 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox), on the number and size of gamma-glutamyltransferase (GGT)-positive putative preneoplastic lesions were examined and compared with their influences on 8-hydroxyguanine formation in DNA and 2-thiobarbituric acid-reacting substance generation in the livers of rats fed a choline-deficient, L-amino acid-defined (CDAA) diet for 12 weeks. A total of 90 male Fischer 344 rats, 6 weeks old, were divided into 18 groups each consisting of five rats. Group 1 received the CDAA diet alone; Groups 2, 3 and 4 received the CDAA diet containing respectively 0.01, 0.05 and 0.10% CV-3611; Groups 5-7, 8-10 and 11-13 similarly received the CDAA diet containing AscA, alpha-T and Trolox, respectively, at these same low, middle and high concentrations; Group 14 received a choline-supplemented, L-amino acid-defined (CSAA) diet alone; Groups 15-18 were given the CSAA diet containing CV-3611, AscA, alpha-T and Trolox, respectively, all at the 0.10% level. While all four vitamin derivatives exerted inhibitory effects on all four parameters, in each case dose-dependently, CV-3611 demonstrated the most pronounced effects. The present results indicated that lipophilic vitamin C derivatives may be particularly effective chemopreventive agents against CDAA diet-associated, oxidative stress-related hepatocarcinogenesis via its superior antioxidative properties.

Amino Acids↗
PubMed1994

Prevention by acetylsalicylic acid of liver cirrhosis and carcinogenesis as well as generations of 8-hydroxydeoxyguanosine and thiobarbituric acid-reactive substances caused by a choline-deficient, L-amino acid-defined diet in rats.

Effects of acetylsalicylic acid (ASA) (aspirin) on the pathogenesis of fatty liver, cirrhosis and hepatocarcinogenesis caused by a choline-deficient L-amino acid-defined (CDAA) diet were examined in male Fischer 344 rats fed a CDAA diet supplemented with 0, 0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrations of > 0.2% prevented the development of both cirrhosis and preneoplastic and neoplastic nodules, but without any directly associated prevention of fatty changes. ASA also prevented hepatocyte proliferation and the generation of thiobarbituric acid-reactive substances and 8-hydroxydeoxyguanosine caused by feeding the CDAA diet, analyzed, respectively, after 1, 12 and 12 weeks. The results clearly indicate that the anti-inflammatory drug ASA, which is not a lipotropic factor, can prevent the pathogenesis of cirrhosis and hepatocarcinogenesis caused by a CDAA diet, which is possibly partly associated with the prevention of reactive oxygen species production.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Different roles of 8-hydroxyguanine formation and 2-thiobarbituric acid-reacting substance generation in the early phase of liver carcinogenesis induced by a choline-deficient, L-amino acid-defined diet in rats.

The present study was performed to assess the roles of hepatocellular oxidative damage to DNA and constituents other than DNA in rat liver carcinogenesis caused by a choline-deficient, L-amino acid-defined (CDAA) diet by examining the effects of the antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD). The parameters used for cellular oxidative damage were the level of 8-hydroxy-guanine (8-OHGua) for DNA and that of 2-thiobarbituric acid-reacting substance (TBARS) for constituents other than DNA. A total of 40 male Fischer 344 rats, 6 weeks old, were fed the CDAA diet for 12 weeks with or without DPPD (0.05, 0.10 or 0.20%) or butylated hydroxytoluene (BHT, 0.25%). In the livers of the rats, the numbers and sizes of glutathione S-transferase (EC 2.5.1.18) placental form (GSTP)- and/or gamma-glutamyltransferase (GGT, EC 2.3.2.2)-positive lesions and levels of 8-OHGua and TBARS were determined. The GSTP-positive lesions of 0.08 mm2 or larger were all stained positively for GGT as well in cross-sectional area, whereas the smaller lesions were generally negative for GGT. DPPD and BHT reduced the size of the GSTP-positive lesions without affecting their total numbers. At the same time, they reduced TBARS generation without affecting 8-OHGua formation in DNA. The present results indicate that oxidative DNA damage (represented by 8-OHGua formation) and damage to constituents other than DNA (represented by TBARS generation) may play different roles in rat liver carcinogenesis caused by the CDAA diet; the former appears to be involved in the induction of phenotypically altered hepatocyte populations while the latter may be related to the growth of such populations.

Animals↗
PubMed1994

Inhibitory effects of exogenously applied met-enkephalin on submandibular ganglion cells.

In this study, effects of exogenously applied Met-enkephalin on hamster submandibular ganglion cells were investigated using an intracellular recording technique. Met-enkephalin (10 microM) was applied to cells by pressure ejection (2 kg/cm2, 50 msec) from a micropipette. More than 30% of the cells caused a hyperpolarization (amplitude: about 3 mV) accompanied by an increase in potassium conductance. After 30-40 ejections, the Ca2+ spike was shortened by 18.1%, and the nicotinic transmission was depressed. The inhibitory effect on presynaptic terminals was blocked by naloxone (10 microM).

Action Potentials↗
PubMed1993

[Antigen-induced dynamic alterations of endothelin receptors--guinea pig lung tissues].

Endothelins (ETs) are a family of peptides with potent constrictive activity in vascular and treacheal smooth muscle. The lung tissues are abundant in these peptides and their receptors; the peptides are produced by endothelial cells and airway epithelial cells, while its receptor is mainly located on smooth muscle. Therefore, it has been proposed that endothelins act in a paracrine fashion on nearby smooth muscle, thus regulating its tone. However, little is known about its physiological and pathological roles in pulmonary functions. We hypothesized that ET plays an important role in bronchoconstriction elicited by antigen challenge. In order to test this hypothesis, we investigated tracheal contractile activities and ET-receptors by employing an animal model in guinea pigs. Here, we report that guinea pigs who were sensitized followed by multiple challenges with the antigens had alterations of ET receptor(s) with respect to number and affinity.

Animals↗
PubMed1993

[Enkephalinase activity in the guinea pig model of asthma].

Enkephalinase exists in airway epithelial cells, smooth muscle, and submucosa near glands, and cleaves tachykinins to inactive metabolites, thereby reducing there effects. To study the role of enkephalinase in asthmatic response, we measured its activity in guinea pig model of asthma. When compared with the control values, the enkephalinase activity was reduced during in immediate asthmatic response (IAR) and late asthmatic response (LAR). Compared with the control values (100%), each value was 79.7%, 73.4% in the trachea and 74.3%, 55.7% in the lung respectively. Tracheal muscle preparation taken from the control, IAR, and LAR groups were made and mounted in oxygenated modified Krebs-Ringer solution. The response was monitored by isometric transducer. Concentration response curves to NKA with or without phosphoramidon were obtained. The contractile responses of the LAR groups were enhanced in potency and efficiency. Phosphoramidon potentiated the NKA induced contraction of control and the IAR groups but was less potent in enhancing the contractile response in the LAR group, showing less enkephalinase activity in the LAR. These results suggest that the enkephalinase plays an important role in LAR. In LAR, the enkephalinase activity may be inhibited and the responsiveness of the smooth muscle to some bronchoconstrictor, such as tachykinins, may be increased.

Allergens↗
PubMed1992

[Effect of enkephalinase inhibitor on endothelin-1 induced bronchoconstriction in guinea pigs].

Endothelin-1 (ET-1) is one of the most potent bronchoconstrictors in the guinea pig. The mechanism of its metabolism is still unclear. Phosphoramidon is known to be an enkephalinase inhibitor. We studied the effect of phosphoramidon on bronchoconstriction induced by ET-1. In the first in vitro study, a tracheal preparation was mounted in oxygenated Krebs-Ringer solution. The response was monitored by isometric transducer. Dose-response curves to ET-1 with or without phosphoramidon were obtained. Phosphoramidon potentiated ET-1 induced bronchoconstriction significantly. Next, the specific airway conductance (sGaw) was measured in conscious guinea pigs exposed to an aerosol of phosphoramidon or saline, followed by ET-1 aerosol inhalation. The ET-1 dose was increased by successively doubling the concentration. sGaw, after inhalation of phosphoramidon, was significantly reduced when exposed to ET-1. Phosphoramidon also potentiated ET-1 induced bronchoconstriction in vivo. Next, lung parenchymal tissues were prepared and placed in oxygenated Krebs-Ringer solution with or without phosphoramidon. ET-1 was added and incubated, and samples were injected into a high performance liquid chromatography column. Phosphoramidon inhibited an analysis of ET-1. These data suggest that enkephalinase plays a role in the break down of ET-1 in the airway of the guinea pig. Under the condition of decreased enkephalinase, ET-1 would potentiate bronchoconstriction.

Animals↗
PubMed1991

[Endothelin-1 induced relaxation of guinea pig trachea after an anaphylactic reaction].

Endothelin-1 (ET-1), one of the most potent constrictors of airway smooth muscles, is reported to act on such inflammatory cells as mast cells and release several chemical mediators. We observed a transient relaxation response to ET-1 after an anaphylactic constriction of guinea pig tracheal smooth muscle. The guinea pig was actively sensitized with ovalbumin, and the tracheal strip was challenged with ovalbumin in vitro. ET-1 induced a transient relaxation followed by a constriction of the tracheal strip. The potency of the relaxation induced by 10(-9) M of ET-1 was 16.0 +/- 1.3%, compared to the response to isoproterenol (2 x 10(-5) M), and the duration of the relaxation was 7.2 +/- 0.7 minutes. Indomethacin (10(-6) M) had no effect on the response, indicated that prostaglandins have no relation. Mechanical denudation of the tracheal epithelium did not reduce the relaxation, but rather augmented it. These results indicate that ET-1 induces a relaxation, associated with a relaxation factor from non-epithelial tissue.

Anaphylaxis↗
PubMed1991

[A case of human tail].

A human tail is a rare anatomical curiosity. A case of a human tail associated with lipomyelomeningocele is reported. The made subject was born, by breech delivery, at the 39th-week with a 3,008 g body weight. He was admitted to our hospital because of the presence of a human tail and subcutaneous mass in the midline lumbosacral region. The tail was about 7.5 cm in length and 2 cm in diameter. It was elastic and covered by normal skin. No systemic anomaly was found. Spina bifida below L5 was revealed, and no bony shadow was found on the plain X-ray film. CT scan showed a low density area in the spinal canal between L3 and lower sacral region that extended into the tail through the spina bifida. MRI also revealed intraspinal long T2 mass which was attached to the spinal cord and extended into the tail. Myelogram indicated intradural extramedullary mass below the L3 level. Surgical treatment was performed on the 3rd month of life with a diagnosis of a human tail with lipomyelomeningocele. At surgery, the tail was found to consist mainly of lipomatous tissue which extended subcutaneously and entered the spinal canal through the spina bifida. The tail and subcutaneous lipomatous tissue were totally excised. The capsule of subcutaneous lipomatous tissue was followed circumferentially down into the spinal canal, and found to be transformed to arachnoid membrane. Intradural lipomatous tissue was excised piece by piece, leaving only a small remnant attached to the conus medullaris to preserve sacral nerve root function.(ABSTRACT TRUNCATED AT 250 WORDS)

Child, Preschool↗