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Biomedical subjects

Y Omori

Publications and source records attributed to Y Omori.

At least 181 records · Page 10Linked to original sources
PubMed1986

Purification and characterization of a form of cytochrome P-450 with high specificity for aflatoxin B1 from 3-methylcholanthrene-treated hamster liver.

A form of cytochrome P-450 highly active in inducing mutagenicity of aflatoxin B1 was purified to a specific content of 15.1 nmol/mg of protein from 3-methylcholanthrene-treated hamster liver. This species of cytochrome P-450, having its absorption maximum at 448.5 nm in carbon monoxide-complex of reduced form and low spin ferric ion, is of molecular weight of 56,000 and distinctly different in physicochemical and catalytic properties from major forms of cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rat liver. In the induction of aflatoxin B1 mutagenicity, this hamster cytochrome P-450 is 50 times more potent than those from rat liver.

Aflatoxin B1↗
PubMed1986

Comparisons of the toxicokinetic parameters in rats determined for low and high dose of gamma-chlordane.

Toxicokinetic parameters of gamma-chlordane (GCD) after oral administration of various doses of radio-labelled GCD (50 micrograms/kg-10 mg/kg) were compared. Absorption of GCD were about 80% in both 0.1 and 1.0 mg/kg groups. Distributions of GCD (50 micrograms/kg and 10 mg/kg) into the liver and kidney were rapid and those into adipose tissues were relatively slow. Concentrations of GCD in adipose tissues became highest at 16 hr after administration and became about 10 times more than those in the liver. The initial concentrations of GCD calculated by two-compartment open model in high dose group (10 mg/kg) were about 200-300 times higher than those in low dose group (50 micrograms/kg). Half lives of GCD in low dose group had a tendency to be a little longer than those in high dose group. This difference seemed to be caused by the accumulation of oxychlordane in low dose group.

Adipose Tissue↗
PubMed1985

Relation between hepatic microsomal metabolism of N-nitrosamines and cytochrome P-450 species.

Effects of SKF 525A (0.1 mM), metyrapone (0.1 mM), alpha-naphthoflavone (ANF) (0.5 mM) and pyrazole (1.0 mM) on N-nitrosodimethylamine (NDMA), N-nitrosomethylbutylamine (NMBuA) and N-nitrosomethylbenzylamine (NMBeA) metabolism by hepatic microsomes from rats pretreated with inducers were investigated. NDMA demethylation was weakly increased by phenobarbital (PB) treatment. The demethylation was inhibited by SKF 525A and enhanced by metyrapone in non-treated and PB-treated microsomes, and weakly inhibited by ANF in 3-methylcholanthrene(MC)-treated microsomes. NMBuA demethylation was increased by PB treatment and inhibited by SKF 525A in all microsomes. Metyrapone inhibited the demethylation in PB-treated microsomes. NMBuA debutylation was increased by PB and MC treatments, and inhibited by metyrapone in all microsomes. The strongest inhibition by metyrapone was observed in PB-treated microsomes. The debutylation was inhibited by SKF 525A in non-treated and PB-treated microsomes and by ANF in MC-treated microsomes. NMBeA demethylation was decreased by MC treatment and weakly inhibited by SKF 525A in all microsomes. The effects of the inducers and inhibitors on NMBeA debenzylation were almost the same as those on NMBuA debutylation except that the increasing effect of MC was small. Pyrazole was a relatively selective inhibitor of NDMA demethylation. These results suggest the following: NDMA demethylation is catalyzed by PB-induced cytochrome P-450 species (P450-PB) and MC-induced cytochrome P-450 species (P448-MC). But their specific activity is low and the other cytochrome P-450 species demethylate NDMA. NMBuA demethylation is catalyzed by P450-PB. But the specific activity is not high and the other cytochrome P-450 species also demethylate NMBuA. NMBuA debutylation is catalyzed by P450-PB and P448-MC. Almost all of NMBeA demethylation is catalyzed by cytochrome P-450 species other than P450-PB and P448-MC. NMBeA debenzylation is catalyzed by P450-PB and P448-MC, but the specific activity of P448-MC is not high.

Animals↗
PubMed1985

Gastroduodenal cytomegalovirus infection after renal transplantation. Fiberscopic observations.

Recently we experienced 2 adult post-renal transplantation cases with gastroduodenal cytomegalic inclusion body. In one case, it was possible to carry out close endoscopic observation from onset to resolution a - very rare opportunity. A 39-year-old man developed continuous occult blood in the stool for 1 month after renal transplantation. Multiple erosive lesions from the upper corpus of the stomach to the bulb of the duodenum were revealed by the endoscopic study. A biopsy specimen from the erosion showed the cytomegalic inclusion body. One month later, the erosive lesions had disappeared. The second case is a 40-year-old man who developed tarry stools 5 days after renal transplantation. Multiple erosions partially covered with blood coagula from the upper portion of the gastric corpus to the antrum were revealed by the endoscopic examination. A biopsy specimen from the erosion in the antrum contained the cytomegalic inclusion body.

Adult↗
PubMed1985

Substrate concentration dependency of N-nitrosodimethylamine and N-nitrosomethylbenzylamine metabolism in rat liver.

Metabolism of N-nitrosodimethylamine (NDMA), a hepatocarcinogen, and N-nitrosomethylbenzylamine (NMBeA), an esophageal carcinogen, was comparatively investigated in rat liver. When these nitrosamines (25 micromole/kg) were administered orally to rats, the clearance of NDMA from the serum and liver was faster than that of NMBeA. The metabolic decomposition of NDMA by rat isolated hepatocytes was slower than that of NMBeA at high concentration (0.5 mM). However, at low concentration (6.7 microM) the metabolic decomposition of NDMA was faster than that of NMBeA. The ratio of NDMA demethylation to NMBeA demethylation and debenzylation by hepatic microsomes also changed depending on nitrosamine concentrations (1 microM to 1 mM), and low concentration of NDMA was demethylated rapidly. These results suggest that NDMA is metabolized to a methylating agent more effectively than NMBeA in liver, when carcinogenic doses of nitrosamines are administered.

Animals↗
PubMed1985

[New apparatus for artificial liver support: PAT resin--removal of protein-bound substances and its effect on hepatic failure in animals].

Hemoperfusion using several materials such as activated charcoal is often performed to treat the patients with hepatic failure. Polyamine triglycidylisocyanulate (PAT) resin is a newly developed artificial liver support material to adsorb protein-bound substances. In this study, the effect of PAT resin on the removal of these toxic protein-bound substances was examined and following results were obtained. PAT resin adsorbed protein-bound substances selectively in vitro. Its adsorbability was superior to those of the other conventional adsorbents such as cellulose-coated charcoal, XAD-4 and XAD-7. Serum bilirubin levels were decreased by 44% in jaundiced dogs and 45% in jaundiced rabbits after 120 minutes hemoperfusion with PAT resin. Leucocyte and thrombocyte count also fell during hemoperfusion. The fall of these blood cell counts, however, was recovered by prostaglandin D2. The survival time of dogs with ischemic hepatic failure was prolonged by hemoperfusion using PAT resin. The mean survival times were 17.6 hrs in the PAT perfusion group and 10.9 hrs in the control group. The difference of survival time between these two groups was statistically significant. (p less than 0.05). These results in animals suggest that PAT resin will be clinically useful in the therapy of hepatic failure or hyperbilirubinemia.

Animals↗
PubMed1985

[Characterization of gastric carcinoma viewed from the primary cancer site].

Character of gastric carcinoma is closely related to the location and the primary site. The 679 cases of gastric carcinoma, curatively resected eleven year period, were studied for the relationship between the primary site and the character. The lower portion of the stomach (A) was characterized by large numbers of protruded type of early cancer, localized type of advanced cancer, and intestinal type histologically. The middle portion of the stomach (M) was characterized by large numbers of depressed type of early cancer, infitrative type of advanced cancer, and diffuse type histologically. The cancer of upper portion (C) involving 2 or 3 portions was characterized by large numbers of infitrative type of advanced cancer. In general, the ratio of intestinal type to diffuse type became inverted in the forties, and percentage of intestinal type increased by aging. In the advanced cancer of the upper portion, the invasion of the ratio occurred in the late fifties. Intestinal metaplasia and changing F-line of the gastric mucosa by aging is thought to be background factors of such characterization of gastric carcinoma.

Adenocarcinoma↗
PubMed1984

Nature of N-nitrosodimethylamine demethylase in hepatic microsomes of rats.

The nature of enzymes involved in demethylation of N-nitrosodimethylamine (NDMA) was investigated in hepatic microsomes of rats. Compared to the other cytochrome P-450-dependent enzymes. NDMA demethylase had anomalous properties as reported in the literature. However, kinetic analysis suggested a qualitative change in NDMA demethylase induced by phenobarbital (PB) and 3-methylcholanthrene (MC) pretreatment. The inhibition of demethylase by alpha-naphthoflavone in MC-treated microsomes also suggested that cytochrome P-450 species induced by MC are active in demethylating NDMA. The enhancement of NDMA demethylase activity by metyrapone in PB-treated microsomes was greater than in non-treated ones, and was not observed in MC-treated ones. The result is almost the same as in acetanilide hydroxylation, depending on cytochrome P-450. Pyrazole, tranylcypromine, and aminoacetonitrile, which are selective inhibitors of NDMA demethylation, interacted with cytochrome P-450 species to produce type-II spectra, and typical type-II compounds (aniline, imidazole, and nicotinamide) were inhibitors of the NDMA demethylation. Tranylcypromine irreversibly inhibited microsomal monoamine oxidase [EC 1.4.3.4], but not NDMA demethylase. Semicarbazide (a copper- and pyridoxal-containing amine oxidase [EC 1.4.3.6] inhibitor) had no effect on demethylation. From these results it is concluded that NDMA demethylation depends only on cytochrome P-450-dependent monooxygenases.

Aminoacetonitrile↗
PubMed1984

Comparison of hepatic drug-metabolizing enzymes induced by 3-methylcholanthrene and phenobarbital between pre- and postnatal rats.

Effects of 3-methylcholanthrene (3MC) and phenobarbital (PB) on the hepatic drug-metabolizing enzyme system in fetal liver of rats were investigated. Intraperitoneal administration of 3MC (25 mg/kg, 72 and 48 hr before death) to pregnant rats significantly increased hexobarbital (HB) and aminopyrine (AM)-metabolizing activities in fetuses on the 21st day of gestation to 148.0 and 150.6% of control fetuses, respectively. In contrast, HB and AM-metabolizing activities in 4-day-old neonates and mothers were decreased by administration of 3MC on the 21st day of gestation. Benzo[a]pyrene (BP)-metabolizing activity, NADPH-cytochrome c reductase activity, and cytochrome P-450 content in 3MC-treated fetuses were significantly increased to 2143.6, 137.6, and 323.8% of the control, respectively. Following 3MC administration, the maximum absorption of the cytochrome P-450-CO difference spectra in liver microsomes of fetuses was observed at 449-450 nm. The induction profile following 3MC administration in the fetal livers was different from that in the neonatal and the maternal livers. On the other hand, intraperitoneal administration of PB (60 mg/kg, 72, 48, and 24 hr before death) significantly increased HB, AM, and BP-metabolizing activities in fetal livers to 263.7, 231.0, and 151.2% of the respective controls. The profile induced by PB in the fetal livers was similar to that in maternal livers. These results suggest that HB and AM-metabolizing enzymes in fetal livers treated with 3MC or PB possess the capacity to be induced, and the responsiveness of the drug-metabolizing enzyme system to 3MC during the prenatal stage may differ from the postnatal stage.

Aminopyrine↗
PubMed1984

Insulin resistance in an infant with leprechaunism.

A Japanese female infant with typical features of leprechaunism exhibited glucose intolerance despite marked hyperinsulinemia, indicating insulin resistance. Circulating insulin appeared to be chemically and biologically normal. There was no evidence of antagonism of insulin action or circulating antibodies to insulin or insulin receptors. Insulin receptor assay of her erythrocytes showed very low affinity despite a six-fold increase in the number of receptors as compared with those of normal adult controls. Our studies indicate that insulin resistance in this patient appears to be due to a qualitative abnormality of insulin receptors or to a postreceptor defect.

Abnormalities, Multiple↗
PubMed1984

Renal aminopyrine demethylation in several species determined by a sensitive radiometric method.

Renal microsomal aminopyrine demethylation activities of several species were measured by a sensitive radiometric method using [dimethylamino-14C-]aminopyrine as a substrate and 2,4-dinitrophenylhydrazine as a trapping agent for the formaldehyde formed. The activity was highest in hamsters (0.75 nmol min-1 mg-1 protein) and that in rabbits, rats, mice, and guinea-pigs was 19.7, 7.0, 4.5 and 3.7%, respectively, of the hamster values. These species differences did not correlate with species differences in cytochrome P-450 content or in NADPH cytochrome c reductase activity. Aminopyrine demethylation activities in sliced renal tissues of several species were also compared. This activity was also found highest in hamsters (0.54 nmol min-1 g-1 wet tissue) and the activities in rabbits, rats, and guinea-pigs were 9.2, 1.8 and 2.5%, respectively, of the hamster values.

Aminopyrine↗
PubMed1984

Renal microsomal N-nitrosodimethylamine demethylase determined by a sensitive radiometric method.

Renal microsomal N-nitrosodimethylamine (NDMA) N-demethylation was measured in several species by a sensitive radiometric method using [14C]NDMA as a substrate and 2,4-dinitrophenylhydrazine (DNPH) as a trapping agent of the [14C]formaldehyde formed. The activities were the highest in mice and lowest in hamsters. The activities in rats could not be detected. Among several strains of mice studied the DDY strain was the highest in its activities. Although nicotinamide adenine dinucleotide supported NDMA demethylation by about 32% of nicotinamide adenine dinucleotide phosphate in kidney and only 16% in liver, other properties (pH profiles, km values, and effects of inhibitors) exhibited almost similar results in liver as compared to kidney.

Animals↗