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Biomedical subjects

H Katayama

Publications and source records attributed to H Katayama.

At least 289 records · Page 16Linked to original sources
PubMed1986

Sarcoplasmic reticulum Ca-ATPase: distinction of phosphoenzymes formed from MgATP and CaATP as substrates and interconversion of the phosphoenzymes by Mg2+ and Ca2+.

In order to characterize the phosphoenzymes (EPs) formed from MgATP and CaATP as substrates, the effects of Mg2+ and Ca2+ outside SR vesicles on the hydrolysis rates of EPs were examined by using purified and unpurified Ca-ATPases of sarcoplasmic reticulum (SR) at low [gamma-32P]ATP (4-10 microM), 0.1 M KCl, pH 7.0, and 0 degrees C. When the phosphorylation reaction was stopped by adding an excess of EDTA over Ca and Mg, two components of EP, EPfast (rate constant, kfast = 15-20 min-1), and EPslow (kslow = 0.3-0.4 min-1), were recognized in the time course of EP decomposition. These two rates did not depend on the Ca2+ or Mg2+ concentration in the medium during the phosphorylation reaction, although the proportions of EPfast and EPslow essentially depended on the concentrations of MgATP and CaATP in the phosphorylation reaction medium. The proportion of EPfast increased with increasing [MgATP]/[CaATP] in the medium, whereas that of EPslow decreased. The rate of EPslow hydrolysis in the presence of excess EDTA was basically the same as that of EP formed from CaATP. These results suggest that EPfast and EPslow are derived from MgATP and CaATP, respectively, and EPfast is a reaction intermediate with Mg bound at the substrate site (MgEP), while the main EPslow is a reaction intermediate with Ca bound at the substrate site (CaEP) which is readily converted to metal-free EP by EDTA addition (Shigekawa et al., (1983) J. Biol. Chem. 258, 8698-8707). Mg2+ added outside SR vesicles stimulated the conversion of CaEP to MgEP and inhibited the hydrolysis of MgEP in the relatively high concentration range (K(Mg) = 7.9 mM). Ca2+ added outside SR vesicles stimulated the conversion of MgEP to CaEP and inhibited the conversion of CaEP to MgEP by Mg2+ addition. The Ca2+ outside SR vesicles did not essentially affect the hydrolysis of MgEP. These results suggest that the interconversion between MgEP and CaEP takes place during the reaction by exchange of the divalent cation on the substrate site. The following scheme is proposed. (formula: see text)

Adenosine Triphosphate↗
PubMed1986

A cell-spreading inhibitor exists in serum and in epidermal basal cells.

A unique monoclonal antibody was obtained by immunizing mice with complement-inactivated fetal bovine serum (FBS). This antibody, named SI-1, stained epidermal basal cells of humans, pig, guinea pig, and rat by an indirect immunofluorescence technique after pretreatment of cryostat sections with alkali buffer (pH 9.6). After dissociating pig epidermal cells by trypsin, the SI-1 antibody stained exclusively and strongly one type of uniquely shaped cells. They were small and hanging-bell or columnar in shape with one convoluted side on the base, consisting of less than 2.8% of the dissociated epidermal cell population. The antigen contained in FBS was partially purified by affinity chromatography using the SI-1 antibody. The affinity-purified antigen inhibited the spreading of PAM cells, a spontaneously transformed murine keratinocyte line, in serum-free medium in a dose-dependent manner at concentrations of 10(-5) to 10 ng/ml. The antigen also inhibited the spreading of trypsinized pig epidermal cells in the range of 10(-2) to 10(3) ng/ml in the presence of 0.05% FBS. Although there have been a few reports indicating that serum inhibited both spreading and attachment, a specific factor in serum has not been purified before. This is, to our knowledge, the first presentation of a cell-spreading inhibitor contained in serum.

Animals↗
PubMed1986

Monoclonal antibodies against epidermal cell surface and dermal-epidermal junction: antigens which may be epidermal cell spreading factors.

Two monoclonal antibodies which reacted with the epidermal cell surface (SF-1) and the dermal-epidermal-junction (SF-2), respectively, were obtained by immunizing mice with partially-purified human epibolin. The corresponding antigens were partially purified from fetal bovine serum by affinity chromatography using these antibodies. SDS-polyacrylamide gel electrophoresis showed that these antigens contained polypeptide components with molecular weights different from that of epibolin (mol. wt. 65,000 daltons); SF-1 antigen had a 68,000 dalton main component, and SF-2 antigen a broad 58,000-61,000 dalton main component. Both of these partially-purified antigens promoted the spreading of dissociated pig epidermal cells. SF-2 antigen also promoted the spreading of Pam cells (a murine keratinocyte line). The results suggest that proteins capable of promoting epidermal cell spreading may be present on the epidermal cell surface and at the dermal-epidermal junction. However, their physiological role in keratinization remains to be elucidated.

Animals↗
PubMed1986

[Effects of chromium compounds on the respiratory system. Part 4. Long-term inhalation of chromic acid mist in electroplating to ICR female mice].

In order to determine the effect on the respiratory system of long-term inhalation of chromic acid in electroplating, histopathological examination was performed on mice (ICR, female, n = 50) exposed to chromic acid mist for 12 months (30 min/d, 2 d/wk), by using the authors' miniaturized chromium electroplating system. After 12 months' exposure, the mice were kept for 6 months without exposure. In the upper respiratory tract, round perforations were found in the nasal septum in 6 mice that were sacrificed or died after 10 months' exposure. The perforations were located near the point of the septum, the thinnest part of the nasal septum, and were of pin-hole sige. On the epithelium of the trachea and bronchus, loss of cilia, proliferation of goblet cells or basal cells, and squamous metaplasia were observed in almost all of the exposed mice. These changes appeared to be more advanced in mice exposed for a longer period. In the lung, development of benign adenoma was observed in one mouse in the 6- to 9-months' exposure group, in three in the 10- to 14-months' exposure group and in one in the group examined after 15 to 18 months. Furthermore, adenocarcinomas were found in two mice, one of which died at 17 months and the other was sacrificed 18 months after initiation of exposure. In conclusion, the finding that adenomas and adenocarcinomas were observed in mice exposed to chromic acid mist suggests the need to give careful attention to the possibility of respiratory cancers in chromium electroplating workers.

Adenocarcinoma↗
PubMed1986

Effects of chronic inhalation exposure to diesel exhaust on the development of lung tumors in di-isopropanol-nitrosamine-treated F344 rats and newborn C57BL and ICR mice.

Long-term exposure to diesel exhaust from a small diesel engine was carried out in order to elucidate the effects of exhaust on the development of lung tumors in F344 rats and newborn ICR and C57BL mice. The deposition of inhaled particles progressed in accordance with duration of exposure in both sets of the animals. No evidence of lung tumor formation was detected following exposure to diesel exhaust alone in rats. However, the combined treatment with DIPN and diesel exhaust led to an overadditive effect in the development of lung tumors. There was a tendency for the diesel-exposed mice to have higher incidences of lung tumors compared with non-exposed mice. The results obtained in the present study suggest that diesel exhaust may act as a factor relating to human respiratory carcinogenesis.

Adenocarcinoma↗
PubMed1986

Carcinogenic effects of a mixture of nitropyrenes in F344 rats following its repeated oral administrations.

The carcinogenic effects of a mixture of 1-nitropyrene and three dinitropyrenes (1,3-, 1,6- and 1,8-dinitropyrene) were investigated in rats. Female F344/Jcl rats were given one of three doses (5, 10 and 20 mg/kg body weight) of the mixture by repeated intragastric instillations twice a week for 55 weeks, and then autopsied 49 weeks later. Mammary adenocarcinomas were induced in rats of all the three experimental groups dose-dependently, while no adenocarcinoma was induced in the control rats which were given only vehicle. Clitoral gland tumors, most of which were diagnosed as squamous cell carcinomas, were also commonly observed in the NP-treated rats in a dose-dependent way. In addition, high incidences of mononuclear cell leukemias were noted in the NP-treated rats. Other tumors were frequently induced in the uterus and endocrine organs, such as the pituitary, adrenal, and thyroid glands. However, the incidences of these tumors were almost equal in both the control and NP-treated groups. The results of the present study indicated the potential carcinogenic activities of nitropyrene compounds in female rats when they were treated by oral route, and suggest that the oral intake of nitropyrene compounds might be related to the incidence of cancer in humans.

Administration, Oral↗
PubMed1985

Reduced hepatic uptake of propranolol in rats with acute renal failure.

The effect of acute renal failure (ARF) on the hepatic uptake and metabolism of propranolol was investigated in relation to the hepatic clearance of the drug. ARF was induced by the subcutaneous injection of uranyl nitrate to rats. The uptake rate of propranolol in the isolated perfused liver was determined by the multiple-indicator dilution method and was found to decrease from 43.6 +/- 2.0 min-1 (mean +/- S.E.) in control to 29.4 +/- 1.7 min-1 in ARF (P less than 0.001). The recovery fraction of propranolol in effluent venous blood increased about twofold in ARF compared to control (P less than 0.05). The metabolic activity for propranolol was examined using the hepatic microsomal fraction prepared from control and ARF rats. There was no significant difference in the kinetics of oxidative metabolism of propranolol between two groups. These results suggest that the previously reported decrease in the hepatic clearance of propranolol in ARF is due to decreased hepatic uptake of the drug from the blood into the liver cells.

Acute Kidney Injury↗
PubMed1985

Subtypes of beta adrenergic receptors mediating pigment dispersion in chromatophores of the medaka, Oryzias latipes.

Actions of the adrenergic beta-2 agonists, salbutamol and terbutaline, and the beta-1 antagonists, metoprolol and atenolol, were examined on denervated melanophores and leucophores of a teleost, Oryzias latipes. Beta-2 agonists depressed the pigment-aggregation response of melanophores to norepinephrine, while beta-1 antagonists inhibited the dispersion response of leucophores to isoproterenol but not the melanophore response. These findings suggest that adrenergic receptors mediating pigment dispersion in melanophores are beta-2 and those of leucophores are beta-1. The possible relations between receptor mechanisms and the responses of chromatophores are discussed.

Albuterol↗
PubMed1985

Familial occurrence of oligomeganephronia.

Oligomeganephronia (OMN) is a rare, renal hypoplasia, consisting of a reduced number of hypertrophied nephrons. This disorder has been considered to be a congenital but not a genetic disease. We describe the first report, to the best of our knowledge, of familial cases of OMN; two male siblings ran rapidly downhill courses and died 11 and 8 days after birth, respectively. In addition, the two patients had similar multiple anomalies; microcephaly, prominent glabella, hypertelorism, antimongoloid slant, epicanthal folds, broad nose, cleft lip and palate, down-turned mouth, short philtrum, micrognathia, low set ears, hypospadias, and cryptorchism. Although the patients and the parents had normal G-banded karyotypes, 4p monosomy syndrome is suggested from clinical features. The implications of this are discussed briefly.

Abnormalities, Multiple↗
PubMed1985

Influence of acute renal failure on pharmacokinetics of phenolsulfonphthalein in rats: a comparative study in vivo and in the simultaneous perfusion system of liver and kidney.

The effect of acute renal failure (ARF) on the disposition of phenolsulfonphthalein (PSP) after intravenous administration was investigated in rats. ARF was induced by the subcutaneous injection of uranyl nitrate to rats. Renal excretion of PSP decreased significantly in ARF compared to that in normal controls. On the other hand, rats with ARF showed an increased biliary excretion of PSP to compensate for reduced renal excretion of the drug. Consequently no significant change was found in total body clearance of PSP between control and ARF. The in vitro binding experiment showed that the binding fraction of PSP to ARF plasma was significantly lower than that to control plasma. In order to clarify the regulatory mechanisms of PSP excretion between liver and kidney in ARF, we developed a simultaneous perfusion system of rat liver and kidney, which could control the flow rate and the constituent of the perfusate. In this perfusion system, neither biliary excretion nor the protein binding of PSP differed significantly between control and ARF, though its renal excretion decreased in ARF in a similar manner as in vivo. These results suggest that alterations in plasma protein binding as well as renal excretory function are determinants of PSP disposition in ARF.

Acute Kidney Injury↗
PubMed1985

Effect of altered plasma protein binding on pharmacokinetics and pharmacodynamics of propranolol in rats after surgery: role of alpha-1-acid glycoprotein.

The pharmacokinetics and pharmacodynamics of propranolol in rats 2 days after laparotomy were compared to control animals. The apparent volumes of distribution and the systemic clearance of propranolol were decreased to about 20 to 40 and 70% of control values, respectively. The area under the blood concentration-time curve (AUC) of propranolol after p.o. administration showed a marked elevation after surgery and its availability increased about 2-fold at doses of 5.0 and 12.5 mg/kg. These changes were associated with a decreased plasma unbound fraction of propranolol after surgery. Immunological determination of alpha-1-acid glycoprotein (AGP) revealed a marked increase after laparotomy and a linear relationship was found between the plasma AGP concentration and the binding capacity of high-affinity binding site for propranolol in plasma (r = 0.961, P less than .001). AUC of p.o. administered propranolol was also correlated with plasma AGP concentration. The beta-blocking activity of propranolol assessed by the reduction in the isoproterenol-induced tachycardia was decreased in rats after laparotomy when it was evaluated in terms of the total plasma concentration of propranolol. In contrast, its activity evaluated by the unbound plasma concentration showed no difference between control and laparotomized rats, suggesting the dependence of the pharmacological activity of propranolol on its unbound level in plasma. Thus, laparotomy-induced changes in both pharmacokinetics and pharmacodynamics could be considered largely due to an increase in its binding to the increased plasma level of AGP.

Animals↗