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Biomedical subjects

K Kamijo

Publications and source records attributed to K Kamijo.

At least 73 records · Page 4Linked to original sources
PubMed1986

Effect of acrylonitrile on the rat pituitary: enlargement of Golgi region in prolactin cells, crinophagy in prolactin cells and growth hormone cells.

Since it has been shown that acrylonitrile prevents the appearance of spontaneous pituitary adenomas, we have investigated its effect in acute experiments on rat pituitaries by histology, immunocytochemistry, electron microscopy and morphometry; in addition, serum prolactin and growth hormone levels were measured by radioimmunoassay. Electron microscopy of prolactin cells revealed hypertrophy of the Golgi region without significant change in volume densities and diameters of forming and storage granules. In the 24 h group, crinophagy was observed in prolactin cells and growth hormone cells. Corticotrophs, thyrotrophs and gonadotrophs were unaltered. Dilation, congestion and rupture of capillaries, as well as pericapillary and intercellular oedema were evident in the 24 h group. One hour after intravenous acrylonitrile injection, serum prolactin levels were within the normal range, whereas at 24 h, hyperprolactinemia was noted. Serum growth hormone concentrations were unchanged. It can be concluded that acrylonitrile has a complex effect on prolactin cells. Hypertrophy of Golgi complex and hyperprolactinemia may reflect increased prolactin synthesis and release. Since volume densities and diameters of secretory granules in prolactin cells remained unchanged, it appears that newly synthesized prolactin was preferentially released and not the prolactin stored in secretory granules. Crinophagy may be the morphological manifestation of a discrepancy between hormone synthesis and release suggesting increased degradation of unused hormone by lysosomes.

Acrylonitrile↗
PubMed1985

Molecular cloning and nucleotide sequence of the cDNA for rat peroxisomal enoyl-CoA: hydratase-3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme.

For the studies on the mechanism of induction of peroxisomal beta-oxidation enzymes and biogenesis of the organelle, we have isolated cDNA clones for rat peroxisomal enoyl-CoA: hydratase-3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme. On blotting experiments with liver RNA, the cDNAs hybridized to a 3.0-kilobase RNA which was increased 5-7-fold by the administration of di-(2-ethylhexyl)phthalate to rats. Nucleotide sequencing was carried out for four cloned cDNAs and one obtained by a primer extension method. By overlapping these sequences with each other, we identified 20 nucleotides of 5'-noncoding, 2,166 nucleotides of coding, and 910 nucleotides of 3'-noncoding regions. The deduced amino acid sequence of the enzyme is composed of 722 residues, and the composition agrees with that of the protein data. The sequence was confirmed by the amino acid compositions and sequence analyses of some of the tryptic peptides. The molecular weight of the mature enzyme is calculated to be 78,511 from the predicted amino acid sequence. The enzyme has no terminal peptide extension as a signal for translocation into peroxisomes.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1985

Membrane lipid environment of carp brain and liver mitochondrial monoamine oxidase.

Delipidation of carp liver mitochondria by treatment with methyl ethyl ketone (MEK) or Triton X-100 and then perchlorate greatly reduced MAO activities. Treatment with only Triton X-100 resulted in less reduction in activity. The Km values of the remaining activities were similar regardless of these treatments. The sensitivities towards clorgyline and l-deprenyl of the remaining activity in the Triton X-100-treated residue and the phospholipase C-treated carp brain mitochondria were found to be unchanged, but those of the activity remaining in the MEK-treated residue were similarly decreased. No evidence was obtained suggesting conversion of carp MAO to either MAO-A or MAO-B by the modification of the mitochondrial lipid environment by the treatments employed.

Animals↗
PubMed1984

Carboxyphenyl chloroanthranilic acid (CCA) in the modulation of immune response in mice.

A study to elucidate the immunopharmacological mechanisms of carboxyphenyl chloroanthranilic acid (CCA) was carried out, employing as a parameter the rosette formation of mouse spleen and thymus cells with red blood cells of sheep. The immunopharmacological properties of CCA and levamisole (LMS) were compared. In C57BL/6 mice, the immune response was either suppressed or enhanced by LMS, whereas CCA caused a suppression of rosette formation. Both drugs enhanced response in adult thymectomized C57BL/6 mice. LMS induced Thy-1 positive rosette-forming cells after adult thymectomy in C57BL/6 mice, whereas CCA did not. CCA was significantly effective in restoring the impaired immune response in C57BL/6 mice pretreated with immunosuppressants. The effect of LMS or CCA on the immune response varied among six different mouse strains (C57BL/6, BALB/c, C3H/He, DBA/2, (NZB X NZW) F1 and BXSB). The results suggest that both drugs have immunomodulation or immunonormalization properties.

Animals↗
PubMed1983

A new type of mitochondrial monoamine oxidase distinct from type-A and type-B.

The characteristics of mitochondrial monoamine oxidase (MAO) in carp liver were studied with MAO inhibitors and substrates. This enzyme was thermolabile, but was stabilized in the presence of bovine serum albumin. With clorgyline and deprenyl, single-sigmoidal curves for inhibition of the activity towards tyramine or 5-hydroxytryptamine were obtained; the sensitivities to the two inhibitors were identical. The activity towards beta-phenylethylamine was not completely inhibited by clorgyline or deprenyl, but the remaining activity was inhibited by semicarbazide and the inhibition curves by either clorgyline or deprenyl and semicarbazide were also identical to the curves with the other two substrates. These results suggest that carp liver mitochondria contain "classical" MAO and a clorgyline- and deprenyl-resistant amine oxidase and that the classical MAO does not seem to be MAO-A or MAO-B, which are present in mitochondria of most mammalian tissues.

Animals↗
PubMed1983

Inhibition of carp liver mitochondrial monoamine oxidase by some commonly-used detergents.

The inhibitory effects of some detergents commonly used in biochemical research on carp liver mitochondrial monoamine oxidase were examined. Sodium dodecylsulfate, octyl-beta-D-glucopyranoside, sodium cholate and Triton X-100 at relatively low concentrations caused strong dose-dependent inhibition of the activity towards tyramine, but digitonin caused only weak inhibition. Sodium dodecylsulfate, octyl-beta-D-glucopyranoside and sodium cholate caused almost complete inhibition of activity in the concentration ranges tested. The extent of inhibition by Triton X-100 was greater after preincubation at 37 degrees C for 30 min than that without preincubation, but with or without preincubation, the inhibition was not substrate-selective and was not complete at a relatively high concentration (2%) of Triton X-100. Without preincubation, the mode of inhibition by Triton X-100 was competitive and reversible with respect to the oxidations of 5-HT, tyramine and PEA, but after preincubation (37 degrees C for 30 min), it became noncompetitive and irreversible, depending on the concentration of detergent used. These findings suggest that it had different actions on the enzyme depending on preincubation. Triton X-100 also slightly changed enzyme sensitivity towards clorgyline and deprenyl, regardless of the preincubation time or the substrate used. Some possible mechanisms of the inhibitory effect of Triton X-100 are discussed.

Animals↗
PubMed1983

Hemodynamics and monoamine oxidase activity in spontaneously hypertensive rats (SHR).

The relationship between the onset of hypertension and changes in monoamine oxidase (MAO) activity in the brains and hearts of spontaneously hypertensive rats (SHR) were studied. After 7-weeks-old, blood pressure of SHR increased rapidly and reached a level of 170 to 180 mmHg; but following 4 weeks of propranolol treatment (10 mg/kg/day), blood pressure decreased significantly compared to that of untreated SHR. Heart/body weights ratio of SHR was higher than that of normotensive Wistar Kyoto rats (WKY). MAO activities in the brain stem, the medulla oblongata and pons of the SHR were significantly higher than those in WKY at 7 weeks of age, and MAO activity in the brain stem of the propranolol-treated SHR was significantly lower than that in the untreated SHR. Propranolol inhibited MAO activity in brain tissue in vitro, and the I50 values of propranolol were identical (1 X 10(-4) M) in SHR and WKY. In both the WKY strain and the SHR, the Vmax values of heart MAO increased with age, and the Vmax values of SHR were twice those of WKY. Km values for tyramine of heart MAO in WKY and SHR were approx. 100 microM and 140 microM, respectively; however, these values were not age-dependent. It was concluded that an increase in MAO activity in SHR brain stem may trigger a reduction in noradrenaline content and that propranolol may be responsible for its restoration, thus reducing peripheral sympathetic activity; moreover, the increase in MAO activity in the hearts of SHR may be of genetic origin.

Animals↗
PubMed1983

Sex difference in the paradoxical response of serum GH to thyrotrophin releasing hormone in cancer patients.

It was demonstrated that thyrotropin-releasing hormone (TRH) elicited a paradoxical increase in basal GH levels in cancer patients. Out of 94 cancer patients, 50 were found to be GH responders and this phenomenon was more frequently recognized in female than in male cancer patients. In cancer patients under 59 years of age, the GH response to TRH was significantly greater in females than in males, although there was no sex difference in the GH response in patients above 60 years of age. In female cancer patients, the GH response to TRH was significantly greater in patients under 59 years of age than in patients above 60 years of age, while there was no age difference in the GH response in male cancer patients. It was concluded that paradoxical responses of serum GH to TRH were recognized in 53 per cent of cancer patients and were more frequently observed in female than in male cancer patients.

Adult↗
PubMed1982

Effects of local anesthetics on monoamine oxidase, and their membrane effects.

The effects of various local anesthetics on rat brain and liver monoamine oxidase (MAO) and their antihemolytic and local anesthetic effects were studied. All local anesthetics tested at 1 x 10(-7) M to 1 x 10(-3) M inhibited MAO activity in rat liver mitochondria with 5-hydroxytryptamine (5-HT) as substrate. The order of potency was tetracaine>procaine>dibucaine>lidocaine>prilocaine. Tetracaine and procaine inhibited 5-HT oxidation much more than beta-phenylethylamine (PEA) oxidation. Dibucaine inhibited PEA oxidation as much as 5-HT oxidation. Inhibition of MAO by local anesthetics other than dibucaine was reversible. Tetracaine and procaine inhibited 5-HT oxidation competitively, whereas dibucaine inhibited it non-competitively. Antihemolytic effects were observed with dibucaine and tetracaine at concentrations of 6 x 10(-5) M and 1 x 10(-4), respectively. The order of surface anesthetic potencies was dibucaine>tetracaine>prilocaine>lidocaine>procaine. These results suggest that the inhibition of MAO activities by local anesthetics depends on both electrostatic and hydrophobic interactions between these drugs and enzyme-associated phospholipids or the hydrophobic regions of proteins.

Anesthetics, Local↗
PubMed1982

Effect of cimetidine on prolactin secretion in normal controls and hyperthyroid patients.

Nine healthy female controls and 10 hyperthyroid female patients were studied. The intravenous administration of 200 mg cimetidine, an H2-receptor antagonist, was followed by a significant and marked rise in serum prolactin levels in all control subjects. There was no significant difference in serum PRL response to cimetidine injection between the euthyroid controls and hyperthyroid patients. But max delta PRL, the change from basal to peak values, is significantly lower in the hyperthyroid patients than in the controls. There was a significant negative correlation between max delta PRL and serum T4 or T3 levels in hyperthyroid patients before and after treatment with MMI or PTU. It appears from our data that cimetidine induced PRL release was blunted in hyperthyroid patients.

Adult↗
PubMed1982

A case with isolated ACTH deficiency accompanying chronic thyroiditis.

An unusual case of isolated ACTH deficiency with coexisting chronic thyroiditis in a 53-year-old man is reported. The patient was admitted with a 2-year history of generalized fatigue, a 13-kg weight loss, muscular weakness, and frequent hypotensive and hypoglycemic attacks. On admission serum thyroxine and triiodothyronine were significantly elevated. Basal TSH concentration was not detected and TSH showed no response to TRH, but one month after replacement therapy with hydrocortisone it was shown that serum T3, T4 and TSH response were all within normal limits. Thyroid antibodies were positive and biopsy of the thyroid gland showed chronic thyroiditis. Arginine and 1-Dopa provoked a subnormal rise in GH with a maximum of 5.6 ng/ml and 5.0, respectively. One month after treatment with hydrocortisone, GH response to 1-Dopa and arginine increased to the normal range. Prolactin response to TRH was normal and FSH response to LHRH was also normal. LH showed an exaggerated response to LHRH, although a normal response was revealed after treatment with hydrocortisone. We also presented a summary of 44 Japanese cases, 23 males (mean age; 46 yrs old) and 21 females (mean age; 48 yrs old), with isolated ACTH deficiency.

Adrenocorticotropic Hormone↗