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  • 1
    Electronic Resource
    Electronic Resource
    Melatonin reduces nitric oxide synthase activity in rat hypothalamus (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of pineal research 20 (1996), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In this report, rat hypothalamic nitric oxide synthase (NOS) activity is shown to be partially inhibited by physiological concentrations of the pineal hormone melatonin. In vitro studies demonstrate that 1 nM melatonin, which approximates the physiological concentration of the hormone at night, significantly inhibited NOS activity. In vivo studies show that administering melatonin or collecting the hypothalamus from animals at night, when endogenous melatonin levels are elevated, results in a significant decrease of NOS activity. Results also show that calmodulin may be involved in this process since its presence in the incubation medium prevents the inhibitory effect of melatonin on NOS activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-079X.1996.tb00260.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    mRNA expression of nuclear receptor RZR/RORα, melatonin membrane receptor MT1, and hydroxindole-O-methyltransferase in different populations of human immune cells (2004)
    Oxford, UK : Munksgaard International Publishers
    Journal of pineal research 37 (2004), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  We characterized the expression levels of the retinoid Z receptor α (RZR α), RORα mRNA isoforms (RORα1, RORα2, and RORα3), and both melatonin receptor MT1 and hydroxindole-O-methyltransferase (HIOMT) genes. For this purpose, the following human peripheral blood mononuclear cells populations were isolated: monocytes (CD14+ cells), B lymphocytes (CD19+ cells), T helper lymphocytes (CD14− CD4+), cytotoxic T lymphocytes (CD56− CD8+ cells), and natural killer (NK) lymphocytes (CD56+ cells). PBMCs subsets were obtained by Dynabeads M-450 (Dynal) isolation procedure. We observed a strong gene expression signal for RZRα in all subpopulations studied, whereas both RORα1 and RORα2 transcripts were amplified only in CD8+ cells. Specific signal for RORα2 was obtained in all subpopulations studied, but we were not able to detect the RORα3 mRNA transcript in human immune cells studied. A weaker signal (especially in CD19+ cells) was also detected in all subsets of cells for the MT1 gene. With regard to HIOMT, a strong signal was achieved among all but one subpopulation of cells; the only exception was CD14+ cells. Thus, in addition to its classical function in the nervous and endocrine system, melatonin could act directly as a paracrine and/or autocrine agent in the human immune system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-079X.2004.00135.x
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  • 3
    Electronic Resource
    Electronic Resource
    Melatonin inhibits telomerase activity in the MCF-7 tumor cell line both in vivo and in vitro (2003)
    Oxford, UK : Munksgaard International Publishers
    Journal of pineal research 35 (2003), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In this study for the first time the relationship between melatonin and telomerase activity was investigated. Melatonin exhibits oncostatic properties, but the actual mechanism of action by which the indole reduces tumor cell activity is not clear. Telomerase is an enzyme responsible of telomere elongation and is activated in most human cancers. In the current in vivo study, eight nude mice received a MCF-7 xenograft and thereafter they were treated for 5 weeks with 0.1 mg/mL of melatonin in the drinking water. Melatonin treatment caused a significant reduction in the weight of tumors and reduced metastases when compared with the control group. As indicated by the Telomerase Repeats Amplification Protocol (TRAP) assay, a significant decrease in telomerase activity was observed in the group treated with melatonin. In related in vitro studies, cultured MCF-7 cells were treated with three different concentrations of melatonin and a control without indole treatment. A significant dose-dependent decrease in Telomerase reverse transcriptase (TERT), the catalytic subunit of telomerase, mRNA expression was observed in the melatonin-treated cells. We also observed a significant reduction in TR, the RNA telomerase subunit, mRNA expression at physiological concentrations of melatonin (1 nm). Significant differences in TEP1, an associated telomerase protein, mRNA expression were also observed. In conclusion, melatonin influences telomerase both in vivo and in vitro, decreasing its activity in the tumors of nude mice and the mRNA expression of the TERT and TR subunits, essential factors for the proper function of the telomerase enzyme.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-079X.2003.00077.x
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  • 4
    Electronic Resource
    Electronic Resource
    Correlation between nuclear melatonin receptor expression and enhanced cytokine production in human lymphocytic and monocytic cell lines (2000)
    Copenhagen : Munksgaard
    Journal of pineal research 29 (2000), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The report shows that melatonin enhances IL-2 and IL-6 production by two human lymphocytic (Jurkat) and monocytic (U937) cell lines via a nuclear receptor-mediated mechanism. Jurkat cells express nuclear (RZRα, RORα1 and RORα2) and membrane (mt1) melatonin receptors, and melatonin binds to Jurkat nuclei and membranes with the same affinity described for human peripheral blood mononuclear cells (PBMCs). Melatonin enhances IL-2 production by Jurkat cells activated by either phytohemagglutinin (PHA) or phorbol myristate acetate (PMA). PHA activation of Jurkat cells does not change the profile of melatonin receptor expression; on the contrary, PMA activation negatively regulates the mt1 receptor. In the absence of the membrane receptor, melatonin still activates IL-2 production. U937 cells express only the mt1 receptor. Although melatonin binds to both U937 nuclei and membranes, CGP 52608, a ligand of the nuclear receptor for melatonin, does not inhibit melatonin binding to U937 nuclei, suggesting that a protein other than the RZR/RORα receptor was involved in the process. In U937 cells, melatonin did not modify basal production of IL-6 or when activated by PMA plus LPS (lipopolysaccharide), a treatment that downregulates the expression of the mt1 receptor. However, in U937 cells activated with IFN-Γ, which induces the expression of the RORα1 and RORα2 nuclear receptors and represses the expression of the mt1 receptor, melatonin can activate IL-6 production. These results show that the expression of nuclear melatonin receptor is sufficient for melatonin to activate cytokine production in human lymphocytic and monocytic cell lines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-079X.2000.290301.x
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  • 5
    Electronic Resource
    Electronic Resource
    Post-traumatic transient cortical blindness (1993)
    Springer
    International ophthalmology 17 (1993), S. 277-283 
    Details
    ISSN: 1573-2630
    Keywords: cortical blindness ; head trauma ; migraine ; vasospasm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Five patients: three children, one adolescent, and one young adult, examined in an emergency room setting were diagnosed with post-traumatic transient cortical blindness. This syndrome is characterized by transient visual loss, normal pupillary response and normal funduscopic examination following minor head trauma. In each case, vision returned to normal within minutes to hours following injury, leaving no neurological sequelae. Headache, confusion, irritability, anxiety, nausea and vomiting were the most common related symptoms. While the mechanism responsible for the transient blindness is unknown, most authors propose an abnormal vascular response to trauma with resultant transient hypoxia and cerebral dysfunction. The similarity between the symptoms accompanying this syndrome and those seen during a classic migraine attack has led many investigators to suggest a common underlying pathophysiology. The purpose of this report is to highlight the salient clinical features and diagnostic approaches to this syndrome, thereby providing ophthalmologists and emergency room physicians a heightened awareness of this entity and the means to detect it.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01007796
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  • 6
    Electronic Resource
    Electronic Resource
    Inhibition of cerebellar nitric oxide synthase and cyclic GMP production by melatonin via complex formation with calmodulin (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 65 (1997), S. 430-442 
    Details
    ISSN: 0730-2312
    Keywords: melatonin ; pineal gland ; cerebellum ; nitric oxide ; nitric oxide synthase ; calmodulin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Constitutive rat cerebellar nitric oxide synthase (NOS) activity is shown to be inhibited by physiological concentrations of the pineal hormone melatonin. The inhibition was dose-dependent and was coupled to an inhibition of the cyclic GMP production activated by L-arginine. Results also show that calmodulin appears to be involved in this process because its presence in the incubation medium was able to prevent the effect of melatonin on both NOS activity and cyclic GMP production. Moreover, polyacrylamide gel electrophoresis studies suggest that melatonin can interact with calmodulin modifying the binding of the peptide to the synthetic NOS peptide encompassing the calmodulin-binding domain of constitutive NOS from rat cerebellum, the natural mechanism by which calmodulin activates cerebellar NOS. J. Cell. Biochem. 65:430-442. © 1997 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
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