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Melatonin’s Effect in Febrile Seizures and Epilepsy

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      Abstract

      Objective

      Recognition of risk factors for febrile seizures (FS) and epilepsy is essential.

      Studies regarding the role of melatonin in these convulsive disorders are limited.

      This study determines the relationship between serum melatonin levels and FS and epilepsy in children.

      Materials & Methods

      A population of 111 children with simple FS, complex FS, and epilepsy (37 children per group, respectively) were included as case groups. In addition, 37 febrile children without seizures comprised the control group. Serum melatonin levels were measured and compared between all groups.

      Results

      The serum melatonin levels in the simple, complex FSs, and epilepsy groups were 2, 2.4, and 2 pg/ml, respectively. The serum melatonin level in the control group was 2.1pg/ml.

      Moreover, there were no significant differences observed while comparing the case groups.

      Conclusion

      The present study reveals that there is no association between serum melatonin level and simple or complex FS and epilepsy. It appears that melatonin plays no significant role in these convulsive disorders.

      Related collections

      Most cited references 35

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      Regulation of antioxidant enzymes: a significant role for melatonin.

      Antioxidant enzymes form the first line of defense against free radicals in organisms. Their regulation depends mainly on the oxidant status of the cell, given that oxidants are their principal modulators. However, other factors have been reported to increase antioxidant enzyme activity and/or gene expression. During the last decade, the antioxidant melatonin has been shown to possess genomic actions, regulating the expression of several genes. Melatonin also influences both antioxidant enzyme activity and cellular mRNA levels for these enzymes. In the present report, we review the studies which document the influence of melatonin on the activity and expression of the antioxidative enzymes glutathione peroxidase, superoxide dismutases and catalase both under physiological and under conditions of elevated oxidative stress. We also analyze the possible mechanisms by which melatonin regulates these enzymes.
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        Physiological effects of melatonin: role of melatonin receptors and signal transduction pathways.

        Melatonin, an endogenous signal of darkness, is an important component of the body's internal time-keeping system. As such it regulates major physiological processes including the sleep wake cycle, pubertal development and seasonal adaptation. In addition to its relevant antioxidant activity, melatonin exerts many of its physiological actions by interacting with membrane MT1 and MT2 receptors and intracellular proteins such as quinone reductase 2, calmodulin, calreticulin and tubulin. Here we review the current knowledge about the properties and signaling of melatonin receptors as well as their potential role in health and some diseases. Melatonin MT1 and MT2 receptors are G protein coupled receptors which are expressed in various parts of the CNS (suprachiasmatic nuclei, hippocampus, cerebellar cortex, prefrontal cortex, basal ganglia, substantia nigra, ventral tegmental area, nucleus accumbens and retinal horizontal, amacrine and ganglion cells) and in peripheral organs (blood vessels, mammary gland, gastrointestinal tract, liver, kidney and bladder, ovary, testis, prostate, skin and the immune system). Melatonin receptors mediate a plethora of intracellular effects depending on the cellular milieu. These effects comprise changes in intracellular cyclic nucleotides (cAMP, cGMP) and calcium levels, activation of certain protein kinase C subtypes, intracellular localization of steroid hormone receptors and regulation of G protein signaling proteins. There are circadian variations in melatonin receptors and responses. Alterations in melatonin receptor expression as well as changes in endogenous melatonin production have been shown in circadian rhythm sleep disorders, Alzheimer's and Parkinson's diseases, glaucoma, depressive disorder, breast and prostate cancer, hepatoma and melanoma. This paper reviews the evidence concerning melatonin receptors and signal transduction pathways in various organs. It further considers their relevance to circadian physiology and pathogenesis of certain human diseases, with a focus on the brain, the cardiovascular and immune systems, and cancer.
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          Melatonin receptors in humans: biological role and clinical relevance.

           C Ekmekcioglu (2006)
          In addition to its antioxidative effects melatonin acts through specific nuclear and plasma membrane receptors. To date, two G-protein coupled melatonin membrane receptors, MT(1) and MT(2), have been cloned in mammals, while the newly purified MT(3) protein belongs to the family of quinone reductases. Screening studies have shown that various tissues of rodents express MT(1) and/or MT(2) melatonin receptors. In humans, melatonin receptors were also detected in several organs, including brain and retina, cardiovascular system, liver and gallbladder, intestine, kidney, immune cells, adipocytes, prostate and breast epithelial cells, ovary/granulosa cells, myometrium, and skin. This review summarizes the data published so far about MT(1) and MT(2) receptors in human tissues and human cells. Established and putative functions of melatonin after receptor activation as well as the clinical relevance of these findings will be discussed.
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            Author and article information

            Affiliations
            [1 ]Department of Pediatrics, Qazvin University of Medical Sciences, Qazvin, Iran.
            [2 ]Department of Pediatric Nephrology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
            [3 ]Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran.
            Author notes
            [* ]Corresponding Author: Mahyar A. MD, Department of Pediatrics, Qazvin Children Hospital, Qazvin University of Medical Sciences, Qazvin, Iran, Tel: +98 281 3334807-9, Email: Abolfazl473@yahoo.com
            Journal
            Iran J Child Neurol
            Iran J Child Neurol
            IJCN
            Iranian Journal of Child Neurology
            Shahid Beheshti University of Medical Sciences (Tehran, Iran )
            1735-4668
            2008-0700
            Summer 2014
            : 8
            : 3
            : 24-29
            25143770 4135277 ijcn-8-024

            This is an Open Access article distributed under the terms of the Creative Commons Attribution License, ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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