ملاتونین: آنتی‌اکسیدان محصول خواب با کیفیت

نوع مقاله : مقاله ترویجی

نویسندگان

1 مرکز تحقیقات بیوشیمی و بیوفیزیک، دانشگاه تهران، تهران، ایران

2 آزمایشگاه شیمی پروتئین، بخش زیستشناسی، دانشکده علوم، دانشگاه شیراز، شیراز، ایران.

چکیده

خواب مرحله بسیار مهمی از زندگی است که سم‌زدایی بدن در آن رخ می‌دهد. میزان دقیق خواب مورد نیاز برحسب سن افراد متفاوت است و تعیین میزان زمان مورد نیاز برای هر فرد بستگی به ویژگی‌های فیزیولوژیک بدن آن فرد دارد. به طور کلی خواب خوب به خوابی در حدود ۸ ساعت گفته می‌شود که در بازه زمانی حدود ۹ یا ۱۰ شب تا ۵ صبح اتفاق می‌افتد. دلیل این پدیده آن است که سازوکارهای ترمیمی و فرایندهای تولید هورمون و آنتی‌اکسیدان‌های لازم بدن در این بازه زمانی شروع، پردازش و تکمیل می‌شود. هورمون ملاتونین طی فرایند خواب تولید می‌شود و تحت عنوان هورمون خواب شناخته شده است. ملاتونین ماده آنتی‌اکسیدانی است که تولید آن منوط به داشتن یک خواب خوب و به‌موقع می‌باشد. همچنین در نبود این هورمون افراد با مشکلاتی نظیر تنش، اضطراب، پیری سریع و دیابت مواجه می‌شوند. بی‌خوابی با افزایش عوامل دخیل در بیماری دیابت و عوارض مرتبط با آن نیز همراه است. داشتن خواب آشفته یا خوابی بی‌کیفیت نظیر اختلال در آغاز خواب و یا حفظ پیوستگی آن سبب افزایش خطر اختلال در سطح گلوکز و درنتیجه افزایش احتمال ابتلا به بیماری دیابت نوع-۲ همراه است. بنابراین عادت به خواب سالم (خواب با کیفیت) می‌تواند به پیشگیری از بروز بیماری‌های مختلف کمک نماید. بهبود سلامت جامعه نیازمند آگاهی افراد از روش‌های اصلاح برنامه خواب و تنظیم ساعت بیولوژیک بدن می‌باشد.

کلیدواژه‌ها


عنوان مقاله [English]

Melatonin: Antioxidant is a quality sleep product

نویسندگان [English]

  • Ali Akbar Moosavi-Movahedi 1
  • Reza Yousefi 2
  • Marjan Soleimanpour 1
1 Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran.
2 Protein Chemistry Laboratory, Faculty of Biology, University of Shiraz, Shiraz, Iran.
چکیده [English]

Sleep is a very important phase of life that the detoxification of the body occurs in this phase. The exact quantity of sleep required varies according to the age of the individual, and determining the amount of time needed per person depends on the physiological characteristics of the individual's body. In general, good sleep is for sleeping at about 8 hours, which occurs at about 9 or 10 in the evening until 5 in the morning. The reason for this phenomenon is that the recovery mechanisms and the processes for producing the necessary hormones and antioxidants are initiated, processed and completed at this interval. The melatonin hormone is produced during the sleep process and is known as the sleep hormone. Melatonin is an antioxidant that produces it in a good, timely manner. Also, in the absence of this hormone, people will endure problems such as stress, anxiety, rapid aging and diabetes. Insomnia is associated with an increase in the incidence of diabetes and its complications. Having distress sleep or poor quality sleep, such as confusion at the beginning of sleep or maintaining its association, increases the risk of impaired glucose levels and, as a consequence, increases the risk of developing diabetes type-2. Therefore, getting used to healthy sleep (quality sleep) can help to prevent various diseases. Improving the health of the community requires people to know how to modify the sleep program and adjust the body's biological clock.

کلیدواژه‌ها [English]

  • sleep quality
  • Melatonin
  • Sleep hormone
  • Biological clock
  • Insomnia
  • Stress
  • Aging
  • Diabetes
[1]. میترا پیرحقی، محمد فرهادی، علی اکبر موسوی موحدی (1395)،" سبک زندگی و پزشکی خواب" نشریه نشا علم، مجلد6، شماره2 صفحات 103-113.
[2]. Smith, H.R., Comella, C.L., Hogl, B. (2008). Sleep medicine, First edition, Cambridge University Press, New York, PP.1-237.
[3]. Akerstedt T., Hume K., Minors D., Waterhouse J. (1994). The Meaning of Good Sleep, Journal of Sleep Research Volume.3 (3), PP. 152-158
[4]. Akerstedt T., Hume K., Minors D., Waterhouse J. (1997). Good sleep - Its Timing and Physiological Sleep Characteristics, Journal of Sleep Research, Volume. 6(4), PP. 221-229
[5]. Lavie, P. (2001). Sleep-Wake as a Biological Rhythm, Annual Review of Psychology, Volume.52, PP. 277-303
[6]. Reiter R.J., Tan D.X., Fuentes-Broto L., Martini, L. (2010). Melatonin: A Multitasking Molecule Neuroendocrinology: The Normal Neuroendocrine System Book Series: Progress in Brain Research, Volume.181, PP127-151
[7]. Hardeland, R. (2013). Reduced Melatonin levels in Aging and Disease, European Journal of Clinical Investigation, Volume.43, PP.58-58
[8]. West, K. E., Jablonski, M. R., Warfield, B., Cecil K.S., James M., Ayers M.A., Maida J., Bowen C., Sliney D.H., Rollag M.D., Hanifin J.P., Brainard G.C. (2011). Blue Light from Light-Emitting Diodes Elicits a Dose-Dependent Suppression of Melatonin in Humans, Journal of Applied Physiology, Volume.110(3), PP. 619-626
[9]. Reiter, R.J. (1993), The Melatonin Rhythm – Both a Clock and a Calendar Experientia, Volume.49(8), PP. 654-664
[10]. Reiter, RJ. (1995). The Pineal-Gland and Melatonin in Relation to Aging, Experimenta Gerontology, Volume.30(3-4), PP. 199-212
[11]. Touitou, Y. ( 2001). Human Aging and Melatonin, Experimental Gerontology, Volume.36(7), PP. 1083-1100
[12]. Rodriguez, C., Mayo, J.C., Sainz, R.M. (2004). Regulation of Antioxidant Enzymes: A Significant Role for Melatonin, Journal of Pineal Research, Volume. 36(1), PP.1-9
[13]. Reiter, R.J. (1998). Oxidative Damage in the Central Nervous System: Protection by Melatonin, Progress Neurobiology, Volume. 56(3), PP.359-384
[14]. Pappolla, M.A., Chyan, Y.J., Poeggeler, B. (2000). An Assessment of the Antioxidant and The Antiamyloidogenic Properties of Melatonin: Implications for Alzheimer's Disease,
Journal of Neural Transmission, Volume. 107(2), PP. 203-231
[15]. da Cunha, P., Alziana, M., Weinlich, R., Mognol, G. (2010), Melatonin Protects CD4(+) T Cells from Activation-Induced Cell Death by Blocking NFAT-Mediated CD95 Ligand Upregulation, Journal of Immunology, Volume.184(7), PP.3487-3494
[16]. Claustrat, B., Chazot, G., Brun, J., Jordan, D., Sassolas, G. (1984), A Chronobiological Study of Melatonin and Cortisol Secretion in Depressed Subjects, Biological Psychiatry, Volume.19(8), PP. 1215-1228
[17]. Srinivasan, V., Smits, M., Spence, P. ( 2006). Melatonin in Mood Disorders, World Journal of Biological Psychiatry, Volume7(3), PP.138-151
[18]. Bellipanni, G., Bianchi, P., Pierpaoli, W. (2001), Effects of Melatonin in Perimenopausal and Menopausal Women, Experimental Geronology, Volume.36(2), PP.297-310
[19]. Tan, D. X., Manchester, L. C., Fuentes-Broto, L. (2011). Application of Melatonin in the Regulation of Brown Adipose Tissue Metabolism: Relation to Human Obesity, Obesity Reviews, Volume. 12(3), PP.167-188
[20]. Ciaran, J., McMullan, M.D., Schernhammer, M.D. (2016).Melatonin Secretion and the Incidence of Type 2 Diabetes, Journal of The American Medical Association, Volume.309(13), PP.1388-1396
[21]. Carlson L.E., Speca, M., Patel, K.D., Goodey, E. (2004).Mindfulness-Based Stress Reduction in Relation to Quality of Life, Symptoms of Stress and Levels of Cortisol and Melatonin in Breast and Prostate Cancer, Psychoneuroendocrinology, Volume.29(4), PP.448-474
[22]. Stevens, R.G. (2005).Circadian Disruption and Breast Cancer from Melatonin to Clock Genes, Epidemiology, Volume. 16(2), PP.254-258
[23]. Schernhammer, E.S., Laden, F., Speizer, F.E., Willett, W.C., Hunter, D.J., Kawachi, I., Colditz, G.A. (2001). Rotating Night Shifts and Risk of Breast Cancer in Women Participating in the Nurses' Health Study, Journal of the National Cancer Institute, Volume. 93(20), PP.1563–1568
[24]. Costa, G., Haus, E., Stevens, R. (2010). Shift Work and Canser, Deutsches Ärzteblatt International, Volume. 108(38), PP.657-662
[25]. Haim, A. (2015). Artificial Light at Night: Melatonin As a Mediator Between the Environment and Epigenome, Philosophical Transactions B, Volume. 370(1667) 20140121
[26]. Krauchi, K. (1997). A Relationship between Heat Loss and Sleepiness,
Journal of Applied Physiology, Volume. 83(1), PP.134-139
[27]. Alberti, A., Mazzotta, G., Gallinella, E. (2005).Headache Characteristics in Obstructive Sleep Apnea Syndrome and Insomnia, ACTA Neurological Scandinavica, Volume.111(5), PP.309-316
[28]. Backhaus, J., Junghanns, K., Born, J. (2006).Impaired Declarative Memory Consolidation During Sleep in Patients with Primary Insomnia, Biological Psychiatry, Volume.60(12) PP.1324-1330
[29]. Horvath, T.L., Gao, X.B. (2005) Input organization and plasticity of hypocretin neurons: Possible clues to obesity's association with insomnia, Cell Metabolism Volume1(4), PP279-286
[30]. Schwartz, S., Anderson, W.M., Cole, S.R. (1999). Insomnia and Heart Disease, Journal of Psychosomatic Research, Volume. 47(4), PP.313-333
[31]. Van der Heijden, K.B., Smits, M.G., Van Someren, E.J.W. (2005).Idiopathic Chronic Sleep Onset Insomnia in Attention-Deficit/Hyperactivity Disorder: A Circadian Rhythm Sleep Disorder, Chronobiology International, Volume.22(3), PP.559-570
[32]. Ananthakrishnan, A. N., Long, M. D., Martin, C. F. (2013). Sleep Disturbance and Risk of Active Disease in Patients with Crohn's Disease, Clinical Gastroenterology and Hepatology, Volume. 11(8), PP.965-971
[33]. Vgontzas, A.N., Liao, D., Pejovic, S., Calhoun, S., Karataraki, M., Bixler, E.O. (2009). Insomnia with Objective Short Sleep Duration Is Associated with Type 2 Diabetes,
Diabetes Care, Volume. 32(11), PP. 1980-1985
[34]. Dauvilliers, M. (2007). Insomnia in Patients with Neurodegenerative Conditions, Sleep Medicine, Volume.8, PP.27-S34
[35]. Iwase, T., Kajimura, N. ( 2002) .Mutation Screening of the Human Clock Gene in Circadian Rhythm Sleep Disorders, Psychiatry Research, Volume.109(2),. PP.121-128
[36]. Baglioni, C., Battagliese, G., Feige, B., Spiegelhalder ,K., Nissen, C., Voderholzer, U., Lombardo, C., Riemann, D. (2011), Insomnia As a Predictor of Depression, Journal of Affective Disorders, Volume.135(1-3), PP.10-12
[37]. Allada, R., White, N.E., So, W.V., Hall, J.C., Rosbash, M. (1998). A mutant Drosophila Homolog of Mammalian Clock Disrupts Circadian Rhythms and Transcription of Period and Timeless. Cell, Volume. 93, PP.805–814.
[38]. Marie, E. Dembinska, R., Jeffrey, C. , Hall, J., Rosbash, M.(1997). Circadian Cycling of a Period-LacZ Fusion Protein in Drosophila: Evidence for an Instability Cycling Element in PER. J. Biol. Rhythms N.12, PP.157-172
[39]. Hall, J.C., Maki, K., Rosbash, M. (1998). a Drosophila Clock and Light-Regulated Cryptochrome, is a Major Contributor to Circadian Rhythmresetting and Photosensitivity. Cell, Volume. 95, PP.669–679.
[40]. Frisch, B., Hardin, P.E., Hamblen-Coyle, M.J., Rosbash, M., Hall, J.C. (1994). A Promoterless Period Gene Mediates Behavioral Rhythmicity and Cyclical Per Expression in a Restricted Subset of the Drosophila Nervous System. Neuron, Volume.12, PP.555–570.
[41]. Hege, D, Stanewsky.R., Hall, J.C. (1997). Rhythmic Expression of a PER-Reporter in the Malpighian Tubules of Interdecapitated Drosophila: Evidence for a Brain Independent Circadian Clock. J. Biol. Rhythms, Volume 12, PP.300–308.
[42]. Saez, L., Young, M.W. (1996). Regulation of Nuclear Entry of the Drosophila Clock Proteins Period and Timeless. Neuron,Volume 17, PP.911–920.
[43]. Price, J.L., Blau, J., Rothenfluh, A., Abodeely, M., Kloss, B., Young, M.W. (1998). Double-Time is a New Drosophila Clock Gene that Regulates PERIOD Protein Accumulation. Cell, Volume 94, PP. 83–95.
[44]. Myers, M.P., Wager-Smith, K., Rothenfluh-Hilfiker, A., Young, M.W. (1996). Light-induced Degradation of TIMELESS and Entrainment of the Drosophila Circadian Clock, Science, Volume. 271, PP.1736–1740.