International Journal of Medical Reviews

International Journal of Medical Reviews

Role of Melatonin Supplementation on Inflammatory and Oxidative Stress Markers in Critically Ill Patients

Document Type : Mini Review

Authors
Naseh Pahlavani
Seyedeh Shabnam Mazloumi Kiapey
Safieh Firouzi
Mahsa Malekahmadi
Department of Nutrition, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
10.29252/IJMR-050403
Abstract
Critically ill patients are diagnosed with signs such as oxidative stress, mitochondrial function impairment, dysfunction of the immune system, and acute inflammation. Inflammation and oxidative stress play a major role in the pathogenicity of most diseases in patients, especially those in intensive care units. Because of the side effects of chemical anti-inflammatory drugs, which include large intestinal ulcers, bleeding, and perforation, it seems that the use of natural anti-inflammatory compounds like melatonin could be very helpful. Melatonin productively interacts with different receptive nitrogen and oxygen species (receptor autonomous activities), up-regulates antioxidant chemicals, and down-regulates pro-oxidant chemicals (receptor-dependent activities). Melatonin attenuates molecular and cellular damage resulting from inflammation and oxidative stress. Previous studies have shown that melatonin reduces inflammation and oxidative stress levels. Thus, the use of safe doses of melatonin can reduce inflammation and oxidative stress. However, further studies are needed to verify these results.
Keywords
Inflammation Mediators
Oxidative Stress
Melatonin
Intensive Care Unit
Inpatients
  1. Rankin JA. Biological mediators of acute inflammation. AACN Clin Issues. 2004;15(1):3-17.
  2. Manzanares W, Dhaliwal R, Jiang X, Murch L, Heyland DK. Antioxidant micronutrients in the critically ill: a systematic review and meta-analysis. Crit Care. 2012;16(2):R66. doi:10.1186/cc11316.
  3. Talmor M, Hydo L, Barie PS. Relationship of systemic inflammatory response syndrome to organ dysfunction, length of stay, and mortality in critical surgical illness: effect of intensive care unit resuscitation. Arch Surg. 1999;134(1):81-87. doi:10.1001/archsurg.134.1.81.
  4. Yousef AA, Amr YM, Suliman GA. The diagnostic value of serum leptin monitoring and its correlation with tumor necrosis factor-alpha in critically ill patients: a prospective observational study. Crit Care. 2010;14(2):R33. doi:10.1186/cc8911.
  5. Cunha BA. Sepsis and septic shock: selection of empiric antimicrobial therapy. Crit Care Clin. 2008;24(2):313-334, ix. doi:10.1016/j.ccc.2007.12.015.
  6. Schacke H, Docke WD, Asadullah K. Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. 2002;96(1):23-43. doi:10.1016/S0163-7258(02)00297-8.
  7. Walsh TS, Stanworth SJ, Prescott RJ, Lee RJ, Watson DM, Wyncoll D. Prevalence, management, and outcomes of critically ill patients with prothrombin time prolongation in United Kingdom intensive care units. Crit Care Med. 2010;38(10):1939-1946. doi:10.1097/CCM.0b013e3181eb9d2b.
  8. Suleyman H, Demircan B, Karagoz Y. Anti-inflammatory and side effects of cyclooxygenase inhibitors. Pharmacol Rep. 2007;59(3):247-258.
  9. Stehle JH, Saade A, Rawashdeh O, et al. A survey of molecular details in the human pineal gland in the light of phylogeny, structure, function and chronobiological diseases. J Pineal Res. 2011;51(1):17-43. doi:10.1111/j.1600-079X.2011.00856.x.
  10. Favero G, Franceschetti L, Bonomini F, Rodella LF, Rezzani R. Melatonin as an Anti-Inflammatory Agent Modulating Inflammasome Activation. Int J Endocrinol. 2017;2017:1835195. doi:10.1155/2017/1835195.
  11. Hebert M, Martin SK, Lee C, Eastman CI. The effects of prior light history on the suppression of melatonin by light in humans. J Pineal Res. 2002;33(4):198-203. doi:10.1034/j.1600-079X.2002.01885.x.
  12. Yu HS, Reiter RJ. Melatonin: biosynthesis, physiological effects, and clinical applications. CRC Press; 1992.
  13. Reiter RJ. The mammalian pineal gland: structure and function. Am J Anat. 1981;162(4):287-313. doi:10.1002/aja.1001620402.
  14. Kennaway DJ, Wright H. Melatonin and circadian rhythms. Curr Top Med Chem. 2002;2(2):199-209. doi:10.2174/1568026023394380.
  15. Morcillo EJ, Estrela J, Cortijo J. Oxidative stress and pulmonary inflammation: pharmacological intervention with antioxidants. Pharmacol Res. 1999;40(5):393-404. doi:10.1006/phrs.1999.0549.
  16. Rahman I, Morrison D, Donaldson K, MacNee W. Systemic oxidative stress in asthma, COPD, and smokers. Am J Respir Crit Care Med. 1996;154(4 Pt 1):1055-1060. doi:10.1164/ajrccm.154.4.8887607.
  17. Steffes MW, Gross MD, Lee DH, Schreiner PJ, Jacobs DR Jr. Adiponectin, visceral fat, oxidative stress, and early macrovascular disease: the Coronary Artery Risk Development in Young Adults Study. Obesity (Silver Spring). 2006;14(2):319-326. doi:10.1038/oby.2006.41.
  18. Sanchez-Munoz F, Garcia-Macedo R, Alarcon-Aguilar F, Cruz M. [Adipocitokines, adipose tissue and its relationship with immune system cells]. Gac Med Mex. 2005;141(6):505-512.
  19. Ouchi N, Parker JL, Lugus JJ, Walsh K. Adipokines in inflammation and metabolic disease. Nat Rev Immunol. 2011;11(2):85-97. doi:10.1038/nri2921.
  20. Fonseca-Alaniz MH, Takada J, Alonso-Vale MI, Lima FB. Adipose tissue as an endocrine organ: from theory to practice. J Pediatr (Rio J). 2007;83(5 Suppl):S192-203. doi:10.2223/JPED.1709.
  21. Fernandez-Sanchez A, Madrigal-Santillan E, Bautista M, et al. Inflammation, oxidative stress, and obesity. Int J Mol Sci. 2011;12(5):3117-3132. doi:10.3390/ijms12053117.
  22. Rahman I, MacNee W. Oxidative stress and regulation of glutathione in lung inflammation. Eur Respir J. 2000;16(3):534- 554. doi:10.1034/j.1399-3003.2000.016003534.x.
  23. Nathan C. Specificity of a third kind: reactive oxygen and nitrogen intermediates in cell signaling. J Clin Invest. 2003;111(6):769-778. doi:10.1172/JCI18174.
  24. Reiter RJ, Calvo JR, Karbownik M, Qi W, Tan DX. Melatonin and its relation to the immune system and inflammation. Ann N Y Acad Sci. 2000;917(1):376-386. doi:10.1111/j.1749-6632.2000.tb05402.x.
  25. Blalock JE. The syntax of immune-neuroendocrine communication. Immunol Today. 1994;15(11):504-511. doi:10.1016/0167-5699(94)90205-4.
  26. Ader R, Cohen N, Felten D. Psychoneuroimmunology: interactions between the nervous system and the immune system. Lancet. 1995;345(8942):99-103. doi:10.5555/uri:pii:S0140673695900667.
  27. Radogna F, Diederich M, Ghibelli L. Melatonin: a pleiotropic molecule regulating inflammation. Biochem Pharmacol. 2010;80(12):1844-1852. doi:10.1016/j.bcp.2010.07.041.
  28. Scheff JD, Calvano SE, Lowry SF, Androulakis IP. Modeling the influence of circadian rhythms on the acute inflammatory response. J Theor Biol. 2010;264(3):1068-1076. doi:10.1016/j.jtbi.2010.03.026.
  29. Alamili M, Bendtzen K, Lykkesfeldt J, Rosenberg J, Gogenur I. Melatonin suppresses markers of inflammation and oxidative damage in a human daytime endotoxemia model. J Crit Care. 2014;29(1):184.e189-184.e113. doi:10.1016/j.jcrc.2013.09.006.
  30. Carrillo-Vico A, Lardone PJ, Naji L, et al. Beneficial pleiotropic actions of melatonin in an experimental model of septic shock in mice: regulation of pro-/anti-inflammatory cytokine network, protection against oxidative damage and anti-apoptotic effects. J Pineal Res. 2005;39(4):400-408. doi:10.1111/j.1600-079X.2005.00265.x.
  31. Gitto E, Karbownik M, Reiter RJ, et al. Effects of melatonin treatment in septic newborns. Pediatr Res. 2001;50(6):756-760. doi:10.1203/00006450-200112000-00021.
  32. Gitto E, Romeo C, Reiter RJ, et al. Melatonin reduces oxidative stress in surgical neonates. J Pediatr Surg. 2004;39(2):184-189; discussion 184-189. doi:10.1016/j.jpedsurg.2003.10.003.
International Journal of Medical Reviews
Volume 5, Issue 4
Autumn 2018
Pages 143-145

  • Receive Date 06 September 2018
  • Revise Date 16 November 2018
  • Accept Date 16 November 2018