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Pharmacological utility of melatonin in reducing oxidative cellular and molecular damage.
Pol J Pharmacol. 2004 Mar-Apr; 56(2):159-70.PJ

Abstract

This review briefly summarizes the actions of melatonin in reducing molecular damage caused by free radicals and associated oxygen- and nitrogen-based reactants. All the mechanisms by which melatonin is protective of such a wide variety of molecules, i.e. lipids, proteins, DNA, etc., and in such widely diverse areas of the cell and different organs are likely not yet all identified. Melatonin actions that have been identified include its ability to directly neutralize a number of toxic reactants and stimulate antioxidative enzymes. Furthermore, several metabolites that are formed when melatonin neutralizes damaging reactants are themselves scavengers suggesting that there is a cascade of reactions that greatly increase the efficacy of melatonin in styming oxidative mutilation. Suggested, but less well defined, processes which may contribute to melatonin's ability to reduce oxidative stress include stimulation of glutathione synthesis (an important antioxidant which is at high concentrations within cells), reducing electron leakage from the mitochondrial electron transport chain (which would reduce free radical generation), limiting cytokine production and inflammatory processes (actions that would also lower toxic reactant generation), and synergistic effects with other classical antioxidants (e.g. vitamins C, E and glutathione). Clearly which of these multiple mechanisms contribute to melatonin's high efficacy in curtailing oxidative damage remains to be clarified. Likewise, it is possible that the key action of melatonin in reducing molecular damage induced by oxygen and nitrogen-based metabolites remains to be identified. Finally, the review summarizes some of the large amount of data documenting the ability of melatonin to limit molecular and organ damage in two situations, i.e. ischemia-reperfusion and ionizing radiation, where free radicals are generally conceded as being responsible for much of the resulting tissue destruction.

Authors+Show Affiliations

Department of Cellular and Structural Biology, University of Texas Health Science Center, 7703 Floyd Curl Drive, MC 7762 San Antonio, TX 78229-3900, USA. Reiter@uthscsa.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15156066

Citation

Reiter, Russel J., et al. "Pharmacological Utility of Melatonin in Reducing Oxidative Cellular and Molecular Damage." Polish Journal of Pharmacology, vol. 56, no. 2, 2004, pp. 159-70.
Reiter RJ, Tan DX, Gitto E, et al. Pharmacological utility of melatonin in reducing oxidative cellular and molecular damage. Pol J Pharmacol. 2004;56(2):159-70.
Reiter, R. J., Tan, D. X., Gitto, E., Sainz, R. M., Mayo, J. C., Leon, J., Manchester, L. C., Vijayalaxmi, ., Kilic, E., & Kilic, U. (2004). Pharmacological utility of melatonin in reducing oxidative cellular and molecular damage. Polish Journal of Pharmacology, 56(2), 159-70.
Reiter RJ, et al. Pharmacological Utility of Melatonin in Reducing Oxidative Cellular and Molecular Damage. Pol J Pharmacol. 2004 Mar-Apr;56(2):159-70. PubMed PMID: 15156066.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pharmacological utility of melatonin in reducing oxidative cellular and molecular damage. AU - Reiter,Russel J, AU - Tan,Dun-Xian, AU - Gitto,Eloisa, AU - Sainz,Rosa M, AU - Mayo,Juan C, AU - Leon,Josefa, AU - Manchester,Lucien C, AU - Vijayalaxmi,, AU - Kilic,Ertugrul, AU - Kilic,Ulkan, PY - 2004/02/17/received PY - 2004/5/25/pubmed PY - 2005/1/19/medline PY - 2004/5/25/entrez SP - 159 EP - 70 JF - Polish journal of pharmacology JO - Pol J Pharmacol VL - 56 IS - 2 N2 - This review briefly summarizes the actions of melatonin in reducing molecular damage caused by free radicals and associated oxygen- and nitrogen-based reactants. All the mechanisms by which melatonin is protective of such a wide variety of molecules, i.e. lipids, proteins, DNA, etc., and in such widely diverse areas of the cell and different organs are likely not yet all identified. Melatonin actions that have been identified include its ability to directly neutralize a number of toxic reactants and stimulate antioxidative enzymes. Furthermore, several metabolites that are formed when melatonin neutralizes damaging reactants are themselves scavengers suggesting that there is a cascade of reactions that greatly increase the efficacy of melatonin in styming oxidative mutilation. Suggested, but less well defined, processes which may contribute to melatonin's ability to reduce oxidative stress include stimulation of glutathione synthesis (an important antioxidant which is at high concentrations within cells), reducing electron leakage from the mitochondrial electron transport chain (which would reduce free radical generation), limiting cytokine production and inflammatory processes (actions that would also lower toxic reactant generation), and synergistic effects with other classical antioxidants (e.g. vitamins C, E and glutathione). Clearly which of these multiple mechanisms contribute to melatonin's high efficacy in curtailing oxidative damage remains to be clarified. Likewise, it is possible that the key action of melatonin in reducing molecular damage induced by oxygen and nitrogen-based metabolites remains to be identified. Finally, the review summarizes some of the large amount of data documenting the ability of melatonin to limit molecular and organ damage in two situations, i.e. ischemia-reperfusion and ionizing radiation, where free radicals are generally conceded as being responsible for much of the resulting tissue destruction. SN - 1230-6002 UR - https://www.unboundmedicine.com/medline/citation/15156066/Pharmacological_utility_of_melatonin_in_reducing_oxidative_cellular_and_molecular_damage_ L2 - http://www.if-pan.krakow.pl/pjp/pdf/2004/2_159.pdf DB - PRIME DP - Unbound Medicine ER -