Abstract Title:

Melatonin's role in preventing toxin-related and sepsis-mediated hepatic damage: A review.

Abstract Source:

Pharmacol Res. 2016 Jan 22 ;105:108-120. Epub 2016 Jan 22. PMID: 26808084

Abstract Author(s):

Eduardo Esteban-Zubero, Moisés Alejandro Alatorre-Jiménez, Laura López-Pingarrón, Marcos César Reyes-Gonzales, Priscilla Almeida-Souza, Amparo Cantín-Golet, Francisco José Ruiz-Ruiz, Dun-Xian Tan, José Joaquín García, Russel J Reiter

Article Affiliation:

Eduardo Esteban-Zubero


The liver is a central organ in detoxifying molecules and would otherwise cause molecular damage throughout the organism. Numerous toxic agents including aflatoxin, heavy metals, nicotine, carbon tetrachloride, thioacetamide, and toxins derived during septic processes, generate reactive oxygen species followed by molecular damage to lipids, proteins and DNA, which culminates in hepatic cell death. As a result, the identification of protective agents capable of ameliorating the damage at the cellular level is an urgent need. Melatonin is a powerful endogenous antioxidant produced by the pineal gland and a variety of other organs and many studies confirm its benefits against oxidative stress including lipid peroxidation, protein mutilation and molecular degeneration in various organs, including the liver. Recent studies confirm the benefits of melatonin in reducing the cellular damage generated as a result of the metabolism of toxic agents. These protective effects are apparent when melatonin is given as a sole therapy or in conjunction with other potentially protective agents. This review summarizes the published reports that document melatonin's ability to protect hepatocytes from molecular damage due to a wide variety of substances (aflatoxin, heavy metals, nicotine, carbon tetrachloride, chemotherapeutics, and endotoxins involved in the septic process), and explains the potential mechanisms by which melatonin provides these benefits. Melatonin is an endogenously-produced molecule which has a very high safety profile that should find utility as a protective molecule against a host of agents that are known to cause molecular mutilation at the level of the liver.

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