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  • Title: Melatonin suppresses markers of inflammation and oxidative damage in a human daytime endotoxemia model.
    Author: Alamili M, Bendtzen K, Lykkesfeldt J, Rosenberg J, Gögenur I.
    Journal: J Crit Care; 2014 Feb; 29(1):184.e9-184.e13. PubMed ID: 24140166.
    Abstract:
    PURPOSE: Melatonin used as an exogenous drug has been documented to have potent antioxidant and anti-inflammatory effects in animal model. We aimed to examine the effect of melatonin in an experimental human sepsis model. MATERIALS AND METHODS: Twelve healthy males were enrolled in a randomized, placebo-controlled, double-blinded cross-over trial. They received lipopolysaccharide endotoxin 0.3 ng/kg of body weight intravenously at 12:00. Before endotoxemia, an 8-hour infusion of melatonin (100 mg) or placebo (saline) was initiated. Blood samples were drawn before and at 2, 4, 6, and 8 hours after lipopolysaccharide administration. Proinflammatory (tumor necrosis factor α [TNF-α], interleukin [IL] 1β, IL-6, and YKL-40), anti-inflammatory markers (IL-1Ra, IL-10, soluble tumor necrosis factor receptor I, and soluble tumor necrosis factor receptor II), a marker for oxidative damage (malondialdehyde), and antioxidants (ascorbic acid and dehydroascorbic acid) were analyzed in plasma. RESULTS: Melatonin significantly reduced proinflammatory markers IL-1β (P < .01) and YKL-40 (P < .05) but not TNF-α and IL-6. None of the anti-inflammatory markers (IL-1Ra, IL-10, soluble tumor necrosis factor receptor I, and soluble tumor necrosis factor receptor II) were lowered by melatonin. Melatonin reduced the levels of ascorbic acid (P < .05) but not dehydroascorbic acid or malondialdehyde. CONCLUSIONS: Melatonin administration before endotoxemia resulted in reduction of certain markers of inflammation and oxidative stress. Further studies are needed to clarify the role of melatonin in clinical setting.
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