• A M Mathes, A Sommerfeld, B Pannen, and I Bauer.
• 1Department of Anesthesiology, Düsseldorf University Hospital, Germany 2Department of Gastroenterology, Hepatology and Infectiology, Düsseldorf University Hospital, Germany.
• Shock. 2015 Oct 1;44 Suppl 2:7.

IntroductionAdministration of melatonin is hepatoprotective in various experimental models of stress; the mechanism of action can be attributed to antioxidant effects. While melatonin reduces hepatocellular injury after oxidative stress in animal models, this effect cannot be observed in human hepatocellular carcinoma cells (HepG2). This study was designed to test the hypothesis that melatonin may influence viability of primary hepatocytes (PH) under oxidative stress.MethodsAfter approval of the animal care and use committee (permission no. 84-02.04.2012.A214), PH were isolated from male Wistar rats (160- 180 g) by means of collagenase perfusion and cultured for 24 h. HepG2 cells and PH (each 3 biological / 4 technical replicates) were exposed to H2O2 (HepG2: 50-500 μM/1 h; PH: 1-10 mM/3 h) in the presence or absence of melatonin (500 μM/3 h pretreatment); DMSO and Triton X-100 (each 1%) served as controls. Cell viability was measured by means of XTT-assay. Data is presented as means ± SD; one- way-ANOVA followed by Tukey[Combining Acute Accent]s test. p < 0.05 is considered significant.ResultsAfter melatonin pretreatment, PH exposed to 1.0-2.5 mM H2O2 presented with a significantly increased viability compared with controls (p < 0.01, Fig. 1); this effect was not noted in HepG2 cells (data not shown).(Figure is included in full-text article.)Conclusion: Melatonin pretreatment increases viability of PH but not of HepG2 cells under oxidative stress. This model of melatonin responsive (PH) and melatonin unresponsive (HepG2) cells will allow us to characterize the molecular pattern of melatonins protective effects under oxidative stress.

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