Melatonin maintains the function of the blood redox system at combined ethanol-induced toxicity and subclinical inflammation in mice

Abstract

Abstract Background The goal of this study was to assess the effect of melatonin on blood redox systems in mice simultaneously exposed to ethanol and low-dose lipopolysaccharide (LPS). Methods Oxidative stress parameters were assessed in eight groups: untreated control, melatonin (10 mg kg−1, 10 days), LPS (injected once intraperitoneally at a dose of 150 μg per mouse), LPS with previous melatonin treatment, acute ethanol-induced stress (AES, 0.75 g kg−1 per day, 10 days), AES with previous melatonin treatment, LPS- and AES-induced toxicity, and melatonin treatment. Results Both ethanol and LPS induced oxidative stress. The combination of these two factors was even more toxic to the organism. Melatonin stabilized erythrocyte membranes and decreased the high level of free radical oxidation at the initial and final stages. Furthermore, melatonin limited protein damage through maintenance in the functional ability of the blood redox system to counteract pathological conditions. Conclusions Melatonin limited the negative effects associated with alcohol consumption and low-intensity inflammation.