We studied the effect of melatonin on morphological and functional disorders using serum markers of liver dysfunction such as cholinesterase and gamma glutamyl transpeptidase, hepatic protein content and malondialdehyde in a burned-rat model. Melatonin (10 mg/kg (−1), i.p) was administered immediately and then 12 h after 30% of total body surface area burns of male Wistar rats. The burns induced an increase of hepatic malondialdehyde levels by 166% (p<0.001), and also vascular congestion, leukocyte infiltration around the central veins, intracellular vacuolization, hepatic cell degeneration and apoptotic bodies (Councilman’s bodies). These changes were associated with significantly reduced serum cholinesterase (36%), gamma glutamyl transpeptidase (76%), hepatic proteins (52%) and serum albumin (37%) (p<0.001–0.0001). Treatment with melatonin reduced elevated hepatic malondialdehyde values by 50% (p<0.01). Melatonin restricted degenerative alteration in the hepatocytes: it protected the burninduced decrease of serum gamma glutamyl transpeptidase activity by 48% (p<0.01), hepatic proteins by 64% (p<0.01), and serum activity of cholinesterase as the only marker of liver damaged synthetic function by 57% (p<0.0001) but did not exert any significant influence on serum albumin concentration. Melatonin repaired the pathomorphological lesions and functional disorders. It could restore liver damage following thermal injury in humans.