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.
Financed by the National Centre for Research and Development under grant No. SP/I/1/77065/10 by the strategic scientific research and experimental development program:
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