PROTECTIVE EFFECT OF MELATONIN AGAINST OXIDATIVE HEPATIC INJURY AFTER EXPERIMENTAL THERMAL TRAUMA

Burns cause thermal injury to local tissue, trigger systemic inflammatory processes and activate lipid peroxidation, leading to multiple distant organ injury. Melatonin is a lipid- and water-soluble antioxidant and membrane stabilizer with antiinflammatary, hepotoprotective and gastroptotective properties, among others. We studied the influence of melatonin on hepatic damage induced by thermal skin injury and its possible relation to hepatic lipid peroxidative status and systemic inflammatory response. Under ether anesthesia the shaved dorsum of rots was exposed to a 90 degrees C both for 10 s. Melatonin was administered intraperitoneally immediately after burns. Malondialdehyde (MDA), aspartate transaminase (AST) and alanine transaminase (ALT) were determined in liver and blood plasma and used as markers of oxidative status. Plasma C-reactive protein (CRP) was used as a marker of systemic inflammatory response. Thermal skin injury caused significant elevation of hepatic MDA by 48%, plasma CRP levels by 30% and plasma AST and ALT activities by 2- and 3.5-fold, respectively, in comparison with normal control rots. Treatment with melatonin (10 mg/kg) significantly inhibited the elevation in hepatic MDA and plasma CRP levels, reaching control values at 24 h. Melatonin treatment restricts the elevation of plasma AST and ALT activities (P < 0.007), which remain significantly increased as compared with controls. In conclusion, the protective effect of melatonin is likely to be due to attenuated lipid peroxidation and interference with reduced oxidative stress and inflammatory response, as evidenced by decreased hepatic MDA and plasma CRP levels.