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Although antioxidant therapy has been introduced into early post burn protocols to prevent oxidative injury, it is still not known how they effect the cellular immunity which was already depressed due to thermal injury. To investigate the effect of antioxidant therapy on postburn immunosuppression following burn injury in a rat model, well known antioxidants: allopurinol (50 mg/kg/day), desferrioxamine (15 mg/kg/day), PEG-catalase (PEG-CAT) (1200 U/kg/day), N-acetylcysteine (NAS) (1 mg/kg/day) and vitamin-C (Vit-C) (0.5 mg/kg/day) were given for 7 days following thermal injury. The immunologic status of the rat was studied using two in vivo measures at seventh day following (30% TBSA) full-thickness burn injury. The contact hypersensitivity response (CHR) of rats, and their ability to induce a host versus graft reaction (HVGR) in the popliteal node were used to assess immune system as in vivo measures. The use of mentioned antioxidants resulted in significant improvement (between P < 0.05 and P < 0.001) of burn induced immunosuppression as reflected by CHR. The treatment with allopurinol and PEG-CAT (P < 0.01) significantly improved, while desferrioxamine, NAS and Vit-C improved, but not significantly, HVG reaction in burned rats. This study demonstrated that a large burn was profoundly immunosuppressive and early intervention of antioxidant therapy was able to significantly restore cell-mediated immunity as reflected by two in vivo assays.

This study was designed to determine the effect of N-acetylcysteine (NAC, a natural hydroxyl radical scavenger) treatment on levels of pulmonary malondialdehyde (MDA, the end product of lipid peroxidation) and glutathione (GSH, a natural antioxidant) in thermally injured rats. Severe skin scald injury (30 percent TBSA) caused a significant decrease in GSH levels, and a significant increase in MDA levels in lung tissue both at 1 h and 1 day postburn injury. Treatment of rats with NAC (15 mg/kg intraperitoneally, 15 min and 12 h following the burn) significantly improved GSH levels, and decreased ongoing lipid peroxidation at 1 day. This study showed that thermal injury resulted in increased pulmonary lipid peroxidation, and this remote organ injury was decreased by treatment with NAC. In addition NAC, a scavenger of hydroxyl radicals, improved GSH levels in the lungs. The higher level of GSH in the lungs of the burned rats treated with NAC could be due to either a decrease in the rate of degradation of GSH or to an increase in its synthesis. No data about these possibilities are provided.