Lecithinized superoxide dismutase suppresses free radical substrates during the early phase of burn care in rats.

Severe hypovolemia is caused by an increase in blood vessel permeability in the early phase after an extensive burn; massive fluid volume replacement has been used for the treatment of this condition. The release of oxygen free radicals and chemical mediators, especially from skin tissue, induces the increase in blood vessel permeability. Free radical burst is associated with ischemia-related skin tissue injury. Although various antioxidant therapies have been used to inhibit the consequences of hypovolemia, an effective method has not been established. To elucidate the protective effects of lecithinized superoxide dismutase (PC-SOD) as an antioxidant agent. Each rat sustained a 30% total body surface area burn (n = 20) on the back by the Walker and Mason method were allocated into three groups: (1) no treatment group (n = 6), (2) a low dose of PC-SOD (0.67 mg/kg) group (n = 7), and (3) a high dose of PC-SOD (1.33 mg/kg) group (n = 7). The concentrations of malondialdehyde and SOD in the serum, skin tissue, and lung tissue were measured in each group 1 hour after burning. Both low and high doses of PC-SOD prevented malondialdehyde concentration associated with free radical burst after burning compared with the no treatment group (P < .05); serum (27.7 +/- 6.8, 10.8 +/- 2.7, and 12.1 +/- 2.8 nmol/L), skin tissue (2251.3 +/- 560.5, 802.7 +/- 228.8, and 790.1 +/- 188.3 nmol/wet.g), and lung (157.3 +/- 19.5, 109.1 +/- 23.9, and 81.9 +/- 20.3 nmol/wet.g). These data suggest that PC-SOD may be a protective agent against free radical-induced vasodilatation caused by severe, extensive burns.