Iron-induced lipid peroxidation in spinal cord: Protection with mannitol and methylprednisolone

Abstract

The ability of the free radical scavenger, mannitol, and the synthetic glucocorticoid, methylprednisolone sodium succinate (MPSS) to reverse the effects of iron catalyzed free radical induced lipid peroxidation was assessed in the feline spinal cord. Ferrous chloride (100 mM) was infused into the gray matter of lumbar spinal cord, the region frozen in situ, removed, and homogenates of the gray matter analyzed for activity of Na⁺, K⁺- ATPase and levels of malondialdehyde (MDA). ATPase activity had declined to approximately 30% of control by 2 h after FeCl₂ infusion and remained at this level through 24 h. Malondialdehyde values were elevated almost twofold at 2 h. Mannitol essentially reversed the effects of FeCl₂ infusion on Na⁺,K⁺-ATPase activity and MDA production. These results may implicate the hydroxyl radical (·OH), or an oxidizing species with ·OH-like reactivity, as the initiating radical species in this model of lipid peroxidation. Similarly, MPSS prevented the decline in spinal cord Na⁺, K⁺-ATPase activity and rise in MDA levels that were induced by FeCl₂ infusion. This demonstrated that at the dosage levels used in this study, MPSS was an effective antioxidant. This finding provides presumptive evidence suggesting that, at least in experimental animals, the effectiveness of MPSS in preventing the tissue necrosis and paralysis that is the sequelae of spinal cord trauma may reside, in part, in the capacity of this glucocorticord to quench peroxidative reactions in the injured tissue.