Formation of malonaldehyde and focal brain edema induced by subpial injection of FeCl2 into rat isocortex.

Subpial injection of iron salts or iron-containing blood products into rat isocortex induces recurrent epileptiform discharges coupled with cavitary necrosis and gliosis. Since aqueous iron or heme compounds cause formation of superoxide radicals and peroxidation of membrane lipids, we studied the rate of formation of malonaldehyde (MDA) after subpial injection of 5 microliters of various concentrations of FeCl2 and CoCl2. Injection of CoCl2 failed to alter isocortical MDA levels. However, significant formation of MDA occurred after injection of 25, 50 and 100 mM FeCl2 into rat isocortex. Formation of peak MDA levels of 13.4 +/- 1.0 nmol.mg protein-1 occurred at 15 in to 1 h after 100 mM FeCl2 injection; levels returned to equal control by 12 h. Tissue fluid accumulation occurred by 2 h after FeCl2 injection and persisted for 38 h. Histopathologic assessment using Nissl staining of tissue from the injection site showed loss of cellular staining, coagulation necrosis, and accumulation of macrophages and glial cells. Although these experiments showed the initiation of lipid peroxidation and formation of focal isocortical edema by injection of aqueous solutions of iron salts, we speculate that decompartmentalization of iron red blood cells after trauma, cerebral hemorrhage or infarction may be important in the propagation of tissue damage from such injuries.