In Vivo Lipid Peroxidation in Rat Brain Following Intracortical Fe 2+ Injection

Abstract: Cerebral contusion, cortical laceration, intracerebral hematoma formation, and hemorrhagic cortical infarction cause extravasation of red blood cells, followed by hemolysis, decompartmentalization of iron, formation and deposition of hemosiderin, and an increased incidence of epilepsy. In this experiment, 10 μl of an aqueous solution containing 100 mmol/L FeCl 2 , 100 mmol/L CoCl 2 , or 0.9% (wt/vol) NaCl were injected at a depth of 1.8 mm into rat isocortex. The rate of formation of fluorescent compounds was measured in chloroform‐methanol extracts of isocortical homogenates. Significant increases in the quantity of fluorescent products of lipid peroxidation were found 120 min after the injection of 100 mmol/L FeCl 2 . Cobaltous chloride and saline injection had no effect on the levels of fluorescent products found in the cortical homogenates. Although the intracortical deposition of aqueous solutions containing CoCl 2 or FeCl 2 , in rodent cortex causes acute epileptiform discharges, the epileptogenic effect of CoCl 2 , is transient, while the injection of iron salts causes persistent seizures. Since CoCl 2 , injection failed to cause formation of lipid peroxidation products while the isocortical injection of iron caused significant increase in fluorescence within the injected hemisphere, we suggest that the occurrence of iron‐induced lipid peroxidation may be of importance in initiation of recurrent seizures in the rat.