ABSTRACT
To observe the role of lipid peroxidation and the effect of liosome-entrapped superoxide dismutase(SOD) on lipid peroxidation experimental cerebral infarct, an infarction model was created by transorbital occlusion of the middle cerebral artery. Malondialdehyde(MDA), which is the degradation product of polyunsatunsaturated fatty acids in the cell wall, were measured at both the cortical and basal ganglia area of cat brain before and after administration of liposome-en-trapped superdioxide dismutase. The results were as follows: 1) There was a more significant increase of MDA in the left cerebral cortex than in the right than in the right cortex after occlusion of the left middle cerebral artery, but there was no significant difference between the 2 sides of the basal ganglia. 2) In the left cerebral cortex of the 1 and 3 hours subgroups with in experimental group, which were treated with liposome-entrapped SOD, there was a more significant decrease of MDA than the left cortex of control group. But there was no significant difference of MDA in the cortex of 6 hours group and the basal ganglia. 3) There was a more significant increase of MDA in the left cortex of control group, which was not treated with liposome-entrapped SOD, than in the right cortex. But there was no significant difference of MDA between both sides of the experimental group. 4) In the basal ganglia, there was no significant difference of MDA between the 2 sides of the control and experimental group. It is suggested that brain damage following cerebral infarction can be prevented or attenuated by the treament of liposome-entrapped SOD.