Indexed on: 27 Jan '99Published on: 27 Jan '99Published in: Experimental Neurology
Oxidative stress can contribute to many neurological disease processes. Because many events known to involve oxidative stress (infection, hemorrhage, brain trauma) are accompanied by hydrocephalus, the present study sought to evaluate the relationship between oxidative stress and the progression of hydrocephalus. Assays for reactive oxygen species (ROS), using dichlorofluorescein (DCF) fluorescence, and lipid peroxidation, using malondialdehyde (MDA), were performed on brain tissue from the cerebral cortex, cerebellum, basal ganglia, and hippocampus of 4-, 10-, and 25-day-old normal and hydrocephalic H-Tx rats. These rats inherit hydrocephalus at a rate of 30-50% and represent a unique model for studying the progression of hydrocephalus. When hydrocephalic and normal H-Tx rats were compared, ROS levels were significantly higher in the cerebral cortex of 4-day-old and in the cerebellum and hippocampus of 4- and 10-day-old hydrocephalic rats. ROS levels also were significantly higher in the basal ganglia of 25-day-old hydrocephalic rats. MDA levels were significantly higher in the hippocampus and basal ganglia of 25-day-old hydrocephalic rats. There were no significant differences in MDA levels at younger ages. These results indicate that, in H-Tx rats, oxidative stress is associated with the progression and molecular pathophysiology of hydrocephalus. This association suggests that oxidative brain damage may represent an important factor resulting from or contributing to the pathogenesis of hydrocephalus.