Regional Changes in Superoxide Free Radicals, Energy Metabolism, and Ca-Calmodulin Binding Protein in the Development of Congenital Hydrocephalus
Interstitial edema has been proposed as a possible mechanism of neuronal damage in congenital hydrocephalus. Recent studies have demonstrated that oxygen-derived free radicals play an important role in the damage of vascular permeability and cell membrane perturbation in various kinds of edema. Therefore, we studied the regional changes of Superoxide free radicals, energy metabolism, and a neuron specific protein, microtubule associated protein 2(MAP2), in the development of congenital hydrocephalus. We present the results in this paper.
Superoxide free radicals increased specifically in the choroid plexus and in periventricular tissue shortly after birth, with degradation of MAP2 in the neural proliferative layer. This specific regional activation of free radicals plays an important role in the development of neural growth and leakage of toxic metabolic substrates from the choroid plexus into the ventricular CSF. In this study, we have demonstrated a free radical trigger mechanism in the development of congenital hydrocephalus.
Key wordsHydrocephalus Free radicals Mapping of Superoxide anions Neural proliferative layer Microtubule associated protein 2(MAP2)
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