Nuclear Cell Regulatory Mechanism in Cerebral Ischemia and Anoxia

Abstract

In cerebral ischemia and anoxia, the depletion of oxygen supply promptly results in a rapid decline of the high energy source, such as adenosine triphosphate or creatine phosphate. However, the effect of reduction in energy state on the transcription step within the nuclear cell regulatory mechanism and the translation step at the polyribosomal level has not been well investigated. Since prolonged cerebral ischemia and anoxia result in irreversible cellular damage leading to cerebral infarction, the disturbance of the macro-molecular regulatory mechanism may play an important role in the reversibility of these pathophysiological conditions. In the past several years, the effort of our laboratory has been focused on the effects of cerebral ischemia and anoxia on the transcription and translation steps, and on comparison of cerebral ischemia and anoxia. For these purposes, we have utilized gerbils as an experimental model for cerebral ischemia and rabbits for an in vitro model of cerebral anoxia. In this communication, protein synthesis with brain slices in vitro, polypeptide synthesis with isolated microsomes, DNA-dependent RNA polymerase activity and phosphorylation of chromatin protein will be compared in cerebral ischemia and anoxia.