Induction of Brain Ornithine Decarboxylase During Recovery from Metabolic, Mechanical, Thermal, or Chemical Injury

Abstract

Metabolic, mechanical, thermal and chemical injury induced ornithine decarboxylase (ODC) activity in rat brain. A 2- to 6-fold increase in ODC activity was measured at 5-9 h after different modes of injury to the brain. During the early phase of recovery from transient ischemia, when average protein synthesis was < 50% of control, ODC activity was increased nearly 5-fold. The rise in activity could be blocked by anisomycin, or reduced by intracerebral injections of actinomycin D. Drilling burr holes into the skull, injection of the vehicle for actinomycin D, hyperthermia, and freezing lesions all caused increased ODC activity. Neurotoxic chemicals (NH3 methionine sulfoximine, acrylamide, CCl4, and anisomycin) also increased brain ODC activity, whereas other chemicals (mannitol and valine) did not. Treatments known to stimulate the synthesis of heat shock proteins (carotid occlusion, hyperthermia, Cd2+, canavanine, and ethanol) induced ODC activity in the liver, whereas only hyperthermia and ethanol caused significant increases in spleen ODC activity. All increases in ODC activity were blocked by difluoromethylornithine, an irreversible inhibitor of ODC. The cellular response to noxious or stressful stimuli includes the synthesis of a small number of proteins of known functions; ODC may be one of these heat shock or trauma proteins.