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 two- to sixfold 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 less than 50% of control, ODC activity was increased nearly fivefold. 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 (ammonia, methionine sulfoximine, acrylamide, carbon tetrachloride, 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 unknown functions; ODC may be one of these "heat shock" or "trauma" proteins.

Effect of trimethyltin on ornithine decarboxylase in various regions of the mouse brain

“…This regional selectivity has been confirmed in studies of neurotransmitter-related parameters [9][10][11] and provides the opportunity to examine for metabolic changes in various brain areas after exposure of animals to TMT. Ornithine decarboxylase (ODC), the rate limiting enzyme of polyamine synthesis, is capable of rapidly responding in cerebral tissues that have been activated or damaged [12][13][14]. This property of ODC can be used to detect the targets of neurotoxic agents [15).…”

Ornithine Decarboxylase Activity and Putrescine Levels in Reversible Cerebral Ischemia of Mongolian Gerbils: Effect of Barbiturate

“…The most pronounced increase in enzyme ac tivity was found after severe metabolic stress such as reversible cerebral ischemia (Kleihues et aI., 1975;Dienel and Cruz, 1984;Dienel et aI., 1985). In contrast to ODC, the activity of the second key enzyme in polyamine synthesis, namely, S adenosylmethionine decarboxylase (SAMDC), was severely depressed after ischemia (Kleihues et aI., 1975;Dienel et aI., 1985), and this suppression con tinued for several hours (Kleihues et aI., 1975) or even days (Dienel et aI., 1985).…”

Differential effects of difluoromethylornithine on basal and induced activity of cerebral ornithine decarboxylase and mRNA

“…Ornithine decarboxylase, a highly inducible enzyme with a very short half-life ( < 10 min), is present at very small concentrations in the adult brain (Russell and Snyder, 1969). The levels of activity of cerebral ornithine decarboxylase are induced very rapidly in response to a variety of stimuli, such as mechanical injury, intense electrical stimulation or chemical toxicity (Dienel and Cruz, 1984;Pajunen, Hietala, Virransalo and Piha, 1978). The rapid responses of omithine decarboxylase to any change in the neuronal environment, implies a relationship between these biogenic compounds and the adaptive mechanisms of the central nervous system.…”