Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.1.17 (ornithine decarboxylase)
 6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the sequence of events that occur in the liver during mirex-induced adaptive liver growth, [3H]thymidine incorporation into DNA, thymidine kinase (TK), and ornithine decarboxylase (ODC) were studied in intact and adrenalectomized (ADX) mirex-dosed rats, and the responses were compared with experimental groups receiving corticosterone. In intact mirex-dosed rats (a response that is both hyperplastic and hypertrophic) there was a 36-h peak in ODC activity, and a 48-h peak in both [3H]thymidine incorporation into DNA and TK activity. This was accompanied by a 72% increase in relative liver weight (RLW). In contrast, in ADX mirex-dosed rats (a predominately hyperplastic response), there was a biphasic ODC response (18- and 36-h peaks), a 36-h TK peak, and a 48-h peak in [3H]thymidine incorporation into DNA. Both TK activity and [3H]thymidine incorporation into DNA were significantly elevated for the remainder of the 96-h study period. There was a 38% increase in RLW. Corticosterone supplements to mirex-dosed intact rats resulted in a biphasic peak of TK activity (30- and 48-h peaks), a reduced ODC peak at 36 h, and a 48-h peak in [3H]thymidine incorporation into DNA. RLW response was similar to the response in intact mirex-dosed rats. Corticosterone supplements to mirex-dosed ADX rats eliminated the 48-h peak of [3H]thymidine incorporation into DNA, reduced TK activity and shifted the peak to 30 h, and eliminated the ODC biphasic response. The RLW increase was similar to the response in intact mirex-dosed rats with a maximum 80% increase at 72 h postmirex dose.
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PMID:The relationship of ornithine decarboxylase and thymidine kinase to mirex-induced liver growth. 378 52

The effect of unilateral removal of the dorsal hippocampus and of glucocorticoid administration was measured on the activity of ornithine decarboxylase (ODC) in the remaining contralateral hippocampus lobe. Unilateral hippocampectomy (Hx) resulted in a rapid rise of ODC activity in the contralateral lobe. The effect on ODC was maximal at 6 h after surgery and lasted two days. In the absence of the adrenals the effect of Hx on the enzyme was more potent and more prolonged. Elevated ODC activity was still detectable at 5 days after surgery, but not at 10 days. Chronic replacement with dexamethasone (DEX) offered in drinking water decreased the Hx-induced ODC response of ADX rats at 3 days after surgery to the level of enzyme activity observed in the S-ADX Hx subject. The effect of the steroid seemed related to the extent of occupation of the pool of glucocorticoid receptor sites in cytosol of rat hippocampus. In contrast, a single injection of a high dose of DEX to Hx-ADX animals at 3 days after surgery increased ODC activity in addition to the lesion-induced ODC in the contralateral lobe. It is concluded that after unilateral removal of the dorsal hippocampus ODC is a biochemical marker for cellular responses taking place in the contralateral lobe. Glucocorticoids modulate the lesion-induced ODC response.
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PMID:Glucocorticoids modulate the response of ornithine decarboxylase to unilateral removal of the dorsal hippocampus. 662 81

Previous results demonstrated that estradiol (E2) treatment of ovariectomized-adrenalectomized (OVX-ADX) rats increased glucocorticoid (GC) binding in brain regions. The experimental protocol was extended to the spinal cord, a GC target tissue in which ornithine decarboxylase (ODC) is markedly induced by GC treatment. First, we measured GC binding to type I and type II receptors in ventral horn, dorsal horn and lateral funiculus of OVX-ADX rats treated during 4 days with E2 or vehicle. In E2-treated rats, type II receptors increased solely in dorsal horn, whereas type I sites remained unchanged. Second, in a group of OVX-ADX rats receiving dexamethasone (DEX), pretreatment with E2 superinduced ODC in ventral horn and lateral funiculus, but not in dorsal horn. Third, we found that the dorsal horn was relatively enriched in E2 receptors compared to other areas. Therefore, E2 stimulation of GC binding to type II sites may be mediated through E2 receptors localized in the dorsal horn. We suggest that combined treatment with E2 and DEX employs a transsynaptic mechanism for ODC induction at the ventral horn and lateral funiculus, with hormonal interaction taking place at the dorsal horn level.
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PMID:Estradiol increases glucocorticoid binding and glucocorticoid induction of ornithine decarboxylase in the rat spinal cord. 842 60