Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:4.1.1.17 (ornithine decarboxylase)
6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal ornithine decarboxylase (ODC) is greatly elevated in rats dosed once with one of several insecticides; chlordecone, p,p'DDT or permethrin. An abrupt rise in the dose-response curve was apparent between 25 and 50 mg chlordecone/kg body wt, corresponding to the range where major behavioral changes occur. The latter dose of chlordecone resulted in a persistent elevation of adrenal ODC for at least 4 days, longer than that caused by the other insecticides examined. No equivalent changes were found in levels of hypothalamic or hippocampal ODC after chlordecone treatment. Hypophysectomy did not reduce the response of adrenal ODC to chlordecone, after the diminished size of the adrenal gland in operated animals was taken into account. Isolated adrenal cortical cells of a mouse tumor line (Y-1), when incubated in media containing 10(-5) M chlordecone, responded with increased ODC activity. These data suggest that the mechanism of adrenal activation by chlordecone may possess a direct component, in addition to the well-characterized stimulation of pituitary ACTH secretion caused by chlordecone acting on the hypothalamo-hypophyseal system.
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PMID:Modulation of adrenal ornithine decarboxylase by chlordecone, p,p'DDT and permethrin. 243 15

The concentrations of polyamines and the activities of ornithine decarboxylase (ODC) and of S-adenosylmethionine decarboxylase (SAM-DC) were measured in the adrenal glands of rats during development. Adrenal spermine content increases gradually during the first month of life whereas spermidine and putrescine decrease. A low spermidine/spermine ratio is obtained. The developmental pattern of adrenal SAM-DC resembles that of spermine content. The activity of adrenal ornithine decarboxylase increases after birth and attains a peak at 17 days of age. It declines sharply thereafter. Induction of adrenal ODC following the stress of immobilization is already observed in the rat at 4 days of age but the induction caused by maternal deprivation or cold exposure is obtained only at 17 days. The results suggest that the developmental pattern of ODC activity is independent of its responsivity to various stressors.
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PMID:Developmental pattern of ornithine decarboxylase activity, S-adenosylmethionine decarboxylase, and polyamines of rat adrenal glands. 359 7

The activity of L-ornithine decarboxylase (EC 4.1.1.17, ODC) has become a useful indicator of hormone responsiveness. Various regimens of dexamethasone, aldosterone and epinephrine, alone or in combination, were administered to adrenalectomized rats either in acute or chronic doses. In addition, adrenalectomized rats, which were chronically treated with aldosterone and epinephrine, were given a single injection of 50 micrograms dexamethasone and sacrificed at various time intervals after hormone treatment. Hepatic and thymic ODC activity was measured. The expected dexamethasone effect, an increase in hepatic and a decrease in thymic ODC, was observed. This study also revealed that aldosterone induced similar responses in these tissues. Epinephrine had the opposite effect since chronic administration of dexamethasone or aldosterone with epinephrine resulted in control levels of ODC. Furthermore, when aldosterone and epinephrine were chronically administered to adrenalectomized rats, to study the acute effects of dexamethasone on rat thymus and liver, the time course of the response in each tissue was found to be distinct. The influence of the adrenal gland on rat thymus and liver is not restricted only to glucocorticoids, but may also involve other hormones which it secretes.
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PMID:Regulation of ODC activity in the thymus and liver of rats by adrenal hormones. 370 32

The effect of a single administration of catecholamines on ornithine decarboxylase activity and polyamine biosynthesis in the rat spleen was investigated. Isoproterenol elicited a dose-dependent increase in spleen ODC activity which reached a maximum 4 hr after the administration of the drug. Putrescine content was also found to increase within a few hours, whereas S-adenosylmethionine decarboxylase activity and spermidine and spermine levels did not change significantly. Adrenaline and noradrenaline proved to be even more effective in increasing splenic ODC activity than isoproterenol. alpha- and beta-adrenergic antagonists prevented the ODC increase by catecholamines to a different extent.
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PMID:Effect of adrenergic stimulation on ornithine decarboxylase activity in the rat spleen. 372 Nov 90

Monocrotaline-induced pulmonary hypertension in rats is preceded by an early and prolonged activation of lung ornithine decarboxylase (ODC) and a resultant increase in lung polyamine levels. These changes coincide in time with a transient period of pulmonary vascular hyperresponsiveness to angiotensin II. We therefore tested the hypothesis that enhanced lung ODC activity is necessary for the occurrence of monocrotaline-induced pulmonary vascular hyperresponsiveness. Adult male rats were given a subcutaneous injection of either 105 mg/kg monocrotaline or its vehicle and were treated concurrently with either alpha-difluoromethylornithine (DFMO), a specific, irreversible inhibitor of ODC, or saline. One week post monocrotaline treatment, animals were sacrificed and vascular responsiveness to angiotensin II and KCl was assessed in isolated, buffer perfused lungs. Relative to control preparations, lungs from monocrotaline-treated animals exhibited significantly larger vasoconstrictor responses upon challenge with 0.1 or 0.5 microgram angiotensin II. In contrast, angiotensin II-induced responses in lungs from rats treated with monocrotaline plus DFMO were not different from control. DFMO treatment alone had no impact on angiotensin responses. Vasoconstrictor responses evoked by 30 and 45 mg KCl were not different in lungs from monocrotaline-treated animals relative to control nor were they influenced by concurrent treatment with DFMO. Neither the polyamines (putrescine, spermidine, or spermine) nor DFMO influenced angiotensin II-induced vasoconstriction in normal lungs when added acutely to the perfusate reservoir. These observations suggest that the polyamines, although not serving as regulators of vascular reactivity in the normal pulmonary circulation, are causally related to the evolution of pulmonary vascular hyperresponsiveness observed in lungs from monocrotaline-treated rats.
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PMID:alpha-Difluoromethylornithine, an inhibitor of polyamine synthesis, attenuates monocrotaline-induced pulmonary vascular hyperresponsiveness in isolated perfused rat lungs. 393 39

Adrenal ornithine decarboxylase activity was stimulated in a dose-related manner after administration of ACTH or dibutyryl ((6)N-2'-O-dibutyryl) cyclic AMP to hypophysectomized rats. Little effect was observed for 2 h, but striking increases in enzyme activity were observed 4 h after administration of these substances. Effects of ACTH and dibutyryl cyclic AMP were not secondary to stimulation of steroidogenesis, since hydrocortisone had no effect on adrenal ornithine decarboxylase although it did stimulate activity of the enzyme in the liver and kidney.ACTH, given subcutaneously to hypophysectomized rats, induced striking increases in adrenal cyclic AMP levels within 15-30 min with a fall towards the base line in 1 h. Increases in ornithine decarboxylase activity lag several hours after this endogenous cyclic AMP peak, in contrast to the stimulatin of steroidogenesis by the nucleotide that requires only 2-3 min. After graded doses of ACTH, increases in adrenal cyclic AMP levels at 30 min were paralleled by proportional increases in adrenal ornithine decarboxylase activity 4 h after hormone treatment. Whereas maximal levels of adrenal steroidogenesis have been observed at tissue cyclic AMP levels of 6 nmol/g. ACTH is capable of inducing increases in nucleotide levels up to 200 nmol/g or more. These high tissue levels of cyclic AMP, although unneccessary for maximal steroidogenesis, appear to stimulate adrenal ornithine decarboxylase activity. Several results in addition to the time lag in the stimulation of ornithine decarboxylase activity suggest a mechanism involving accumulation of the enzyme or some factor needed for its activity rather than direct activation of the enzyme by cyclic AMP. Thus, the addition of cyclic AMP directly to the ornithine decarboxylase assay mixture in vitro was without stimulatory effect. In addition, actinomycin D or cycloheximide in doses sufficient to block adrenal RNA and protein synthesis, respectively inhibited the stimulation of ornithine decarboxylase activity by ACTH in vivo. An adrenocortical cancer was found to maintain ornithine decarboxylase activity at very high levels, but did so at much lower cyclic AMP levels than those of ACTH-stimulated adrenals. It is concluded that ACTH stimulates adrenal ornithine decarboxylase activity and that this effect may be mediated by cyclic AMP. However, cyclic AMP be mediated by appear to be a determinant of the high level of enzyme activity found in adrenocortical cancer.
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PMID:Regulation of adrenal ornithine decarboxylase by adrenocorticotropic hormone and cyclic AMP. 435 78

Epinephrine, norepinephrine, and isoproterenol produced dose-dependent stimulation of ornithine decarboxylase (EC 4.1.1.17) activity in isolated porcine granulosa cells maintained under defined conditions in vitro. beta- but not alpha-receptor-blocking agents prevented enzyme stimulation by catecholamines. Application of preferential beta-1 and beta-2-receptor antagonists and agonists localized the epinephrine effect to beta-2-adrenergic mediation. Epinephrine action was enhanced by the phosphodiesterase inhibitor, 1-methyl-3-isobutyl-xanthine, but not by saturating concentrations of the cyclic AMP analogue, 8-bromocyclic AMP, of follicle-stimulating hormone, or of prostaglandin E2. However, stimulation by epinephrine was additive to that of luteinizing hormone. Follicular fluid obtained from immature Graafian follicles contained concentrations of norepinephrine and epinephrine active in vitro. Thus, catecholamines may participate in the regulation of ornithine decarboxylase activity in the ovary. Catecholamine effects may be mediated by beta-2-receptors linked to the adenylate cyclase system.
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PMID:Beta-2-Adrenergic stimulation of ornithine decarboxylase activity in porcine granulosa cells in vitro. 615 44

The concentrations of cyclic AMP and cyclic GMP were measured in the denervated rat diaphragm at various times following unilateral phrenicectomy. Cyclic AMP concentration was raised by the second day after operation, reached a peak by the third day, followed by another increase at around 10 days. By contrast, cyclic GMP concentration was decreased within a day after denervation and remained below control levels at all subsequent times studied. Epinephrine in vitro produced a comparable increase in the concentration of cyclic AMP in both normal and denervated tissue. The concentration of adenosine appeared unchanged in the denervated diaphragm by comparison with its innervated control. Activity of ornithine decarboxylase was elevated in the diaphragms of rats treated with dibutyryl cyclic AMP, but this effect could also be achieved with sodium butyrate alone. Adenosylmethionine decarboxylase activity, was unaffected after treatment with either compound. These observations and others discussed are taken to indicate a lack of direct relationship between cyclic AMP concentrations and the activity of the rate-limiting enzymes of polyamine biosynthesis in the rat diaphragm.
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PMID:Cyclic nucleotides in the denervated rat diaphragm and the effect of cyclic AMP on ornithine and adenosylmethionine decarboxylases. 627 18

Adrenal corticosterone (CORT) levels and ornithine decarboxylase (ODC) activities in thyroid intact, thyroidectomized, and thyroxine (2 micrograms/ml in drinking water for 3 weeks) supplemented rats were measured 11 days after adrenal sham surgery or enucleation. Thyroidectomy decreased and thyroxine supplementation increased adrenal CORT significantly (p < 0.05) at 0600 h and 1800 h. The ODC activity was not significantly affected by thyroidectomy. Thyroxine supplementation however, inhibited ODC activity significantly (p < 0.05) at 1800 h in the regenerating adrenal cortex. Results indicated that, while CORT response in normal and regenerating adrenals are positively related to thyroid manipulation, inhibition of adrenal ODC activity by thyroxine may affect adrenal regeneration.
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PMID:In vivo response of the normal and regenerating adrenal glands to thyroid manipulation in rats. 909 Jul 58

The effects of immobilization stress and/or dexamethasone (DEX) on the adrenal ornithine decarboxylase (ODC) activities of sham-operated and adrenal-medulloectomized (enucleated) male Sprague-Dawley rats were investigated. On day 11 after surgery, rats were injected with saline or DEX (1 mg/kg), 3 h before the time of sacrifice (0600 h or 1800 h). Four groups, from sham-operated and enucleated rats (ENU) treated with saline or DEX were subjected to immobilization stress for 1 h prior to sacrifice. Groups of rats from stress-sham-DEX, non stress-sham-DEX, stress-sham, non stress-sham, stress-ENU-DEX, non stress-ENU-DEX, stress-ENU, and non stress-ENU were sacrificed at 0600 h or 1800 h on day 11 after surgery. Adrenal glands were excised and later analyzed for ODC activities. Results indicated that DEX and/or immobilization stress inhibited ODC activities (p<0.05) in normal and regenerating adrenal glands at 1800 h and ODC activity varies diurnally, the activity being greater at 1800 h than at 0600 hours (p<0.001).
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PMID:Inhibition of the rat adrenal ornithine decarboxylase activity by immobilization stress and/or dexamethasone. 919 82


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