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)

This study was designed to characterize mouse kidney ornithine decarboxylase (ODC) activity as an androgenic end point and to use ODC activity to detect an androgenic effect of antiandrogens. Enzyme activity was not affected by freezing the whole kidney or the 15,000 X g supernatant for up to 7 days. ODC activity in female mice had a diurnal variation that peaked at midday. This diurnal variation did not affect the androgenic response of ODC. Enzyme activity was lower in females than in males and, in both sexes, could be induced further to similar levels with testosterone treatment. A single dose of crystalline testosterone induced a marked increase in activity, which peaked sharply, up to 100-fold above baseline, 12-17 h after treatment. Enzyme activity could be maintained with continued treatment for at least 28 days and reached levels up to 1,000-fold above baseline. The response was specific for androgens and required a functional androgen receptor. Other hormones had permissive effects. The early androgen-stimulated response (less than 24 h) was partially diminished by hypophysectomy. Propylthiouracil reduced both early and chronic responses. Genetic factors were also involved. The testosterone-stimulated response of C57BL/6J mice was consistently approximately half that of DBA/2J mice. Using this very specific and sensitive increase in ODC activity as an end point, we did not detect an androgenic response to treatment with the antiandrogens, cyproterone acetate (6-chloro - 17 alpha - acetoxyl - 1,2 alpha - methylene - 4,6- pregnadiene- 3,20-dione) and flutamide (4'-nitro-3'-trifluoromethylisobutyranilide), despite an increase in RNA polymerase activity. The functionality of the polymerase activity induced by antiandrogens thus remains in question. These data suggest that mouse renal ODC activity can be a useful tool for future study of androgen action at the physiological and molecular level.
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PMID:Androgen and progestin stimulation of ornithine decarboxylase activity in the mouse kidney. 668 54

We studied the effects of daily ip administration of T4 (200 micrograms/100 g BW) or T3 (50 micrograms/100 g) to the rat (six per group) for 3 days with or without sodium ipodate (6 mg/100 g), propylthiouracil (PTU; 2 mg/100 g), propranolol (0.5 mg/100 g), or amiodarone (2.5 mg/100 g) on cardiac weight, 3',5'-diiodothyronine (3',5'-T2) to 3'-monoiodothyronine monodeiodinating activity (MA), mitochondrial alpha-glycerophosphate dehydrogenase (alpha GPD), and/or cytosolic ornithine decarboxylase (ODC). T4 treatment caused a 28% increase in cardiac weight, about an 11-fold increase in 3',5'-T2 MA, about a 27% increase in alpha GPD activity, and about a 129% increase in ODC activity. Administration of ipodate with T4 abolished all effects of T4 on the heart. PTU abolished the effect of T4 on alpha GPD and markedly reduced its effect on 3',5'-T2 MA and ODC activity; it had little effect on cardiac hypertrophy caused by T4 treatment. Propranolol reduced the increase in cardiac weight following T4 administration from 28% to 11%, but had a modest or no effect on T4-induced changes in other metabolic variables studied. Amiodarone also reduced the effect of T4 on heart weight, but had little or no influence on 3',5'-T2 MA, the only metabolic variable studied. T3 treatment of the rat caused a 35% increase in heart weight, about a 15-fold increase in 3',5'-T2 MA, about a 35% increase in alpha GPD, and about a 100% increase in ODC activity. Ipodate and PTU reduced the increase in 3',5'-T2 MA following T3 administration, but had no appreciable influence on heart weight, alpha GPD, and/or ODC activity. Propranolol and amiodarone had no significant effect on any of the changes studied after T3 administration. It was concluded that: 1) ipodate markedly lessens or abolishes the effects of T4 on the heart; 2) propranolol and amiodarone decrease cardiac hypertrophy in response to T4 administration, but have little or no effect on metabolic changes due to T4; 3) PTU curtails the metabolic effects of T4 on the heart but has little effect on cardiac hypertrophy; 4) none of the drugs studied affects cardiac changes occurring after T3 administration. The changes observed in 3',5'-T2 MA after ipodate and PTU treatment may have been a result of direct interaction of the drugs with the deiodinase.
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PMID:A study of cardiac effects of thyroid hormones: evidence for amelioration of the effects of thyroxine by sodium ipodate. 672 73