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)

The development of pre-neoplastic and neoplastic changes has been documented in the urinary tract of the rat after portacaval shunting (PCS) and has been attributed variously to circulating carcinogens, the development of bladder stones, or deficiency of vitamin A. Therefore, an investigation of the pathogenesis of bladder tumors after PCS was undertaken in 120 PCS and 120 sham-operated male Sprague Dawley rats. Ten rats from each group were sacrificed at monthly intervals for 1 year after surgery. The incidence of calculus formation in the bladder increased from 20% at 2 months to 80% at 12 months after PCS. Hyperplastic mucosal changes occurred 3 months after surgery. After 5 months, distinct papillomas developed, and after 7 months, increasingly severe papillary changes and squamous metaplasia were evident. Interestingly, these urothelial changes were seen both in animals with and without bladder stones. Significantly decreased serum vitamin A levels were observed at 6 months (54.0 +/- 8.8 IU/dl, n = 10) (P less than .01), and 12 months (41.0 +/- 7.9 IU/dl, n = 10) (P less than .01), compared to those in sham-operated controls of 126.0 +/- 12.5 IU/dl (n = 10) and 122.7 +/- 19.2 IU/dl (n = 10). In addition, PCS resulted in a significantly increased activity of urothelial ornithine decarboxylase (ODC), a marker of neoplastic changes, at 6 months (3.1 +/- 0.4 nmoles CO2 in 60 min/mg protein, n = 5) (P less than .05) and 12 months (8.1 +/- 0.6 nmoles CO2 in 60 min/mg protein, n = 5) (P less than .05), when compared to ODC activity in controls (0.9 +/- 0.2 nmoles CO2 in 60 min/mg protein, n = 5). These data suggest that the development of urinary bladder tumor after PCS in the rat may be due to vitamin A deficiency rather than to bladder calculi or urinary carcinogens.
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PMID:Pre-neoplastic changes in rat urothelium following portacaval anastomosis. 279 51

We present a rapid and uncomplicated in situ assay for measuring ornithine decarboxylase activity in small cell quantities. This method is more economic than the in situ methods described by others. In addition, our system is faster and less complicated since it avoids manipulation of the CO2-trapping paper. Applying this method we demonstrate that parathyroid hormone, PGE1, and other inducers of intracellular cAMP levels, like IBMX and forskolin can induce ODC activity in primary cultures of chicken osteoblasts. Salmon calcitonin does not induce ODC activity, and 1.25 (OH)2D3 at higher concentrations can even give an inhibition of ODC activity. We confirm the recent findings that ODC activity is also dependent on calcium.
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PMID:An in situ assay system to measure ornithine decarboxylase activity in primary cultures of chicken osteoblasts: effects of bone-seeking hormones. 300 May 45

Ornithine decarboxylase from the African trypanosome is an important target for antitrypanosomal chemotherapy. Despite this, the enzyme had not been previously purified or extensively characterized as it is a very low level protein. In this paper we describe the purification of Trypanosoma brucei brucei ornithine decarboxylase from bloodstream form trypomastigotes by 107,000-fold to a specific activity of 2.7 x 10(6) nmol CO2/h/mg of protein in the parasite. T. brucei ornithine decarboxylase had a native molecular weight of 90,000 and a subunit molecular weight of 45,000. The isoelectric point of the protein was 5.0. The Km for ornithine was 280 microM and the Ki for the irreversible inhibitor alpha-difluoromethylornithine (DFMO) was 220 microM with a half-time of inactivation at saturating DFMO concentration of 2.7 min. T. brucei ornithine decarboxylase appears similar to mouse ornithine decarboxylase, further supporting our previous suggestion that the selective toxicity of DFMO to the parasite is not due to catalytic differences between the two proteins. Although a small quantity of T. brucei ornithine decarboxylase was purified from T. brucei, extensive structural and kinetic studies will require a more ample source of the enzyme. We therefore expressed our previously cloned T. brucei ornithine decarboxylase gene in Escherichia coli using a vector that contains an inducible lambda promoter. T. brucei ornithine decarboxylase activity was induced in E. coli to levels that were 50 to 200 fold of that present in the long-slender bloodstream form of T. brucei. Ornithine decarboxylase activity in the crude E. coli lysate was 1500-6000 nmol of CO2/h/mg of protein and represented 0.05-0.2% of the total cell protein. The recombinant T. brucei ornithine decarboxylase was purified to apparent homogeneity from the transformed E. coli. The purified recombinant enzyme had kinetic and physical properties essentially identical to those of the native enzyme.
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PMID:Trypanosoma brucei ornithine decarboxylase: enzyme purification, characterization, and expression in Escherichia coli. 305 33

Glucocorticoid hormones induced a stringent dependence on serum for the in vitro proliferation of Fu5 rat hepatoma cells by suppressing the growth rate and final quiescent cell density. Treatment of dexamethasone-suppressed quiescent Fu5 with serum plus insulin caused a rapid reinitiation of cellular proliferation and DNA synthesis that peaked at 16 h. RNA dot blot analysis of this time course showed that the transcript levels for the proto-oncogenes c-fos, c-myc, and c-rasKi peaked at 0.5, 2, and 4 h, respectively, while expression of c-rasHa and ornithine decarboxylase transcripts rose steadily during 16 h. Microspectrofluorimetric measurements of cytosolic calcium (Ca2+i) with fura-2 showed that insulin and serum, alone or in combination, elicited no changes in Ca2+i over a 50-min time course, although ATP, which is not a mitogen, induced large increases in Ca2+i. Cytosolic pH, pHi, was also measured using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. Insulin and serum, alone or in combination, did not cause pHi to increase in either 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid (HEPES) (pHi 7.17)- or HCO3/CO2 (pHi 7.19)- buffered media. Acid-loading of cells with NH4Cl indicated that both quiescent and proliferating Fu5 cells have equally active, amiloride-sensitive Na/H exchangers. Therefore, induction of DNA synthesis and proto-oncogene expression occurs in Fu5 epithelial tumor cells in the absence of any short term increases of pHi or Ca2+i.
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PMID:Glucocorticoids confer normal serum/growth factor-dependent growth regulation to Fu5 rat hepatoma cells in vitro. Sequential expression of cell cycle-regulated genes without changes in intracellular calcium or pH. 305 98

We quantitated the activity of ornithine decarboxylase (ODC) in homogenates and subcellular fractions of inner ear tissues from the rat and guinea pig and demonstrate inhibition of cochlear ODC by the aminoglycoside neomycin. Subcellular fractionation showed the enzyme associated with the post-mitochondrial supernatant fraction in each of the tissues: Specific activities of ODC, defined as alpha-difluoromethylornithine (DFMO)-sensitive decarboxylation of ornithine, in the supernatant fractions of combined inner ear tissues were: guinea pig = 44 +/- 4 pmoles CO2 produced/hour/mg protein, and rat = 133 +/- 30. In the guinea pig, supernatant fractions of the lateral wall tissues (stria vascularis and spiral ligament) had specific activities of 62 +/- 25, those of the organ of Corti (plus VIIIth nerve) 64 +/- 41. The ototoxic aminoglycoside neomycin produced a dose-dependent inhibition of ODC with half-maximal inhibition observed at 50 microM drug and almost complete inhibition at 100 microM. This is the first report of the presence of ODC in the inner ear and its inhibition by neomycin. Since both the ODC-inhibitors, DFMO and neomycin, can cause hearing loss in patients and experimental animals it is suggested that inhibition of ODC may be an important factor in the ototoxicity of these drugs.
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PMID:Inhibition of inner ear ornithine decarboxylase by neomycin in-vitro. 312 50

A new type of phorbol ester, which has a macrocyclic dicarboxylic acid diester structure, was isolated from the seed oil of Jatropha curcas L. (Euphorbiaceae). Based on the results of spectroscopic analyses of the compound and its chemical degradation products, its structure is proposed to be an intramolecular 13,16-diester of 12-deoxy-16-hydroxyphorbol, 12-deoxy-16-hydroxyphorbol-4'-[12',14'-butadienyl]-6'-[16',18',20' - nonatrienyl]-bicyclo[3.1.0]hexane-(13-O)-2'-[carboxylate]-(16-O)-3 '- [8'-butenoic-10']ate (DHPB). DHPB showed slightly weaker biological and biochemical activities than 12-O-tetradecanoylphorbol-13-acetate (TPA). DHPB induced ornithine decarboxylase in mouse skin (2.8 nmol CO2/30 min/mg protein/34 nmol application), inhibited the specific binding of [3H]-12-O-tetradecanoylphorbol-13-acetate to phorbol ester receptors (50% effective dose, 17.0 nM), and activated protein kinase C in vitro (50% effective dose, 36.0 nM). Also, a weak tumor-promoting activity of DHPB was found in a two-stage carcinogenesis experiment on mouse skin. One week after initiation of mice with 100 micrograms of 7,12-dimethyl-benz(a)anthracene, topical application, twice a week, of 2 micrograms of DHPB until week 17, followed by application of 5 microgram of DHPB until week 30 at the same rate, resulted in 46.7% incidence of tumors by week 30. The groups treated with 7,12-dimethylbenz(a)anthracene alone or DHPB alone did not produce significant numbers of tumors. These results indicate that the new phorbol ester, DHPB, is a tumor promoter with weaker activity than 12-O-tetradecanoylphorbol-13-acetate.
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PMID:A new tumor promoter from the seed oil of Jatropha curcas L., an intramolecular diester of 12-deoxy-16-hydroxyphorbol. 316 37

The abilities of sn-1,2-didecanoylglycerol (sn-1,2-DDG) to induce epidermal ornithine decarboxylase (ODC) activity and epidermal hyperplasia were tested using SENCAR, DBA/2 and C57BL/6 mice. Following a single application of 5000 nmol of sn-1,2-DDG, ODC activity reached a maximum at 4 h after treatment with a peak activity of 6.03 nmol CO2/mg protein/60 min in C57BL/6, 1.50 in SENCAR and 0.73 in DBA/2, respectively. The time course and magnitude for induction of ODC activity after multiple treatments was very similar to that after a single application in these three mouse lines. Interestingly, the induced ODC activity in C57BL/6 was always higher than that in SENCAR and DBA/2 mouse epidermis regardless of the treatment protocol. Induction of hyperplasia and dark basal keratinocytes (DCs) and changes in the labeling index (LI) of basal keratinocytes in DBA/2 and C57BL/6 mice following treatment with sn-1,2-DDG were investigated. Multiple treatments (twice weekly for 2 weeks) of 5000 nmol sn-1,2-DDG did not induce substantial increases in epidermal thickness or DCs 24 or 48 h after the last treatment. In contrast, TPA induced a marked increase in epidermal thickness in DBA/2 rather than C57BL/6 and a considerably higher induction of DCs in DBA/2 (37.3 +/- 2.2%) than in C57BL/6 (9.6 +/- 2.5%) 48 h after the last treatment. The LIs after topical application of sn-1,2-DDG were elevated at 24 h, but returned to basal levels by 48 h in both strains, whereas TPA treatment significantly elevated the LI in both strains at 48 h after the last application. In addition, the effects of various doses and frequencies of application of sn-1,2-DDG were investigated using SENCAR mice. High doses (20,000 nmol) or more frequent applications (5000 nmol once daily for 7 days) of sn-1,2-DDG still produced only weak hyperplasia. These results suggest that the induction of epidermal ODC activity can be dissociated from the induction of epidermal hyperplasia and may provide an explanation for the lack of complete promoting activity presently observed with membrane permeable diacylglycerol derivatives.
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PMID:sn-1,2-didecanoylglycerol effectively induces epidermal ornithine decarboxylase but only weak hyperplasia in mouse skin. 319 67

Cell-cycle progression of rat thymocytes stimulated with concanavalin A and interleukin 2 was monitored at 12-h intervals by pulse labeling aliquots of the cell culture with [3H]thymidine, by measuring cellular DNA and protein content and by counting the number of cells in the cultures. The cell cycle was completed after 96 h of culture with the S phase peaking at 48 h. Early events in thymocyte activation were enhanced phosphatidylinositol turnover and the induction of ornithine decarboxylase. Concomitant changes were observed in the rates of DNA synthesis and glycolysis accompanied by a 20-fold increase in glucose uptake 48 h after stimulation. However, the maximal increment in the glycolytic rate preceded that of DNA synthesis by 12 h. Apart from the quantitative changes which occurred during the cell-cycle progression, there was also a change from partial aerobic glucose degradation to CO2 (26%) to almost complete anaerobic conversion of glucose to lactate (85%) and less than 3% to CO2. Glycolytic enzyme levels increased fourfold to tenfold and reached their maxima 48 h after mitogenic stimulation. Maximal increments of glycolytic enzyme activities preceded or coincided with the maximal increments of the glycolytic rate. Actinomycin D (1.5 ng/ml) completely inhibited DNA and RNA synthesis but did not show any inhibitory effect either on glycolytic enzyme induction or on enhanced glycolysis. During mitosis and return of the cells to the non-proliferative state, all of the enhanced metabolic rates returned to their initial levels and the elevated enzyme activities were decreased also. The marked changes of metabolic rates and enzyme activities observed at the various phases of the cell cycle suggest that these biochemical events may also serve as suitable parameters for evaluating the response of lymphocytes towards mitogens and lymphokines.
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PMID:Cell-cycle-related metabolic and enzymatic events in proliferating rat thymocytes. 325 38

Ornithine decarboxylase (ODC) activity in human breast cancer tissues was correlated with prolactinemia (Prl), estradiol and progesterone cytosol receptors (ER and PR), and histopathologic pattern. Ninety-two cases of breast cancer, six benign mammary disease, and three normal breast tissues were studied for ER, PR, and ODC. Prolactinemia was assessed in 59 cancer patients, 14 of whom showed hyper-Prl along with significantly higher ODC than in patients with normal-Prl [(20.01 +/- 6.33) 10(-2) vs (5.20 +/- 0.90) 10(-2) pmol CO2/micrograms protein/h; P less than 0.0125]. A direct correlation was found between Prl and ODC in postmenopausal women (n = 40). Prl was assayed in seven of 13 ER-PR breast cancer patients; a highly significant, direct correlation was found between Prl and ODC in this group (r = 0.934, P less than 0.0025). ODC did not correlate with ER or PR. Carcinomas with higher ODC (n = 17) had higher cellularity, lower histologic differentiation, and higher nuclear anaplasia than those in which ODC was not detectable (n = 13). In normal breast and five of six benign mammary disease tissues, ODC was not detectable. These findings suggest that ODC could be a reliable marker for prognosis.
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PMID:Ornithine decarboxylase activity, prolactin blood levels, and estradiol and progesterone receptors in human breast cancer. 344 Feb 34

We have investigated the role of ornithine decarboxylase activity in rectal mucosa as a marker for colorectal neoplasia. Biopsies of normal rectal mucosa were taken from 18 patients with adenomas greater than 1 cm diameter, 11 with carcinomas and 16 controls. The mean ornithine decarboxylase activity in normal rectal mucosa of adenoma patients, 6.52 nmol CO2 released h-1 (mg cell protein)-1, was significantly lower than that in controls, 16.8, P = 0.006. The difference in rectal ornithine decarboxylase activities between cancer patients, 3.58, and controls was also significant, P = 0.001. These preliminary results suggest that ornithine decarboxylase may be a useful marker in screening for colorectal neoplasia.
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PMID:Assessment of ornithine decarboxylase activity in rectal mucosa as a marker for colorectal adenomas and carcinomas. 359 25


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