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)

Fetal lung beta-receptors become effectively coupled to lung fluid reabsorption and enzymes involved in surfactant synthesis on the day before birth, a period when circulating catecholamine levels are high. Accordingly, we examined the effects of repeated maternal terbutaline exposure on beta-receptor binding capabilities and beta-receptor-mediated processes in the fetal rat lung. Administration of terbutaline to pregnant rats on gestational day 17-20 produced significant reductions in beta-receptor binding to membrane preparations. Similarly, beta-receptor-mediated stimulation of adenylate cyclase activity and ornithine decarboxylase activity showed marked desensitization in the terbutaline-exposed fetuses. However, the linkage of beta-receptors to lung fluid reabsorption and phosphatidic acid phosphatase, an enzyme involved in surfactant synthesis, did not desensitize with chronic terbutaline pretreatment; both of these processes displayed the normal onset of responsiveness on gestational day 21 in the treated animals, as well as a normal magnitude of response. Hence, beta-receptor-mediated events in the developing lung may be differentially regulated during exposure to agonists, allowing the selective expression or depression of function when circulating catecholamine levels are high.
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PMID:Regulation of beta-adrenergic receptor-mediated processes in fetal rat lung: selective desensitization caused by chronic terbutaline exposure. 196 39

During lung development, beta adrenergic receptors undergo transient coupling to enzymes and physiological processes which govern respiratory function and trophic responses to neural stimulation. To determine the role of endogenous catecholamines in mediating these processes, we examined the gestational and postnatal effects of chronic propranolol infusion (10 mg/kg/day) throughout fetal development. The effectiveness of receptor blockade in dam and fetus were confirmed through measurements of heart rate and enzymatic stimulatory responses to acute challenge with beta agonists (terbutaline to isoproterenol). Propranolol antagonized the ability of terbutaline to stimulate fetal lung fluid resorption and phosphatidic acid phosphatase, a key enzyme in surfactant synthesis. After birth, basal lung compliance and the compliance response to beta adrenergic stimulation were compromised in the neonates that had been exposed to propranolol before birth, despite the fact that direct receptor antagonism had disappeared by that time. After weaning, animals exposed to prenatal propranolol showed interference with basal activity of ornithine decarboxylase (an enzyme involved in transduction of neuronal and hormonal trophic stimuli) and its response to acute beta adrenergic challenge. These results suggest that endogenous fetal catecholamines participate in perinatal respiratory adaptation to air-breathing and help to program future cellular responsiveness to neuronal input.
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PMID:Prenatal exposure to propranolol via continuous maternal infusion: effects on physiological and biochemical processes mediated by beta adrenergic receptors in fetal and neonatal rat lung. 215 10

Neurotransmitter receptors may exhibit transient linkage to specific developmental processes involved in physiological adaptation to extrauterine life and in cell maturation. We have examined the responsiveness of the developing rat lung to beta-adrenergic agonists, using fluid reabsorption, phosphatidic acid phosphatase (an enzyme involved in surfactant synthesis) and ornithine decarboxylase (an enzyme related to cellular development) as markers of these activities. The ability of beta-adrenergic agonists to stimulate phosphatidic acid phosphatase and to cause liquid reabsorption first appeared just before birth, a period in which few receptor binding sites are present; the reactivity of both these processes declined after birth, but the enzymatic stimulation reached a second peak of response during the second and third postnatal weeks. The ability of beta-adrenergic challenge to elicit stimulation of lung phosphatidic acid phosphatase then declined into adulthood, despite the fact that receptor binding sites are increasing during the same period. Lung ornithine decarboxylase activity was poorly linked to beta-receptors in the immediate perinatal period and reached a peak of reactivity during the late postnatal period in which the coupling to phosphatidic acid phosphatase was lost. The pattern for phosphatidic acid phosphatase and liquid content was selective for the lung, as no stimulatory effects were seen for these variables in the liver, despite the comparable beta-adrenergic effects on ornithine decarboxylase in the two tissues. These data suggest that, during development, the coupling of receptors to specific cellular events is more important than the number of receptor sites in determining the pattern of physiological and cellular responses mediated by neurotransmitters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective linkage of beta-adrenergic receptors to functional responses in developing rat lung and liver: phosphatidic acid phosphatase, ornithine decarboxylase and lung liquid reabsorption. 257 76

6-Methylene progesterone (6MP) is an irreversible in vitro kcat inhibitor of rat prostate 5 alpha-reductase, the enzyme which converts testosterone (T) to dihydrotestosterone (DHT). Treatment of adult rats with 6MP or diethylstilbestrol (DES) decreased the weight of the ventral prostate (VP) by 45%, while castration reduced it by 86%. Histologically, the 6MP-treated VP were indistinguishable from those of controls, while the VP from DES-treated rats showed fibrous stromal hypertrophy as in castrated rats. The prostatic hydroxyproline content, an index of collagen levels, was enhanced by castration or DES, but was not significantly increased by 6MP. Within 2 days of 6MP treatment, the 5 alpha-reductase activity was reduced by 46% and ornithine decarboxylase (ODC) activity was lowered by 27%. During this time the prostatic acid phosphatase activity increased 42% and remained elevated with continued exposure to 6MP up to 13 days. The castration-induced involution of the VP was accompanied by a reduction in serum T and an increase in serum luteinizing hormone (LH). 6MP had no effect on T and LH serum levels but reduced the DHT content within the VP by 64%. Our results indicate that the structure and secretory acid phosphatase activity of the VP are less sensitive to changes in the ratio of T:DHT than is cell proliferation. Thus, the relative amounts of DHT and T within the VP may prove to be more significant than the absolute amount of either androgen in controlling prostate growth or its attendant neoplasms.
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PMID:A comparison of the effects of castration and 6-methylene progesterone, a 5 alpha-reductase inhibitor, on the rat ventral prostate. 343 60

Epithelial-cell-enriched primary cultures were established from canine prostate. Minced tissue was dissociated with 750 units/ml of collagenase in F12K tissue culture medium containing 1% fetal bovine serum. This treatment resulted in the gradual removal of stromal elements from the base of the epithelial cells. After 30 minutes of digestion, aggregates of epithelial cells free of stroma were dislodged from the minced pieces of prostate. These aggregates were washed and plated at high density in F12K plus 10% fetal bovine serum. After 12-16 hours in vitro the unattached cellular aggregates were removed from the culture dishes, washed, and reinoculated into new culture vessels containing fresh medium. After 48 hours in vitro, the aggregates had attached to the culture vessels and spread out to yield discrete patches of epithelial cells. By 120 hours in vitro the patches of cells had grown and coalesced to form a confluent monolayer of epithelial cells. Ultrastructural examination of these cultures indicated that adjacent cells were joined by desmosomes and tight junctions and had tonofilaments and microvilli, giving the cells an epithelial appearance. The cells contained rough endoplasmic reticulum, Golgi apparatus, and secretory granules similar to those of the epithelial cells in the intact organ. In addition, intracellular "blebs" containing acid phosphatase were observed in the monolayers and were found to increase in size and number with time in vitro. Differentiated function of the cultures was demonstrated by the presence of ornithine decarboxylase and acid phosphatase and the ability of the cultures to metabolize testosterone to primarily 5 alpha-reduced metabolites.
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PMID:Primary epithelial cell cultures derived from canine prostate: isolation, culture, and characterization. 713 51

The influence of diets containing combinations of high protein and low calcium on discrete stages of bone formation was investigated in 28-day-old rats. A bone matrix-induced bone forming system was utilized to determine the stages of endochondral ossification that were being affected. Mesenchymal cell proliferation as assessed by [3H]-thymidine incorporation and ornithine decarboxylase activity were unchanged in animals fed a high protein (80% casein)/normal calcium (0.61% Ca; 0.40% P) diet. However, osteogenesis was reduced by 78% in the rats fed high protein/normal calcium as measured by 45Ca incorporation. Alkaline and acid phosphatase activities in bone were increased 2.5 and 2.3 times, respectively, reflecting increased matrix turnover induced by the high protein availability. Bone that did form was not remodeled nor was there evidence of marrow formation. The animals were normocalcemic and normophosphatemic and showed no evidence of acidosis. A combination diet of high protein and low calcium resulted in a 62% reduction of cell proliferation and chondrogenesis and a 98% inhibition of bone formation. High dietary protein-induced osteoporosis in animals is due to a failure of osteogenesis of the stage of ossification possibly a result of restricted availability of calcium at the site of mineralization.
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PMID:Influence of high protein diets on cartilage and bone formation in rats. 722 30

The trifunctional enzyme CAD catalyzes the first three steps of pyrimidine biosynthesis. By using fluorescence in situ hybridization we have localized the Chinese hamster CAD gene on chromosome 7q11-q13 of diploid fibroblasts. Other genes previously assigned to chromosome 7 include acid phosphatase-1, the M2 subunit of ribonucleotide reductase and ornithine decarboxylase. These genes are also syntenic with CAD on human chromosome 2p. We have then mapped CAD on the pericentromeric region of two different rearranged chromosomes (Z8p and R2q) in a cell line derived from Chinese hamster ovary. The presence of CAD on Z8 and R2 indicates that they derive from rearrangements involving chromosome 7.
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PMID:Localization of the Chinese hamster CAD gene reveals homology between human chromosome 2p and Chinese hamster 7q. 810 Aug 5

We compared the Sp1 binding activity of Rat2 fibroblasts in nuclear extracts prepared from quiescent cells and cells stimulated with 20% serum. Increased DNA-binding activity was observed in extracts from serum-stimulated cells when an Sp1 oligonucleotide was used as radiolabeled probe in electrophoretic mobility shift assays. This increase in Sp1 DNA-binding activity is not due to changes in the amount of Sp1 in the nucleus as shown by immunoblot analysis. The transcriptional activity of a reporter construct containing six Sp1 sites upstream of a minimal adenovirus promoter or an Sp1-dependent promoter such as ornithine decarboxylase (ODC) containing Sp1 sites was enhanced following serum stimulation in transient transfection assays. Dephosphorylation of the nuclear extracts with potato acid phosphatase abolished the Sp1 DNA-binding activity, demonstrating a possible correlation between phosphorylation of Sp1 and DNA-binding activity. These results implicate a potential role for Sp1 in mediating signal transduction pathways in response to mitogenic signals.
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PMID:Serum responsive gene expression mediated by Sp1. 982 63

Two luminous marine bacterial strains, LC2-005(T) and LC2-102, were isolated from seawater at Kuroshio Region and Sagami Bay in Japan, respectively. These bacteria were Gram-negative, oxidase-positive, catalase-positive, motile and rod-shaped. On the basis of 16S rRNA gene sequence analysis, strains LC2-005(T) and LC2-102 formed a cluster within the Vibrio harveyi species group. However, multilocus sequence analysis using five loci (pyrH, ftsZ, mreB, gyrB and gapA) and DNA-DNA hybridization experiments indicated that these strains were distinct from the currently known Vibrio species. Additionally, these strains differ from related Vibrio species in utilization of glucose, mannitol, inositol, sorbitol, rhamnose, sucrose, melibiose and arabinose, production of lysine decarboxylase, ornithine decarboxylase, tryptophan deaminase, esterase (C4), lipase (C4), chymotrypsin, acid phosphatase, alpha-glucosidase, beta-glucosidase and N-acetyl-beta-glucosaminidase and the ability to reduce nitrate to nitrite. The major fatty acids were C(15 : 0) iso 2-OH and/or C(16 : 1)omega7c, C(16 : 0), C(18 : 1)omega7c and C(14 : 0). The DNA G+C contents of strains LC2-005(T) and LC2-102 were 45.2 and 45.5 mol%, respectively. On the basis of the polyphasic taxonomic evidence presented in this study, it can be concluded that strains LC2-005(T) and LC2-102 belong to the same genospecies and represent a novel species of the genus Vibrio, for which the name Vibrio azureus sp. nov. is proposed. The type strain is LC2-005(T) (=NBRC 104587(T) =KCTC 22352(T)).
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PMID:Vibrio azureus sp. nov., a luminous marine bacterium isolated from seawater. 1954 36

We examined the functional and morphological characteristics of the liver in rats acclimatized to a simulated altitude of 5500 m. We examined the metabolic activity and cytoplasmic distribution of liver mitochondria and the capacity of the liver to regenerate after partial hepatectomy. Mitochondrial respiration, oxidative phosphorylation, the respiratory control ratio (RCR), and the morphological characteristics of mitochondria in liver sections were studied after 3 months acclimatization to high altitude (HA). Partial hepatectomy was performed in a subset of animals after 30 days acclimatization to 5500 m. The rate of hepatic regeneration, induction of ornithine decarboxylase and uridine diphosphate glucuronyltransferase (UGT1a1), and plasma bilirubin were measured 24, 48, 72, and 96 hours after hepatectomy. Acclimatization to 5500 m did not affect the mitochondrial respiratory capacity or oxidative phosphorylation. The RCR decreased and acid phosphatase activity increased, which suggests that there were subtle changes in mitochondrial integrity. In addition, mitochondria were distributed more homogeneously in hepatocytes. Hepatic regeneration, which was associated with 25-fold induction of the ornithine decarboxylase, did not differ between controls and the altitude-exposed animals. Plasma bilirubin levels rose markedly 24 hours after hepatectomy, but returned to control levels 48 hours after the operation in the altitude-exposed animals. Thus, the remarkable functional capacity of the liver was retained at simulated HA. Redistribution of hepatic mitochondria seems to play an important role in maintaining hepatic function despite severe cellular hypoxia.
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PMID:Liver function in rats acclimatized to a simulated altitude of 5500 m. 2437 45


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