Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandins biosynthesized from 3H-arachidonic acid by trypsin-dispersed cat adrenocortical cells were isolated by silicic acid and thin layer chromatography. PGE, PGF, and a third component with mobility properties indistinguishable from either PGA or PGB were identified both in cortical cell homogenates and incubation medium. Concentrations of ACTH (125-250 muU) which stimulate steroidogenesis enhanced the conversion of labeled precursor to all three of these prostaglandins. These findings provide further evidence for the proposal that prostaglandins function as a critical link in ACTH-induced steroidogenesis.
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PMID:ACTH-induced prostaglandin biosynthesis from 3H-arachidonic acid by adrenocortical cells. 17 81

Calcium and folic acid absorption were studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on diphenylhydantoin alone, calcium absorption was abnormal in 9. In 12 patients on both diphenylhydantoin and phenobarbital, calcium absorption was abnormal in 3 patients. Folic acid (3H-PGA) absorption was normal in all but one patient, while serum folate (less than 6.4 ng/ml) was reduced in all patients. Hypocalcemia (less than 8.5 mg/100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. These findings support the proposal that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorption. The effect of these drugs appears to be the acceleration of the metabolism of vitamin D and an increase in the excretion of polar metabolites. This may result in reduced levels of 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol which are necessary for normal absorption of calcium. Since calcium absorption may be impaired secondary to a relative vitamin D deficiency, a supplemental increase in vitamin D intake by patients on anticonvulsant drugs is recommended.
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PMID:Calcium and folic acid absorption in patients taking anticonvulsant drugs. 17 36

The concentration of different prostaglandins (PG's) was determined in both cells and culture medium of growing BALB/3T3 and BALB/3T3 (3T3) cultures transformed by simian virus 40 (SV3T3). Most PG's were found in the culture medium rather than in the cells. Further, the larger PG measurements were PGE and a composite measurement of PGA and PGB. PGF was detected at lower levels. The sum of PGE and the composite measurement (PGA+PGB) was the best indication of PG production in culture. When 2-day medium collections from 3T3 and SV3T3 cells were measured by radioimmunoassay for PGs, higher concentrations of PG were detected in the media of SV3T3 cultures. This difference in PG production was not due merely to differences in cell density, since SV3T3 cells produced higher PG concentrations, even at equal cell densities. PG production for a 2-day interval was more a function of cell type than cell density.
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PMID:Prostaglandin production in cultures of BALB/3T3 and SV3T3 mouse fibroblasts. 17 97

The property of the neuronal membrane to be permeable to metabolic modifiers of two regulatory enzymes has been utilized to manipulate the spike activity of inspiratory (I) and expiratory-inspiratory (EI) neurons of the bulbar respiratory centre. The neurons have been classified according to their response to lung distention or collapse (alpha- or beta-type) and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). Using extracellular microelectrodes for single unit recording, the medulla oblongata was superfused with a metabolite-containing CSF. The various neuronal sub-types exhibited a differential activating or inhibitory response to one or several metabolic effectors. For example Ialpha+ units were activated by 5 mM glucose-6-phosphatase (G-6-P) and 3.5 mM 3-phosphoglycerate (3-PGA), which both inhibited Ibeta+ neurons, while 5 mM AMP inhibited Ialpha+ much more strongly than Ibeta+ cells. The spike density of Ialpha- and Ibeta- neurons was increased in the presence of 2.5 mM fructose-6-phosphate and 3.5--5 mM AMP, but became reduced by G-6-P. In contrast, 3 mM fructose-1,6-diphosphate and 5 mM 3-PGA activated the Ialpha- but inhibited the Ibeta- neurons. The EIbeta units were characteristically activated by 10 mM citrate, which inhibited all I-type neurons. Activations of the Ialpha and Ibeta neurons led to an accelerated respiratory rate and a higher tidal volume, while the opposite was true for EIbeta neurons. Intravenous injection of metabolites could not duplicate the striking effects under local applications.
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PMID:Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. 1. Mainpulation of inspiratory and expiratory-inspiratory neurons. 18 80

The effects of prostaglandin (PG) E1, E2, A1, F1alpha, F2alpha or D2 on the rat renal cortical, outer medullary and inner medullary adenylate cyclase-cyclic AMP systems were examined. While high concentrations (8X10-4M) of each prostaglandin stimulated adenylate cyclase activity in each area of the kidney, PGE1 was the only prostaglandin to stimulate at 10-7M. PGA's were the only prostaglandins tested besides PGE's which stimulated adenylate cyclase at less than 10-4M. This effect of PGA's was limited to the outer medulla. PGD2 was the least stimulatory. Observations with renal slices yielded qualitatively similar results. The PGE's were the most potent in each area with PGA's only stimulatory in the outer medulla. O2 deprivation (5% O2) lowered the slice cyclic AMP content in each area of the kidney. In the cortex and outer medulla, prostaglandin mediated increases in cyclic AMP content were either lower or absent at 5% O2 compared to 95% O2. However, in the inner medulla PGE stimulation was observed only at 5% O2 and not 95% O2. No other prostaglandins were found to increase inner medullary cyclic AMP content at 95% or 5% O2. These results illustrate that the adenylate cyclase-cyclic AMP system responds uniquely to prostaglandins in each area of the kidney. Consideration of these results along with correlative observations suggests that inner medullary produced PGE's may act as local modulators of inner medullary adenylate cyclase.
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PMID:Effects of prostaglandins on rat renal adenylate cyclase-cyclic AMP systems. 19 51

1 The report of the depression by indomethacin of vasoconstrictor responses to noradrenaline and their partial restoration by prostaglandin E(2) (PGE(2)) and PGE(1) in rat isolated perfused mesenteric blood vessels was investigated. The further suggestion that prostaglandins may be necessary for the combination of noradrenaline with the alpha-adrenoceptor in this tissue was also studied.2 The reported depression by indomethacin was confirmed and was further shown to be in the form of a concentration-dependent flattening of the noradrenaline concentration-effect curve.3 A concentration-dependent restorative effect was observed for all prostaglandins studied. The decreasing order of potency for the restoration towards normal of the indomethacin-depressed responses to noradrenaline was: PGE(2), PGE(1), PGA(1), PGF(2alpha), PGA(2).4 The prostaglandins studied were not uniform in their restorative actions and could be separated into two groups. PGE(2) and PGE(1) restored responses towards the control level whereas PGA(1), PGA(2) and PGF(2alpha) increased responses to an above control level and did so over a smaller concentration range. The possibility of several prostaglandin receptors is discussed.5 At concentrations equi-effective in restoring depressed responses to control levels PGA(1) but not PGE(2), caused a parallel shift of the noradrenaline concentration-effect curve to the left and a small, gradual rise in the basal perfusion pressure.6 The reason for the differing effects remains obscure but does not seem to involve a change in the alpha-adrenoceptor as indicated by the pA(2) of phentolamine. Furthermore, the restorative and potentiating effect of PGA(1) is not mediated by blockade of neuronal uptake of noradrenaline.7 It appears that prostaglandins are required for the vasoconstrictor action of noradrenaline in rat mesenteric blood vessels and that this effect is distal to the drug-receptor interaction. The possible involvement of prostaglandins with intracellular calcium ions is discussed.
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PMID:The influence of prostaglandins on noradrenaline-induced vasoconstriction isolated perfused mesenteric blood vessels of the rat. 20 65

The NAD+-linked 15-hydroxyprostaglandin dehydrogenase (PGDH) of swine lung was purified to a high specific activity by affinity chromatographies on prostaglandin (PG)-and NAD+-Sepharose. The affinities of the enzyme for various synthetic analogues of PGA, E, F, and I and their inhibitory effects on the enzymatic reaction were examined. The modification of the alkyl side chain of PG, particularly at C-15 or C-16, reduced the affinity of the enzyme for these PG analogues. Furthermore, 14-methyl-13,14-dihydro-PGE1 and 16-cyclopentyl-omega-trinor-15-epi-PGE2 were potent inhibitors of PGDH.
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PMID:Studies on 15-hydroxyprostaglandin dehydrogenase with various prostaglandin analogues. 21 66

Prostaglandins (PG) have been shown to raise the level of cyclic AMP (cAMP) in various tissues, and to increase permeability. Whether both events are linked, is at present a matter of speculation. We have investigated the effects of PGE1, E2, A1, A2, F1alpha and F2alpha on an isolated rat mesentery placed in a diffusion cell (surface area : 2 sq.cm). The PGs (5 microgram/ml) increased the passage of (I 125) - Albumin across the mesentery. In other experiments, diks of rat mesentery (surface area : 2 sq.cm) have been incubated in assay tubes, and cAMP levels measured by a binding protein assay. We have observed an excellent correlation between increases in permeability and cAMP levels (r=0.961). In order of increasing potency on both parameters, the PGs may be classified as follows : PGF, PGA and PGE. In the rat mesentery, under the influence of prostaglandins, increases in permeability and in cAMP levels are apparently connected.
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PMID:The role of various prostaglandins on the correlation between permeability to albumin and cAMP levels in the isolated mesentery. 21 45

Ribulose-diphosphate carboxylase from Thiobacillus novellus has been purified to hemogeneity as observed by polyacrylamide gel electrophoresis and U.V. light observation during sedimentation velocity analysis. The optimum pH for the enzyme with Tris-HCl buffers was about 8.2. Concentrations of this buffer in excess of 80 mM were inhibitory. The apparent Km for RuDP was about 14.8 muM with a Hill value of 1.5, for HCO3- the apparent Km was about 11.7 mM with an n value of 1.18 and for Mg2+ about 0.61 mM. The enzyme was specific for this cation. Relatively high concentrations of either Hg2+ or pCMB were required before significant inhibition was observed. Activity declined slowly during a 4-hr incubation period in either 3.0 M or 8.0 M urea. Incubation for 12 hrs resulted in complete loss of activity which was not prevented by 10 mM Mg2+ and was not reversed by dialysis and subsequent addition of 10 mM cysteine. Polyacrylamide gel electrophoresis revealed a loss of the major band and the appearance of 2 new bands. SDS polyacrylamide gel electrophoresis gave an average M.W. of 73500 +/- 2500 for the slower moving band and 12250 +/- 2500 for the faster moving. However, incubation in urea for up to 40 hrs revealed a decrease in the M.W. of the slower moving band to about 60000. The Ea for the enzyme was calculated to be about 18.85 kcal mole-1, with the possibility of a "break" between 40 and 50 degrees C. The Q10 was 3.07 between 20 and 30 degrees C whereas between 30 to 40 degrees C it was 3.31. Only phosphorylated compounds caused significant inhibition of enzyme activity. They included ADP, FDP, F6P, G6P, PEP, 6PG, 2-PGA, R1P, R5P, and Ru5p.
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PMID:Properties and regulation of ribulose diphosphate carboxylase from Thiobacillus novellus. 24 94

This study compared the osteogenic potential and tissue compatibility of biodegradable copolymers--PLA/PGA--and a biodegradable ceramic--Ca3(PO4)2. These compounds were placed in experimentally created defects in rat tibias, both in combination and singly, and evaluated at 14, 28, and 42 days. The ceramic served as a format to result in uniform osteogenesis throughout the defect. The copolymer implants resulted in a more gradual bone formation, progressing slowly from the would peripheries. The ceramic and copolymer combination behaved little differently from the copolymer alone. All experimental materials were extremely tissue tolerant, with minimal inflammation and no foreign-body reactions.
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PMID:Evaluation and comparisons of biodegradable substances as osteogenic agents. 26 77


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