Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A mutant strain (ttr-3) of Escherichia coli was originally isolated as a strain resistant to tributyltin exhibiting temperature-sensitive depressions of growth and ATP synthesis on succinate plates at 42 degrees C. The ttr gene was mapped between the pyrE and dnaA genes (in the 82-83 min region) on the chromosome by P1-transduction experiments. Comparison of proline transport and oxygen uptake by membrane vesicles of the wild-type transductant and the mutant (ttr-3) transductant showed that membrane vesicles of the mutant exhibited temperature-sensitive decrease of proline transport and increase of oxygen uptake at the restrictive temperature (42 degrees C), compatible with depression of growth of the mutant at this temperature. Therefore, the ttr gene seems to code for some factor involved in the respiratory chain that is present in the inner membrane of Escherichia coli.
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PMID:A new gene responsible for an energy-transducing system in Escherichia coli. 269 85

Injection of progesterone for 3 days before treatment with relaxin inhibited the trophic effect of the peptide in both estrogen-primed and unprimed uteri. The depression in collagen concentration and increase in apparent rate of proline incorporation into collagen induced by relaxin alone were also eliminated, indicating a fundamental blockade of the effect of relaxin in this experimental design as well as a close association of changes in collagen concentration with tissue hypertrophy. The effect of relaxin on incorporation of proline into soluble protein was not blocked by progesterone, however, suggesting a separate mechanism for this anabolic effect of relaxin.
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PMID:Progesterone inhibits the uterotrophic effect of relaxin in immature rats. 272 81

Depression of lung endothelial cell metabolic function may be an early and sensitive indicator of lung damage. When such functions are measured in vivo, substrates injected usually must be limited to "trace" doses due to the significant hemodynamic effects of high doses of substrate. Under first-order conditions (i.e., trace doses) the enzyme or transport system rate constant Vmax/Km may be calculated, but independent estimates of each variable (Vmax and Km) are not available. We therefore used multiple indicator-dilution methods and higher substrate concentrations to apply a mathematical model, based on saturable kinetics that yield independent estimates of the apparent kinetic parameters Vmax and Km for pulmonary angiotensin-converting enzyme (ACE). We used the ACE substrate, [3H]benzoyl-phenylalanyl-alanyl-proline ([3H]BPAP) and made these measurements and also estimates of serotonin [5-hydroxytryptamine (5-HT)] removal, before and after acute lung injury induced by intratracheal administration of phorbol myristate acetate (PMA). PMA significantly depressed the percent 5-HT removal (62 +/- 3 to 44 +/- 4%) and BPAP percent metabolism (74 +/- 2 to 66 +/- 2), when trace amounts of either compound were injected as a bolus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary angiotensin-converting enzyme kinetics after acute lung injury in the rabbit. 284 Dec 74

beta-Pyrazol-1-yl-DL-alanine, an uncommon amino acid from plants of the Cucurbitaceae, was fed to mice. Although pyrazole is known to affect the liver enzymes UDP-glucose dehydrogenase, UDP-glucuronyl transferase and UDP-glucuronic acid pyrophosphatase, and also depresses their liver glycogen concentrations, beta-pyrazol-1-ylalanine had no such effects. beta-Pyrazol-1-ylalanine could not be detected in the liver of the experimental animals but was present in the urine. No other change in urinary amino acid content was observed. Studies with [14C]-beta-pyrazol-1-yl-DL-alanine showed the administered amino acid was excreted over a 4-day period, 93% of the compound supplied was recovered. Similar recoveries were obtained with the L-enantiomer from cucumber seed. The metabolic inertness of beta-pyrazol-1-ylalanine was also apparent in experiments involving subcutaneous injection of this compound. Administration of pyrazole confirmed an earlier report of resultant increased activity of liver UDP-glucose dehydrogenase and UDP-glucuronyl transferase, and of the depression of activity of liver UDP-glucuronic acid pyrophosphatase. A concomitant 40% decrease in liver glycogen content was seen. The urine contained a novel metabolite, identified as a peptide conjugate of a pyrazole derivative. Mass spectrometry and p.m.r. spectroscopy indicate that this derivative is 3,4,4-trimethyl-5-pyrazolone. The amino acid constituents are aspartic acid, threonine, serine, glutamic acid, proline, glycine, alanine, valine and leucine. The urine of mice receiving pyrazole contained less free glycine and alanine than controls. From the results, it is concluded that pyrazole is not a catabolite of dietary beta-pyrazol-1-ylalanine but to the contrary, the amino acid is essentially excreted unchanged. Formation of 3,4,4-trimethyl-5-pyrazolone from pyrazole would imply C-methylation, a process that has not been previously observed in a mammalian detoxication context.
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PMID:Metabolism of the amino acid beta-pyrazol-1-ylalanine and its parent base pyrazole. 298 41

Single pass extraction of a new iodinated inhibitor of angiotensin-converting enzyme (ACE) was measured by means of indicator-dilution techniques applied to rabbit lungs, perfused in situ at 20 ml/min with Krebs bicarbonate solution containing 3% bovine serum albumin. A bolus containing the inhibitor, N-[1(S)-carboxy-(4-OH-3-125I-phenyl)ethyl]-L-Ala-L-Pro (CPAP), and an intravascular marker, [14C]dextran, was injected and extraction calculated at the peak of the resulting venous outflow-time curve. In 13 of 21 lungs used, a synthetic substrate for ACE, [3H]benzoyl-phenylalanyl-alanyl-proline (BPAP), was added to the bolus and appearance of its hydrolysis product, [3H]benzoyl-Phe, measured in effluent samples. When low amounts (0.15 nmol) of [125I]CPAP were injected, pulmonary extraction (E) of CPAP was 67 +/- 14% (X +/- S.D; n = 21) and metabolism (M) of BPAP was 56 +/- 9% (n = 13). Addition of unlabeled CPAP (3, 34 or 340 nmol) to the Addition of unlabeled CPAP (3, 34 or 340 nmol) to the injected bolus caused dose-dependent reduction of E(CPAP) and M(BPAP) that was no longer evident 10 min after the largest dose of CPAP. Coadministration of the ACE inhibitor, captopril (3, 6, 8 and 28 nmol), also caused dose-dependent, reversible depression of both E(CPAP) and M(BPAP). Accordingly, extraction of CPAP by perfused rabbit lung is saturable. Inasmuch as CPAP inhibits ACE activity (as reflected by BPAP metabolism) and CPAP uptake is inhibited by captopril (which also inhibits BPAP hydrolysis), it appears that a large portion of this saturable process probably reflects binding to vascular ACE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uptake of N-[1 (S)-carboxy-(4-OH-3-125I-phenyl)ethyl]-L-Ala-L-Pro, an inhibitor of angiotensin-converting enzyme by rabbit lungs in situ. 301 13

Pulmonary angtiotensin-converting enzyme (ACE) is located on the luminal surface of pulmonary microvasculature. Multiple indicator-dilution techniques have been used to measure pulmonary ACE activity in vivo and in isolated lungs. These studies suggest that ACE activity is depressed in several forms of acute lung injury. Depression of ACE activity may reflect impaired substrate delivery to enzyme sites because of flow-related reduction of perfused surface area. To assess the role of altered microvascular flow and surface area in the measurement of ACE activity, we utilized similar techniques to estimate the apparent Km and Vmax of pulmonary ACE in isolated, Krebs-perfused rabbit lungs. Km is an estimate of the affinity of a synthetic ACE substrate, [3H]benzoyl-phenyl-alanyl-alanyl-proline ([3H]BPAP), for ACE and should not be influenced by the rate of substrate delivery to luminal enzyme sites. Conversely, Vmax is an index of the number of ACE sites and should be influenced by perfusion changes that alter the number of perfused sites (recruitment or derecruitment). When isolated lungs were subjected to physiological maneuvers designed to increase or decrease perfused surface area, apparent Vmax increased or decreased respectively. Apparent Km was not altered by these maneuvers. Km and Vmax were independent of changes in perfusion rate when surface area was held constant. Thus these parameters should be useful in evaluating perfusion changes in normal and injured lungs.
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PMID:Effect of flow and surface area on angiotensin-converting enzyme activity in rabbit lungs. 303 60

Carcasses and organs of 36 broiler chicks originating from an extensive fattening experiment with differing proportions of tryptophan (0.65 and 0.93 g/16 g N) to the neutral amino acids (15.2, 18.3 and 22.0 g/16 g N) in feed were analyzed for amino acid contents. Aside from the whole carcasses, a selected muscle (M. fibularis longus), liver, small intestine, and brain were prepared from the animals and analyzed. The organ weights differed according to the live-weights with the exception of the brain, where no group differences were measured. The patterns of amino acids of carcasses and organs remained nearly constant with differing amino acid supply. The only remarkable effect was the increase of the proportions of proline and hydroxyproline in the carcass protein from 6.4 to 7.4 and from 1.6 to 1.8%, respectively, with the higher tryptophan supply indicating increasing proportions of connective tissue. No relationship between weight gain and collagen content (calculated from hydroxyproline content) could be detected. The frequently supposed antagonism between tryptophan and the neutral amino acids, especially at the border of blood and brain, caused no reduction in tryptophan content of brain with increasing supply of neutral amino acids. There was, however, a significant depression of the development of the animals and the other inner organs.
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PMID:[Amino acid pattern in the bodies and several organs of broilers fed different provisions with tryptophan and neutral amino acids]. 322 54

L-[3H]Proline binds specifically and saturably to rat hippocampal synaptic membranes in the absence of inorganic ions. Saturation isotherms constructed in Hepes-Tris buffer best fit a model of a single independent population of binding sites with a dissociation constant of 1.6 microM and maximum density of 16 pmol/mg protein. The rank order of displacement of radioligand by proline analogues suggests that binding sites of this type could be receptors responsible for proline-induced retinal spreading depression and inhibition of memory consolidation.
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PMID:Sodium-independent binding of L-[3H]proline to hippocampal synaptic membranes. 379 55

Preadaptation of adult rats to hypoxia (10% O2 for 5 days) results in tolerance to oxygen-induced lung injury (greater than 95% O2 for 2 days). This study investigated whether hypoxia preadaptation maintained an endothelial cell metabolic function, angiotensin-converting enzyme (ACE) activity, despite exposure to hyperoxia. Lung ACE activity was measured as the capacity of isolated, ventilated, perfused lungs to hydrolyze an ACE substrate, benzoyl-phenylalanyl-alanyl-proline (BPAP), after in vivo hypoxia, hyperoxia, or sequential hypoxia-hyperoxia exposure. The results indicated that (1) hyperoxia decreases BPAP hydrolysis in isolated lungs, (2) hypoxia preadaptation does not affect BPAP hydrolysis (measured at ambient PO2), and (3) hypoxia preadaptation prevents hyperoxia-induced depression of lung ACE activity. These data imply that lung microvascular endothelial cells participate in the development of oxygen tolerance in this model.
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PMID:Hypoxia preadaptation prevents oxygen-induced depression of lung angiotensin-converting enzyme activity. 608 27

The influence of 1 mM-L-proline on electrically stimulated release of endogenous glutamate from slices of rat frontal cortex was measured. One mM-L-proline approximates the in vitro concentration that inhibits glutamate-induced spreading depression. Also, this L-proline level has been reported to be present in brain after an intraperitoneal injection that induced amnesia in chicks. L-Proline but not D-proline exhibits an inhibitory effect on glutamate release, thus supporting the suggestion that this mechanism may play a role in memory retention and/or formation.
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PMID:L-Proline inhibition of glutamate release. 611 6


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