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)

Treatment of 24 male patients with 3 g/day of xanthinol nicotinate did not change the in vitro measurements of ADP-induced platelet aggregation but produced a marked inhibition of collagen-induced platelet aggregation. This effect may be connected with the drug-induced depression of the ATP level in platelet-rich plasma. Changes in the platelets in the patients' blood or in the lipid composition and the concentration of uric acid in their serum were ruled out as reasons for the decrease of the collagen-induced aggregation. The activity of the three serum enzymes y-GT, GOT, and GPT and the concentration of the blood sugar did not change.
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PMID:Effect of xanthinol nicotinate treatment on platelet aggregation. 84 33

At time of admission 50 hospitalized male patients assigned to one of two groups judged as depressed and nondepressed completed one form of the Depression Adjective Check List (DACL). Depressed patients were placed in a highly specific treatment regime: Antidepressive program (adp), which required display of assertive behavior for termination of treatment. After removal from the program ADP patients received an alternate form of the DACL, and 2 weeks postadmission all patients completed a third form of testing. Significant decrease in number of dysphoric mood items selected posttreatment was found for the ADP group as compared with nondepressed patients. Lower depression scores were obtained after ADP across the period studied. Length of time in ADP was related negatively to initial depression scores. Results are interpreted in terms of reinforcement contingencies that sustain depressive verbal behavior.
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PMID:Effects of antidepressive program on verbal behavior. 85 98

Oxidative phosphorylation was measured polarographically in mitochondria isolated from rat heart. With regard to ADP/O ratio and respiratory control index, no differences were found among mitochondria isolated from normal, acutely (increased pneumatic resistance of the heart-lung preparation) and chronicly (renal hypertension) stressed heart. However, the acute stressed heart induced by strangulating the outflow tract of the heart-lung preparation showed clear depression and tendency to depression, respectively, in the level of ADP/O ratio and respiratory control index in mitochondria. The results indicate that there is no change in the oxidative phosphorylating mechanism of the myocardial mitochondria of nonfailed heart despite acute or chronic pressure loadings; however, there is an uncoupling of oxidative phosphorylation in mitochondria of the failed heart after acute strangulation of the outflow tract.
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PMID:Oxidative phosphorylation in mitochondria isolated from stressed rat heart. 121 39

Rats aged 7, 30 days and 3-5 months were given intraperitoneally single doses (2.5 mg/kg) of reserpine. The content of the adenyl system compounds (ATP, ADP, AMP and inorganic phosphorus) was determined. It was shown that as regards the extent of ATP and ADP depression the 7-day old animals proved more sensitive to reserpine than were adult animals.
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PMID:[Age-related characteristics of the reaction of the myocardial adenyl system to pharmacological sympatholysis]. 122 80

The present study investigated whether reduced adenylate cyclase activity and an increase in inhibitory guanine nucleotide binding proteins (Gi alpha), which have been observed in the failing human heart, already occur in myocardial hypertrophy before the stage of heart failure. In membranes of hypertrophic hearts from rats with different forms of experimentally induced hypertension without heart failure (one-kidney, one clip rats, deoxycorticosterone-treated rats, and rats with reduced renal mass), basal as well as isoprenaline-, 5'-guanylylimidodiphosphate-, and forskolin-stimulated adenylate cyclase activity was reduced. The activity of the catalyst was depressed in deoxycorticosterone but unchanged in one-kidney, one clip and reduced renal mass compared with controls. The number of beta-adrenergic receptors was similar in all groups. Radioimmunological quantification of Gi alpha proteins revealed an increase by 73% in one-kidney, one clip, 67% in reduced renal mass, but only 20% in deoxycorticosterone compared with sham-operated, age-matched control rats. The increase of Gi alpha was accompanied by smaller changes of pertussis toxin-induced [32P]ADP-ribosylation of a 40-kd membrane protein. It is concluded that Gi alpha contributes to the reduced adenylate cyclase activity in cardiac hypertrophy in one-kidney, one clip and reduced renal mass and to a smaller extent in deoxycorticosterone. It is suggested that an enhanced expression of Gi alpha could occur not only in severe heart failure but also in cardiac hypertrophy and could, therefore, contribute to myocardial depression and progression of disease in heart failure. In addition, Gi alpha might represent an important regulatory mechanism for cardiac adenylate cyclase activity and thus, might play an important role in various cardiac diseases.
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PMID:Desensitization of adenylate cyclase and increase of Gi alpha in cardiac hypertrophy due to acquired hypertension. 131 58

The effect of gentamicin on both glutamate synthesis and glutamate deamination was studied in kidney-cortex mitochondria and tubules isolated from both control and gentamicin-treated animals. In kidney-cortex mitochondria which were permeabilized in order to make a free access of substrates and antibiotic to the glutamate dehydrogenase, gentamicin appeared to be a very potent inhibitor of glutamate synthesis, resulting in about 60% decrease of the enzyme activity at 5 mM concentration. Other aminoglycoside antibiotics decreased the enzymatic activity, in the following order: gentamicin > neomycin = tobramycin = kanamycin > biodacyna > amikacin > streptomycin. This, in principle, corresponds to their known nephrotoxic potential observed in vivo. The inhibitory action of antibiotics was abolished by neither ADP nor leucine, allosteric activators of glutamate dehydrogenase. Surprisingly, gentamicin did not decrease the rate of ammonia formation from glutamate when added to both renal tubules and mitochondria isolated from control rabbits. This indicates that the antibiotic exerts its inhibitory effect on glutamate dehydrogenase activity in the direction of glutamate synthesis only. In contrast, the rate of both glutamate deamination and glutamate synthesis was about 40% lower in renal tubules and mitochondria isolated from kidney-cortex of animals which were given antibiotics for 10 days. In view of these results it seems that (i) the depression of ammoniagenesis in gentamicin-treated animals may be due to a decrease of glutamate dehydrogenase content and (ii) under conditions in vitro the aminoglycoside inhibits the enzyme activity in the direction of glutamate synthesis while it does not affect the glutamate deamination.
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PMID:Differential in vivo and in vitro effect of gentamicin on glutamate synthesis and glutamate deamination in rabbit kidney-cortex tubules and mitochondria. 136 90

To determine the effects of dietary protein level on cardiac and hepatic mitochondrial oxidative phosphorylation, chicks were fed on semi-purified diets of different protein levels (7, 25, 43 and 61% of metabolizable energy content) for 7, 14 and 21 d. All diets were formulated to contain equivalent fat, mineral and vitamin contents on a gross energy basis. Cardiac and hepatic mitochondrial oxidative phosphorylation rates were assessed polarographically with pyruvate and malate as substrates. Cardiac mitochondria isolated from chicks fed on a 43 or 61% protein-energy diet for 7 d exhibited significantly reduced ADP:oxygen (ADP:O) ratios when compared with mitochondria isolated from chicks fed on a lower-protein-energy diet. Feeding low- (7%) protein-energy diets for 14 d resulted in a relatively increased ADP:O ratio in the heart. Responses of ADP:O ratios to protein level in hepatic mitochondria showed more dependency on protein level than in heart muscle; at all feeding periods the ADP:O ratio decreased with an increase in protein level. As a result, ATP synthesized in the liver, expressed as nmol/mg mitochondrial protein per min, significantly decreased with increased dietary protein level. A parallel correlation was observed, in chicks fed on diets with different levels of protein, between ADP:O ratio for liver mitochondria and body fat. These results suggest that the reduction in oxidative phosphorylation in the heart and liver of animals fed on a higher protein-energy diet may partly contribute to the depression of body fat.
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PMID:Dietary protein level alters oxidative phosphorylation in heart and liver mitochondria of chicks. 139 Jun 19

1. Orthophosphate (P(i), 0.1-2.0 mM) was photogenerated within the filament lattice of isometrically contracting glycerinated fibres of rabbit psoas muscle at 10 and 20 degrees C. The P(i) was produced by laser flash photolysis of the photolabile compound 1-(2-nitrophenyl)ethylphosphate (caged P(i)). Caged P(i) caused a depression of tension that was much smaller than that caused by P(i). 2. Photolysis of caged P(i) produced a decline in isometric force composed of four phases: phase I, a lag phase (e.g. 1-4 ms at 10 degrees C) during which force did not change; phase II, an exponential decline by as much as 20% of the pre-pulse force; phase III, a partial force recovery (0-3% of the pre-pulse force); and phase IV, a further slow (0.5-3 s) decline to the steady value. Phases I, III and IV were largely independent of [P(i)] and are likely to be indirect effects caused by the caged P(i) photolysis. 3. Both the rate and amplitude of phase II depended markedly on [P(i)]. The amplitude of phase II was similar to the reduction of steady-state force by P(i). The rate of phase II increased with increasing temperature and [P(i)]. At high [P(i)] the rate began to saturate, and approached limits of 123 s-1 at 10 degrees C and 194 s-1 at 20 degrees C. 4. The rate of phase II was independent of sarcomere overlap, while the amplitude was proportional to tension at partial filament overlap. A control experiment using caged ATP showed that phase II was not produced by the photolytic by-products or the light pulse. The results suggest that phase II is associated with the force-generating transition of the cross-bridge cycle. 5. Sinusoidal length oscillations at 0.5 and 2 kHz were used to measure muscle stiffness during phase II. Stiffness declined in a single exponential phase, with the same time course as phase II of the tension transient. The change in stiffness was 83 +/- 6% (mean +/- S.E.M., n = 10, 0.5 kHz) of the change in tension when both signals were normalized to their pre-flash values. 6. Analysis of the data shows that two steps are involved in force generation and P(i) release. The non-force exerting AM-ADP-P(i) cross-bridge state first isomerizes to form a force-exerting cross-bridge state (AM'-ADP-P(i)). P(i) is then released to form a second force-generating state, AM'-ADP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reversal of the cross-bridge force-generating transition by photogeneration of phosphate in rabbit psoas muscle fibres. 140 12

1. Pyruvate kinase was partially purified from the foot, mantle, and digestive gland of active and aestivating snails. 2. At pH 7.0 the apparent Km values for phosphoenolpyruvate (PEP) were 0.064 mmol/l for the enzyme from foot and 0.071 mmol/l for the enzyme from mantle; those for ADP were 0.35 mmol/l for the foot enzyme and 0.33 mmol/l for the mantle enzyme. 3. Both enzymes were inhibited by alanine, and this could be reversed by fructose 1,6-bisphosphate (FBP), although FBP alone was a weak activator. 4. Decreasing the pH to 6.5 markedly increased the inhibition by alanine and reduced the response to FBP. 5. The enzymes from these tissues of aestivating snails showed a small decrease in their affinity for PEP and a small increase in the effectiveness of alanine as an inhibitor. 6. These changes are indicative of a down-regulation of this enzyme which is consistent with the observations in other species during metabolic depression. 7. In contrast the enzyme from the digestive gland of active animals showed sigmoidal saturation kinetics for PEP with a S0.5 of 1.2 mmol/l, but had a markedly higher affinity for PEP, S0.5 = 0.20 mmol/l during aestivation. This may be indicative of other metabolic changes occurring in the digestive gland.
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PMID:The effects of aestivation on the catalytic and regulatory properties of pyruvate kinase from Helix aspersa. 152 37

Methapyrilene (MP) is a rat-specific liver carcinogen that alters mitochondrial number and morphology both in vivo and in vitro. This biological phenomenon may be due to the effects of MP on mitochondrial function. To test this hypothesis, studies were conducted to examine the effects of MP on DNA and protein synthesis and respiration in isolated mitochondria. DNA and protein synthesis activities were measured using [3H]thymidine and [3H]leucine incorporation. Mouse liver mitochondria were also examined for comparison since no tumor formation or alterations in mitochondrial morphology have been associated with MP treatment in mice. A significant decrease in basal DNA and protein synthesis levels was observed in mitochondria isolated from rats and mice following in vivo MP treatment. This effect could not be reproduced when mitochondria were exposed to 0 or 100 microM MP following isolation, despite the presence of an S9 activation system. Electron microscopic examinations were performed on isolated rat mitochondria and revealed morphologic differences between mitochondria from naive and MP-treated rats. Although significant differences in State 3 and State 4 respiratory rates were noted, the respiratory control ratio, ADP/O ratio, and uncoupler-stimulated respiratory rates were unaffected. Results demonstrate that: (1) MP irreversibly depresses DNA and protein synthesis in a majority of mitochondria, despite only localized morphologic changes; (2) these changes are not reflected by a decrease in respiratory function; and (3) depression of DNA and protein synthesis does not correlate with carcinogenic susceptibility.
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PMID:Effects of methapyrilene measured in mitochondria isolated from naive and methapyrilene-treated rat and mouse hepatocytes. 152 42


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