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)

Depression of the activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase [mevalonate:NADP(+) oxidoreductase (CoA-acylating); EC 1.1.1.34] was elicited by the removal of serum from the growth medium of HeLa S3G cells with a concomitant expected increase in cellular sterol biosynthesis; if dexamethasone (9alpha-fluoro-11beta,17alpha,21-trihydroxy-16alpha-methyl-1, 4-pregnadiene-3,20-dione) was present in the serumless medium, there was an augmentation of HMG-CoA reductase activity but a suppression of sterol biosynthesis. When human serum, human low density lipoprotein, or calf serum was present in the medium, there was a reduction of both the enzyme activity and sterol biosynthesis, but the presence of dexamethasone resulted in an increase in HMG-CoA reductase activity as compared to the controls containing human serum, low density lipoprotein, or calf serum alone. In contrast, either low density lipoprotein or whole serum supplementation eliminated the differences in acetate incorporation into sterols between glucocorticoid-treated and untreated cells. Human high density lipoproteins had little effect on the enzyme activity and abolished the difference in sterol biosynthesis only at relatively high concentrations. Addition of low density lipoproteins to cells after preincubation in serumless medium elicited the same rate of decay of HMG-CoA reductase (t(1/2) 3.8-4.2 hr) regardless of the presence of glucocorticoids in the medium, but there was an exaggerated lag before the onset of suppression in the hormone-treated cells. If free cholesterol was present in the medium, the dexamethasone augmentation of HMG-CoA reductase was maintained, but the addition of either 7-ketocholesterol or 25-hydroxycholesterol abolished the difference between glucocorticoid-treated and control cells. These observations suggest that, under certain physiological conditions, HMG-CoA reductase activity no longer accurately reflects cellular sterol biosynthesis.
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PMID:Regulation of cholesterol biosynthesis in HeLa S3G cells by serum lipoproteins: dexamethasone-mediated interference with suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase. 20 49

Intravenous administration of lead acetate to rabbits for 10 weeks at 2 week intervals resulted in significantly elevated blood lead levels, slight anemia with marked microspherocytosis and moderate basophilic stippling, and marked depression of red cell delta-aminolevulinic acid (ALA) dehydratase activity. However the decrease in red cell pyrimidine 5'-nucleotidase (P5N) activity was slight when compared to the red cell P5N activity of comparable reticulocyte-rich blood, and intracellular accumulation of pyrimidine nucleotides could not be demonstrated. In the in vitro inhibition test the same degree of inhibition of red cell P5N activity seen in hereditary red cell P5N deficiency was obtained by using a lead concentration 200--400 times higher than the lead levels detected in human plumbism. Most importantly, there were no differences in the lead-induced inhibition of human and rabbit red cell P5N. From the results of the in vitro inhibition test, lead-induced red cell P5N deficiency appears to be one of several pathogenic mechanisms in chronic lead exposure associated with the accumulation of lead in bone marrow. A decrease in rec cell P5N activity could not be demonstrated despite the marked depression in red cell ALA dehydratase activity, and slight anemia with marked microspherocytosis and moderate basophilic stippling in this experiment. These results suggest that lead affects red cells at multiple metabolic loci.
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PMID:A role of red cell pyrimidine 5'-nucleotidase in experimental lead poisoning. 23 20

Membrane potentials in single barnacle muscle fibres of Megabalanus psittacus, internally perfused with 200 mM K-acetate (KAc) solution of pH 7.5 were in the range --53 to --60 mV. These were followed as a function of pH of the external chloride saline. Decrease of pH of the Cl-saline from 8.5 to 3.5 hyperpolarized the membrane reversibly by about 8 mV. On further decrease of pH to 3.0, a transient hyperpolarization (from --60 to --65 mV) followed by a sudden and irreversible drop of potential to --40 mV was observed. Replacement of the external Cl-saline by acetate saline in the pH range 8.5 to 6.5 had no effect on the membrane potential. Further decrease of pH to 5.0 brought about an irreversible reduction of membrane potential. For fibres bathing in Cl- or Ac-saline at pH 7.5 when the internal pH was changed to 5.5, a transient hyperpolarization in Cl-saline and a sustained hyperpolarization in Ac-saline were observed. Further studies of membrane potential changing the concentration of external K, keeping the concentration of Cl or Ac constant, and changing the concentration of Cl or Ac, keeping the concentration of K constant, at different internal and external pHs showed that as the pH was reduced the membrane became more permeable to anions, Cl being more permeable than Ac. Experiments in which the membrane potential was controlled showed that when the internal pH of 200 mM KAc solution was reduced from 7.5 to 6.5 or raised to 8.5, the changes in outward K currents at various depolarizations were negligible. However, when the pH was reduced to 5.5 or 5.0, there was a progressive decrease in the outward K currents. The leakage currents in all these cases were relatively small. Use of high ionic strength solution of 580 mM KAc internally protected the K system in that when the pH was lowered the depression of the outward K current was smaller than that observed at a corresponding pH when the internal solution was 200 mM KAc. Use of low ionic strength solution of 50 mM KAc had the opposite effect. The results have been explained in terms of the ion exchange theory by postulating that the membrane has fixed amphoteric groups.
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PMID:Effects of pH and ionic strength on the potassium system in the internally perfused giant barnacle muscle fibre. 24 Oct 51

Treatment of unanesthetized castrated adult male rats every 3 h for 48 h with either 5 microgram of arginine vasotocin (AVT) and/or 1 microgram luteinizing hormone-releasing hormone (LRH) caused a significant inhibition of plasma levels of luteinizing hormone (LH) and compared to castrated control rats receiving diluent only. However, the intravenous (iv) injection of 1 microgram of AVT into urethane-anesthetized male rats which had been castrated for 0, 24 or 48 h did not affect plasma levels of LH at 10, 20 or 60 min following injection compared to their respective diluent-treated castrated control rats. Similarly, the iv injection of either 100 ng, 1 microgram or 10 microgram AVT was unable to acutely affect plasma levels of LH in intact male rats. Following the iv injection of 2 doses of 50 ng LRH spaced 1 h apart in anesthetized castrated male rats, 2 peaks of equal magnitude in plasma LH were noted. Castrated rats treated with 2 injections spaced 1 h apart of LRH + AVT had significantly higher plasma levels of LH than did rats treated with LRH alone. In subsequent studies, both AVT and arginine vasopressin were observed to augment the plasma response of LH to an injection of LRH whereas oxytocin had no effect. A single injection of AVT + LRH significantly augmented the plasma titers of LH compared to levels observed in LRH-treated control rats as did a second injection 1 h later. The administration of cyproterone acetate sc for 2 days by itself had no effect on plasma LH but in conjunction with LRH caused a marked rise in plasma LH compared to intact rats treated with LRH alone. AVT in combination with LRH and cyproterone acetate caused a significant elevation in plasma LH at 60 min post-injection when compared to plasma levels of rats treated with LRH alone or the combination of LRH and cyproterone acetate. It is concluded that acute intravenous injections of AVT augment the LH-releasing activity of LRH; chronic treatment for 48 h, however, with LRH + AVT leads to a significant depression of plasma LH perhaps due to an exhaustion of the releasable pool of LH in the anterior pituitary.
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PMID:Interaction of luteinizing hormone-releasing hormone, cyproterone acetate and arginine vasotocin on plasma levels of luteinizing hormone in intact and castrated adult male rats. 37 36

In the teleost, Fundulus grandis, injections of prolactin early in the light phase cause an immediate 50% depression in the rate of hepatic lipogenesis ([14C]acetate incorporation); 10 h later, that rate has returned to levels not different from controls. Injections of prolactin late in the light phase cause an even more dramatic immediate depression of lipogenesis (79%) followed by a gradual increase in lipogenic rate which is 2.6 times higher than the control rate after 24 h. The stimulation of lipogenesis by prolactin is blocked by simultaneous treatment with indomethacin, an inhibitor of prostaglandin synthesis. These circadian phase-dependent effects of prolactin on hepatic lipogenesis are discussed with reference to possible mechanisms of action exerted by endogenous prolactin rhythms.
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PMID:Circadian phase-dependent prolactin mechanisms in hepatic lipogenesis of a teleost. 51 47

Rats were kept in barochamber for 2 hours at the pressure of 240 mm Hg after subcutaneous administration of (1)14C-acetate. Hypobaric hypoxia caused depression in the incorporation of labeled acetate similar in both phospholipid (PL) components. But the dependence of depression in the metabolic rate upon hypothermia which accompanied hypoxia was more pronounced for hydrophobic portion of PB (carbon skeleton of fatty acids) than for hydrophilic one. Similarity in the degree of the hypoxia induced depression of incorporation of the precursors containing labeled phosphorus and carbon allows one to suggest that the carbon-containing parts of PL hydrophilic components (glycerol and nitrogen bases) and residues of ortho-phosphoric acid respond to hypoxia as a whole.
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PMID:[Effect of hypobaric hypoxia on the acetate-1-14C incorporation rate in hydrophilic and hydrophobic brain phospholipid components]. 51 97

The effect of verapamil on Ca2+ and Mg2+ accumulation was investigated in isolated rat kidney cortex mitochondria. For the 50% inhibition of Ca2+ accumulation, 2 x 10(-4) M verapamil concentration was required in the presence of ATP (2 mM) and phosphate (5 mM). Omission of phosphate from the medium increased the inhibitory effect of verapamil on Ca2+ accumulation. Verapamil had no effect on Ca2+ accumulation in the presence of both ATP and succinate (7.8 mM), but further addition of phosphate resulted in a significant inhibition of Ca2+ accumulation by verapamil. Mg2+ accumulation of mitochondria was similarly depressed by verapamil. The same tendency was found as for the modification of verapamil effect by acetate in mitochondrial Ca2+ and Mg2+ accumulation. Succinate oxidation of mitochondria was not affected by verapamil in the absence of phosphate, but was inhibited by verapamil in the presence of phosphate. Therefore, it seemed reasonable to assume that the depression of Ca2+ and Mg2+ transport of mitochondria by verapamil is modulated by permeant anions.
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PMID:Effect of verapamil on the calcium and magnesium transports of rat kidney cortex mitochondria. 53 83

Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.
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PMID:Acetate fails to reverse myocardial depression in dogs anesthetized with halothane. 56 99

The effect of cyproterone acetate (CA) on the production of the male-originating oestrus-inducing pheromone in the Indian field mouse, Mus booduga Gray was investigated. The anoestrus induced in regularly cycling females by unisexual grouping was reversed by exposure to intact males. The majority of male-exposed females returned to oestrus within seven days, with a peak on the fourth-day. By contrast, exposure to CA-treated males failed to induce oestrus in grouped females. Since CA is a potent antiandrogen, the inability of CA-treated males to induce oestrus in females is interpreted as due to the depression of the production of the androgen-dependent pheromone. The results provide evidence in favour of the concept that the oestrus-inducing pheromone in the Indian field mouse is associated with androgens either directly or indirectly through some androgen-dependent gland.
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PMID:Suppression of oestrus-inducing pheromone production in the Indian field mouse, Mus booduga Gray, by treatment with an antiandrogen. 57 50

The effect of regular hemodialysis (HD) with dialyzate containing acetate was evaluated in 20 patients. After dialysis, a significant increase in limb blood flow was found (P less than 0.01) while the mean arterial blood pressure remained unchanged indicating a significant decrease in peripheral vascular resistance after HD (P less than 0.01). Cardiac function was evaluated using the ratio of the preejection period to left ventricular ejection time (PEP/ET); this value showed a significant increase after HD suggesting depression of cardiac function (P less than 0.001). The study was repeated substituting bicarbonate for acetate in 13 of the 20 patients. Under these conditions, limb blood flow and peripheral vascular resistance showed no significant change though mean arterial blood pressure decreased significantly (P less than 0.01). The ratio, PEP/ET, showed a significant increase after HD (P less than 0.01), but the value was significantly lower than that found after HD with dialyzate containing acetate (P less than 0.05). Changes in the serum levels of calcium, potassium, pH and body weight could not explain the differences found after HD with the two kinds of dialyzate. The results of the present study suggest strongly that acetate exerts a depressant action on the cardio-vascular system.
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PMID:Depressant action of acetate upon the human cardiovascular system. 58 78


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