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: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in locomotor activity, body temperature, and body weight gain, and the enhancement of thiopental-induced sleep were investigated in rats as indices of the functional changes in the CNS caused by methyl bromide (CH3Br) exposure. The correlations of these behavioral changes with CH3Br metabolism are discussed. The LC50 value and its 95% confidence limits for an 8-hr exposure of CH3Br was 302 ppm (267-340) ppm. Effects were examined following exposure to 63, 125, 188, or 250 ppm CH3Br for 8 hr. CH3Br concentrations as low as 63 ppm remarkably enhanced the sleep-inducing potency of thiopental, but CH3Br exerted no effect on thiopental metabolism. The body temperature and body weight gain were decreased at exposure to concentrations of 125 ppm or higher, and locomotor activity was reduced at 188 ppm or higher. These effects were reversible and, at 24 hr after the exposure, locomotor activity and body temperature were almost the same as in control rats. In a time-course study of CH3Br, bromine, and methyl alcohol, CH3Br was rapidly eliminated from rat tissues following the cessation of exposure, with a half-life of about 30 min in the early post-exposure period. In contrast, the elimination rate of bromine was very slow, with a half-life about 5 days. The methanol amount was below that reported to induce the changes in CNS functions. These results suggest that the CNS depression caused by CH3Br exposure may be due to the CH3Br molecule or the methyl moiety incorporated into tissues and may not be attributable to bromine or methanol. A linear relationship was obtained between bromine amounts in blood and the exposure concentration or duration. This result suggests the possibility that the extent of CH3Br exposure may be estimated from the bromine quantities in blood.
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PMID:Neurotoxicity and metabolism of methyl bromide in rats. 406 Jan 47

The neuromuscular junctions from diaphragm, soleus, and extensor digitorum longus (EDL) muscles of male albino rats were assessed for morphological alterations following acute (30-min) and subacute (2-day) exposure to pyridostigmine bromide in Mestinon-equivalent buffer. These muscles were selected to compare the effects of the drug on muscles of different fiber type composition. The diaphragm has approximately equal numbers of type I and type II fibers while the soleus and EDL possess primarily type I and type II fibers, respectively. Pyridostigmine was administered to each acute-exposure animal by a single subcutaneous injection of 0.36 mg/kg pyridostigmine and to each subacute-exposure animal by a subcutaneously implanted osmotic minipump containing 10 mg/ml pyridostigmine. Both treatments resulted in whole blood cholinesterase (ChE) depression of approximately 60-70% as determined by radiometric assay. Control animals received only Mestinon-equivalent buffer. Both acute and subacute exposures resulted in morphological alteration of the neuromuscular junctions (NMJs) of all three muscles, although considerable variation in the extent of damage occurred even within individual NMJs. The most frequently observed presynaptic alterations were mitochondrial damage and partial withdrawal of nerve terminal branches (partial denervation). Post-synaptic changes included occasional rarefaction of mitochondrial matrices and disruption of the myofibrillar organization in small numbers of subjunctional sarcomeres. The data indicate that acute or subacute exposure to pyridostigmine bromide at a whole blood ChE depression of 60-70% results in similar alterations to the NMJs of three muscles with substantially different fiber type compositions. Although the severity of the damage varies from fiber to fiber, the variability appears random and not related to a specific fiber type or dosage regimen.
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PMID:Neuromuscular toxicity of pyridostigmine bromide in the diaphragm, extensor digitorum longus, and soleus muscles of the rat. 409 93

The inotropic effects of five non-depolarizing muscle relaxants were examined using an isolated canine heart muscle preparation. Except for fazadinium, all drugs were studied in their commercially available forms. d-Tubocurarine chloride (dTc) and metocurine iodide (MTC) produced dose-dependent decreases in isometric force (F) and the maximum velocity of force development (dF/dt) at concentrations greater than 22.5 x 10(-3) g/L for dTc and greater than 15.0 x 10(-3) g/L for MTC, concentrations which are 3 and 6 times higher than estimated clinical serum concentrations, respectively. Myocardial depression was about 3 times less with MTC than with dTc at equipotent concentrations. The degree of depression in F and dF/dt produced by MTC was almost identical with that produced by phenol, a preservative of MTC, indicating that MTC-induced myocardial depression may be due to the effect of the preservative. Pancuronium bromide (PC) produced a dose-dependent increase in F and dF/dt and decrease in the time to peak force. PC-induced changes in F, dF/dt, and time to peak force were inhibited by administration of propranolol 10(-6) M. The results indicate that PC possesses a positive inotropic effect mediated by beta-adrenergic stimulation. Alcuronium chloride did not change F or dF/dt at concentrations from 5.0 x 10(-3) to 60.0 x 10(-3) g/L. Frazadinium bromide increased F and dF/ dt slightly at a low concentration (1.875 x 10(-2) g/L), but further increases in its concentration returned the values of F and dF/dt to control levels. F and dF/dt were not altered in vitro by concentrations of relaxants that would be anticipated in plasma in vivo in patients given clinically effective doses of 0.3 mg/kg of dTc, 0.1 mg/kg of MTC or PC, 0.2 mg/kg of alcuronium chloride, or 0.75 mg/kg of fazadinium bromide.
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PMID:Inotropic effects of non-depolarizing muscle relaxants in isolated canine heart muscle. 610 62

The accessibility of immobilized DNA has been shown to depend more crucially on the method of immobilization than on the type of support used for fixation. When sonicated denatured DNA is coupled via diazotization or via cyanogen bromide reaction to solid Sephadex G-25 and Cellex 410 or to macroporous Sephacryl S-500 and Sepharose C1-6B its accessibility varies from 100 to 24 percent. Generally the loss of accessibility is linked to a depression of the melting temperature of DNA helices formed on the support. This correlation shows a characteristic course for a particular coupling method. DNA coupled under denaturing conditions may become totally inaccessible when only 3 percent of its bases are involved in the covalent linkage. Kinetic experiments with sonicated E.coli DNA have shown that the rate constants for renaturation or hybridization reactions are very similar for DNA immobilized by different methods to solid or macroporous supports. Generally the second order rate constant for a heterogeneous reaction (between mobile and immobilized DNA) is about one order of magnitude smaller than that of the analogous homogeneous reaction (in solution).
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PMID:Immobilization of denatured DNA to macroporous supports: II. Steric and kinetic parameters of heterogeneous hybridization reactions. 618 22

Cell lines resistant to ethidium bromide have been developed from cultured mammalian BHK21/C13 cells and these same cells transformed by Rous sarcoma virus (C13/B4). Cells resistant to 2 micrograms ethidium bromide per milliliter have been cloned. One clone of the control and one of the virus-transformed cell lines has been employed for characterization. The resistant cells, in the presence of 2 micrograms ethidium bromide/ml, grow at approximately the same rate as the untreated parental cells. The control cells possess a "normal" karyotype (44 chromosomes), while the corresponding ethidium bromide mutant has a reduced chromosome number of 41 and a number of translocations. The mitochondria displayed morphological alterations compared to the parental lines during the transition phase prior to the isolation of the ethidium bromide-resistant cells. The mitochondria of the ethidium bromide-resistant mutants appear somewhat enlarged with a normal morphology. The effect of ethidium bromide on selected respiratory enzymes in normal and virus-transformed ethidium bromide-resistant baby hamster kidney cells was determined. Ethidium bromide-resistant cells exhibited a depressed level of cytochrome aa3. This depression could not be reversed by growth in ethidium bromide-free media. Ethidium bromide-resistant cells possessed the same cytochrome b, c, and c1 levels per cell as their corresponding parental lines. Purified mitochondria isolated from virus-transformed ethidium bromide-resistant cells exhibited a depression in cytochrome oxidase-specific activity, while the ethidium bromide-resistant control cells did not. All cell lines studied showed a depression in NADH-ferricyanide and NADH-cytochrome c reductase-specific activities relative to their parental BHK21/C13 cells. No increase was observed in virus-transformed ethidium bromide-resistant cells. Ethidium bromide-resistant control cells exhibited a two-fold increase in oligomycin-insensitive adenosine triphosphatase activity relative to their parental cells. All of the cell lines studied possessed equivalent oligomycin-sensitive adenosine triphosphatase-specific activity except for the virus-transformed, dye-resistant mutant, whose activity was increased.
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PMID:Control and virus-transformed baby hamster kidney cells resistant to ethidium bromide. I. Characterization and the respiratory enzymes. 625 Oct 98

Effects of TRH and pentobarbital alone, and in combination, on local cerebral glucose utilization of rats were studied by the autoradiographic 2-deoxy[14C]glucose method. TRH (5 mg/kg i.v.) reduced the rate of cerebral glucose utilization slightly in the whole brain. Locally, significant depression was observed in the following structures: frontal and visual cortices, hippocampus Ammon's horn and dentate gyrus, medial and lateral geniculate bodies, nucleus accumbens, caudate-putamen, substantia nigra, pontine gray matter, superior colliculus, superior olivary nucleus, vestibular nucleus, lateral lemniscus and cerebellar cortex. Pentobarbital (30 mg/kg i.v.) produced a marked and diffuse reduction in the rate of glucose utilization throughout the brain. TRH given 15 min after the administration of pentobarbital markedly shortened the pentobarbital sleeping time and caused some reversal of the depression in local cerebral glucose utilization produced by pentobarbital. These effects were almost completely abolished by pretreatment with intracerebroventricular injection of atropine methyl bromide (20 microgram/rat). These results indicate that although TRH acts to cause a reduction in the rate of cerebral glucose utilization, it reverses the depression induced by pentobarbital, via a cholinergic mechanism, in a number of structures, some of which are related to monoaminergic systems and the reticulo-thalamo-cortical activating system.
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PMID:Effect of thyrotropin-releasing hormone (TRH) on local cerebral glucose utilization, by the autoradiographic 2-deoxy[14C]glucose method, in conscious and pentobarbitalized rats. 677 68

Stimulation of taste receptors with sodium chloride, sodium acetate, sodium propionate, and the respective potassium salts gave concentration-response profiles, measured electrophysiologically, which are remarkably consistent with a two-state allosteric mechanism. The allosteric constant or equilibrium constant for the transition between the active and inactive receptor states is low, resulting in a condition in which small differences in ion affinities for the two states are sufficient to significantly alter the equilibrium. Receptor activators, such as sodium ion, displaced the equilibrium toward the active receptor state by virtue of a higher affinity for that state, whereas receptor inhibitors, such as acetate and propionate ions, displaced the equilibrium in the opposite direction as a result of a higher affinity for the inactive state. The low allosteric constant increased about 10-fold after treatment with the protein modification reagent dimethyl(2-hydroxy-5-nitrobenzyl)sulfonium bromide, resulting in a marked reduction in the response to sodium chloride and sodium propionate without a significant change in ion affinities. In order to fully resolve the potassium response characteristics, it was necessary to consider both a potassium activation site and a potassium inhibition site. Analysis of the response from sodium chloride/potassium chloride mixtures showed that sodium ion is competitive with potassium binding at the activation site but not the inhibition site. With potassium propionate as the stimulus, the effect of both a receptor activator and a receptor inhibitor was quantitatively consistent with depression of the response below a water baseline level at low stimulus concentrations. Estimation of active and inactive state dissociation constants for each anion and cation permitted accurate prediction of the response magnitude for a range of cation ratios in sodium chloride/potassium chloride mixtures and anion ratios in sodium chloride/sodium propionate mixtures. The association of salty taste with receptor activators and bitter taste with receptor inhibitors may be relevant to the generation of these taste qualities.
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PMID:Sodium and potassium salt stimulation of taste receptor cells: an allosteric model. 692 15

The level of thymus-derived lymphocytes was assessed by determining the per cent of cells which formed non-immune rosettes with 2-Aminoethyl isothiouronium bromide treated sheep erythrocytes in the peripheral blood of 20 (14 bullocks and 6 cows) histopathologically confirmed cases of bovine squamous cell carcinoma of horn (horn cancer) and an equal number of age-matched control animals. A significantly marked (P less than 0.01) depression in the per cent erythrocyte-rosette forming cell count was observed in horn cancer affected bullocks and cows as compared to the values in unaffected control animals. The decrease in the level of these cells was comparatively more marked in animals which were clinically in advanced stages of the disease.
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PMID:Rosette forming T-lymphocyte levels in the peripheral blood of cattle affected with squamous cell carcinoma of horn. 698 5

Acute administration of triethyltin (TET) produces a well-described sequence of pathological events characterized by intramyelinic vacuolation, edema, and histotoxic hypoxia. Recent behavioral studies have attempted to characterize the functional consequences of TET exposures. In this study, the effects of exposure on the visual evoked response (VER) and hippocampal afterdischarge (AD) were determined. Rats were administered either 0, 0.188, 0.375, 0.75, or 1.50 mg/kg TET bromide IP each day for 6 consecutive days. TET increased latencies of P1, N1, P2, N2, and N3 peaks of the VER. The increased latencies are consistent with delayed conduction produced by alterations in the myelin of the optic nerve. TET increased the frequency of spikes within ADs, increased the severity of postictal EEG depressions, and prolonged recovery of excitability following ADs. These effects may be partially explained as reflecting a generalized CNS depression.
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PMID:Acute triethyltin exposure: effects on the visual evoked potential and hippocampal afterdischarge. 708 57

1 Intracellular recordings were made from cells of the sinoatrial (S-A) node region and from atrial muscle fibres of rabbit hearts. The effects of sodium salicylate and 5-bromo salicylate on various parameters of the membrane action potential were studied.2 5-Bromo salicylate (30-100 muM) and sodium salicylate (300-500 muM) caused a dose-dependent decrease in the frequency of discharge of the SA node cells. Applications of atropine (2.6 muM) with propranolol (3.3 muM) did not affect the negative chronotropic effect, whereas adrenaline (5 muM) reversed it.3 Depolarization and shortening of the action potential duration were found in atrial muscle fibres after the application of 5-bromo salicylate (60-100 muM). The reduction of the action potential duration (APD) was not affected by atropine (2.6 muM).4 Higher concentrations of 5-bromo salicylate (> 100 muM) also caused a dose-dependent reduction in the action potential amplitude (APA), in the overshoot (OS) of the action potential and in the maximum rate of rise of the action potential (V(max)). All these effects were completely reversed on washing.5 Substitution of the NaCl of the bathing Tyrode solution by an equimolar concentration of Na isethionate did not affect the plateau depression induced by the salicylates in atrial muscle fibres.6 After increasing the K concentration to 27 mM in the presence of isoprenaline (1 muM), ;slow responses' were obtained upon stimulation. 5-Bromo salicylate (20-60 muM) and sodium salicylate (100 muM) decreased reversibly the amplitude and the rate of rise of the ;slow response'.7 A four fold increase in Ca concentration of the standard Tyrode solution did not antagonize the plateau depression of atrial muscle fibres or the negative chronotropism induced by salicylates.8 Addition of CsCl (10 mM) to the Tyrode solution did not affect the shortening of the APD induced by the salicylates in atrial muscle fibres.9 When the K concentration in the Tyrode solution was increased from 2.7 mM to 5.4 mM, the effects of 5-bromo salicylate on the APA, OS and V(max) were potentiated. However, a significant reduction in the shortening of the APD produced by the salicylate was observed.10 It is suggested that the salicylates possibly depress the slow inward current in both S-A node cells and atrial muscle fibres of the rabbit heart. In atrial muscle fibres, a concomitant increase in the outward potassium current is probably involved.
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PMID:Electrophysiological effects of the salicylates on isolated atrial muscle of the rabbit. 713 89


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