UMLS:C0011570 - FACTA Search

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Wadi El Raiyan is a great depression located southwest of Cairo in the western desert of Egypt, one of the most arid regions of the world. In 1973, Wadi El Raiyan was connected with the agricultural wastewater drainage system of the El Faiyum province to provide a reservoir for the wastewater that exceeded the capacity of Lake Qarun north of the province. Pollutants from agricultural waste including pesticides and fertilizers as well as other effluents of industrial activities and runoffs certainly will pass into the biotic elements of the ecosystem. This report presents the status of inorganic pollutants including anions, cations, and trace metals in the two lakes and the surrounding springs of Wadi El Raiyan using ion chromatography, ion-selective electrodes, and inductively coupled plasma emission spectroscopy. The report also includes the levels of selected metals in the vegetation community of the area. The result of this investigation revealed a great improvement in water quality of the Wadi El Raiyan lakes compared to 1988 report by Saleh et al. Mercury was not detected in any of the samples and the level of lead was significantly reduced. Cadmium levels were much higher than those seen earlier. The higher level of cadmium might be used as an indicator to track the contamination of water by human waste. Concentrations of common anions were not significantly different from those reported earlier. However, an increase in the level of cyanide was observed. Levels of heavy metals in vegetation around the lakes were also found to be lower than previously reported.
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PMID:Monitoring Wadi El Raiyan lakes of the egyptian desert for inorganic pollutants by ion-selective electrodes, ion chromatography, and inductively coupled plasma spectroscopy. 1070 52

Nitric oxide (NO) is endogenously generated from two constitutively expressed nitric oxide synthase (NOS) isoforms, i.e., neuronal (NOS-1) and endothelial (NOS-3). Both isoforms are localized within the carotid body. Previous studies have shown endogenously generated NO modulates carotid body activity. In the present study, we examined the relative contribution of NO generated by NOS-1 and NOS-3 in respiratory reflexes arising from the carotid body. Experiments were performed on mutant mice deficient in NOS-1 or NOS-3. Wild-type (WT) mice, which contained both isoforms, served as controls. Respiration was monitored in unanesthetized mice by plethysmography. In anaesthetized mice, efferent phrenic nerve activity was monitored as index of breathing. We examined the effects of hypoxia (12% O2), cyanide and brief hyperoxia (Dejour's test) on respiration. In NOS-1 mutant mice, the ventilatory response to hypoxia (12% O2) were significantly augmented, compared to wild-type (WT) mice. By contrast, NOS-3 mutant mice displayed significantly blunted respiratory responses to hypoxia compared to WT controls. The responses to cyanide were augmented in NOS-1; whereas they were blunted in NOS-3 mutant mice. Respiratory depression in response to brief hyperoxia was more pronounced in NOS-1, while it was nearly absent in NOS-3 mutant mice. These results demonstrate that NO produced by the neuronal and endothelial NOS isoforms have different modulatory roles in carotid body chemosensitivity.
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PMID:Peripheral chemosensitivity in mutant mice deficient in nitric oxide synthase. 1084 97

Ethylazinphos increases the passive proton permeability of lipid bilayers reconstituted with dipalmitoylphosphatidylcholine (DPPC) and mitochondrial lipids. A sharp increase of proton permeability is detected at insecticide/lipid molar ratios identical to those inducing phase separation in the plane of DPPC bilayers, as revealed by differential scanning calorimetry (DSC). Ethylazinphos progressively depresses the transmembrane potential (DeltaPsi) of mitochondria supported by piruvate/malate, succinate, or ascorbate/TMPD. Additionally, a decreased depolarization induced by ADP depends on ethylazinphos concentration, reflecting a phosphorylation depression. This loss of phosphorylation is a consequence of a decreased DeltaPsi. A decreased respiratory control ratio is also observed, since ethylazinphos stimulates state 4 respiration and inhibits ADP-stimulated respiration (state 3). Ethylazinphos concentrations up to 100 nmol/mg mitochondrial protein increase the rate of state 4 together with a decrease in DeltaPsi, without significant perturbation of state 3 and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP)-uncoupled respiration. For increased insecticide concentrations, the state 3 and FCCP-uncoupled respiration are inhibited to approximately the same extent. The perturbations are more pronounced when the energization is supported by pyruvate/malate and less effective when succinate is used as substrate. The present data, in association with previous DSC studies, indicate that ethylazinphos, at concentrations up to 100 nmol/mg mitochondrial protein, interacts with the lipid bilayer of mitochondrial membrane, changing the lipid organization and increasing the proton permeability of the inner membrane. The increased proton permeability explains the decreased oxidative phosphorylation coupling. Resulting disturbed ATP synthesis may significantly underlie the mechanisms of ethylazinphos toxicity, since most of cell energy in eukaryotes is provided by mitochondria.
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PMID:Ethylazinphos interaction with membrane lipid organization induces increase of proton permeability and impairment of mitochondrial bioenergetic functions. 1155 19

1. L-type Ca2+ channels play an important role in vital cell functions such as muscle contraction and hormone secretion. Both a voltage-dependent and a Ca2+-dependent process inactivate these channels. Here we present evidence that inhibition of the mitochondrial Ca2+ import mechanism in rat (Sprague-Dawley) ventricular myocytes by ruthenium red (RR), by Ru360 or by carbonyl cyanide m-chlorophenylhydrazone (CCCP) decreases the magnitude of electrically evoked transient elevations of cytosolic Ca2+ concentration ([Ca2+]c). These agents were most effective at stimulus rates greater than 1 Hz. 2. RR and CCCP also caused a significant delay in the recovery from inactivation of L-type Ca2+ currents (I(Ca)). This suggests that sequestration of cytosolic Ca2+, probably near the mouth of L-type Ca2+ channels, into mitochondria during cardiac contractile cycles, helps to remove the Ca2+-dependent inactivation of L-type Ca2+ channels. 3. We conclude that impairment of mitochondrial Ca2+ transport has no impact on either L-type Ca2+ currents or SR Ca2+ release at low stimulation frequencies (e.g. 0.1 Hz); however, it causes a depression of cytosolic Ca2+ transients attributable to an impaired recovery of L-type Ca2+ currents from inactivation at high stimulation frequencies (e.g. 3 Hz). The impairment of mitochondrial Ca2+ uptake and subsequent effects on Ca2+ transients at high frequencies at room temperature could be physiologically relevant since the normal heart rate of rat is around 5 Hz at body temperature. The role of mitochondria in clearing Ca2+ in the micro-domain near L-type Ca2+ channels could be impaired during high frequencies of heart beats such as in ventricular tachycardia, explaining, at least in part, the reduction of muscle contractility.
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PMID:Mitochondria regulate inactivation of L-type Ca2+ channels in rat heart. 1160 Jun 74

Beyond their role in generating ATP, mitochondria have a high capacity to sequester calcium. The interdependence of these functions and limited access to presynaptic compartments makes it difficult to assess the role of sequestration in synaptic transmission. We addressed this important question using the calyx of Held as a model glutamatergic synapse by combining patch-clamp with a novel mitochondrial imaging method. Presynaptic calcium current, mitochondrial calcium concentration ([Ca(2+)](mito), measured using rhod-2 or rhod-FF), cytoplasmic calcium concentration ([Ca(2+)](cyto), measured using fura-FF), and the postsynaptic current were monitored during synaptic transmission. Presynaptic [Ca(2+)](cyto) rose to 8.5 +/- 1.1 microM and decayed rapidly with a time constant of 45 +/- 3 msec; presynaptic [Ca(2+)](mito) also rose rapidly to >5 microM but decayed slowly with a half-time of 1.5 +/- 0.4 sec. Mitochondrial depolarization with rotenone and carbonyl cyanide p-trifluoromethoxyphenylhydrazone abolished mitochondrial calcium rises and slowed the removal of [Ca(2+)](cyto) by 239 +/- 22%. Using simultaneous presynaptic and postsynaptic patch clamp, combined with presynaptic mitochondrial and cytoplasmic imaging, we investigated the influence of mitochondrial calcium sequestration on transmitter release. Depletion of ATP to maintain mitochondrial membrane potential was blocked with oligomycin, and ATP was provided in the patch pipette. Mitochondrial depolarization raised [Ca(2+)](cyto) and reduced transmitter release after short EPSC trains (100 msec, 200 Hz); this effect was reversed by raising mobile calcium buffering with EGTA. Our results suggest a new role for presynaptic mitochondria in maintaining transmission by accelerating recovery from synaptic depression after periods of moderate activity. Without detectable thapsigargin-sensitive presynaptic calcium stores, we conclude that mitochondria are the major organelle regulating presynaptic calcium at central glutamatergic terminals.
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PMID:Presynaptic mitochondrial calcium sequestration influences transmission at mammalian central synapses. 1212 46

We investigated how inhibition of mitochondrial Ca2+ uptake affects transmitter release from mouse motor terminals during brief trains of action potentials (500 at 50 Hz) in physiological bath [Ca2+]. When mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria with antimycin A1 or carbonyl cyanide m-chlorophenyl-hydrazone, the stimulation-induced increase in cytosolic [Ca2+] was greater (> 10 microM, compared to < or = 1 microM in control solution), the quantal content of the endplate potential (EPP) depressed more rapidly (approximately 84 % depression compared to approximately 8 % in controls), and asynchronous release during the stimulus train reached higher frequencies (peak rates of approximately 6000 s-1 compared to approximately 75 s-1 in controls). These effects of mitochondrial depolarization were not accompanied by a significant change in EPP quantal content or the rate of asynchronous release during 1 Hz stimulation, and were not seen in oligomycin, which blocks mitochondrial ATP synthesis without depolarizing mitochondria. Inhibition of endoplasmic reticular Ca2+ uptake with cyclopiazonic acid also had little effect on stimulation-induced changes in cytosolic [Ca2+] or EPP amplitude. We hypothesize that the high rate of asynchronous release evoked by stimulation during mitochondrial depolarization was produced by the elevation of cytosolic [Ca2+], and contributed to the accelerated depression of phasic release by reducing the availability of releasable vesicles. During mitochondrial depolarization, the post-tetanic potentiation of the EPP observed under control conditions was replaced by a post-tetanic depression with a slow time course of recovery. Thus, mitochondrial Ca2+ uptake is essential for sustaining phasic release, and thus neuromuscular transmission, during and following tetanic stimulation.
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PMID:Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals. 1258 98

Single skeletal muscle fibres from rat and cane toad were mechanically skinned and stimulated either electrically by initiating action potentials in the sealed transverse (t-) tubular system or by ion substitution causing depolarisation of the t-system to pre-determined levels. Depression of mitochondrial ATP-producing function with three diverse mitochondrial function antagonists (azide: 1-10 mM; oligomycin 1 microg ml-1 and carbonyl cyanide 4-trifluoromethoxyphenylhydrazone (FCCP) 1 microM), under conditions in which the cytosolic ATP was maintained high and constant, invariably reduced the excitability of rat fibres but had no obvious effect on the excitability of toad fibres, where mitochondria are less abundant and differently located. The reduction in excitability linked to mitochondria in rat fibres appears to be caused by depolarisation of the sealed t-system membrane. These observations suggest that mitochondria can regulate the functional state of mammalian muscle cells and have important implications for understanding how the balance between ATP utilisation and ATP production is regulated at the cellular level in general and in mammalian skeletal muscle fibres in particular.
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PMID:A novel signalling pathway originating in mitochondria modulates rat skeletal muscle membrane excitability. 1261 17

Using optical recording methods in the rat lateral septal nucleus (LSN) slice, we examined the question of whether antecedent hypoglycemia protects neurons from the adverse effects of subsequent hypoglycemic stimuli. The first exposure of LSN neurons to glucose deprivation for 15 min produced a marked depression of neuronal activity. The neuronal activity recovered by reapplication of glucose to the neurons. In neurons previously exposed to glucose deprivation, subsequent applications of glucose-free artificial cerebrospinal fluid (ACSF) produced only weak depression of the neuronal activity. The contribution of monocarboxylate transporters to this adaptation of neuronal activity to repeated glucose deprivation was examined in LSN neurons. alpha-Cyano-4-hydroxycinnamate (4-CIN, 100 microM), an inhibitor of the monocarboxylate transporters, did not significantly affect the depression of the neuronal activity induced by the first glucose deprivation. However, in the presence of 4-CIN (100 microM), a second glucose deprivation produced a typical depression of the neuronal activity, indicating that 4-CIN had nullified the adaptation of neuronal activity to a second glucose deprivation. Cytochalasin B (CCB, 20 microM), an inhibitor of glucose transporters, depressed the neuronal activity in the presence of 11 mM glucose. Pyruvate (11 mM) partially restored the neuronal activity depressed by pretreatment with CCB (20 microM) for 30-40 min. These results suggest that antecedent glucose deprivation stimulates monocarboxylate-transporters to supply energy substrates to LSN neurons, thus protecting the neurons against subsequent glucose deprivation. .
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PMID:Monocarboxylate transporters contribute to the adaptation of neuronal activity to repeated glucose deprivation in the rat lateral septal nucleus. 1274 Aug 65

It has been shown that helium has the ability to affect variously the rates of certain metabolic reactions in vitro as compared to nitrogen. An attempt has been made to approximate the sites of action in mouse liver preparations. The following results have been obtained by the substitution of a mixture of 80 per cent helium and 20 per cent oxygen for air: (a) An increase in the rate of oxygen consumption and carbon dioxide production to the same degree, the respiratory quotient remaining unchanged. (b) A decrease in the magnitude of cyanide inhibition. The effectiveness of helium increases with the degree of the cyanide inhibition. (c) No effect on the activity of slices which have been poisoned with fluoride when either lactate or pyruvate has been added as a substrate. (d) A change in the rate, and the slope of the curve of oxygen consumption in liver homogenates which are utilizing pyruvate as a substrate. The use of helium relative to nitrogen under anaerobic conditions causes: (a) A depression of the glycolytic rates in both mouse liver slices and diaphragm. (b) An increase in the carbon dioxide evolution and lactic acid production of mouse liver homogenates oxidizing either glucose and hexose diphosphate, or hexose diphosphate alone. In neither slices nor homogenates does the addition of fluoride and the use of pyruvate as the hydrogen acceptor alter the fundamental response of the preparations. The following hypotheses have been advanced and discussed in order to explain the observed phenomena: 1. Helium does not alter the substrate utilized by the tissue. 2. The gas interferes in some way with the cyanide-cytochrome oxidase bond, but may not affect cytochrome oxidase in the absence of cyanide. 3. The citric acid cycle is not subject to the influence of helium in tissue slices, but is altered in an unexplained fashion in homogenates. It is postulated that a rearrangement of particulate surfaces may be the significant factor here. 4. The glycolytic cycle is the site of both an inhibitory and an acceleratory effect of helium. The locus of the inhibition lies above the aldolase reaction and that of the acceleration between the aldolase and enolase reactions.
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PMID:Effect of helium on the respiration and glycolysis of mouse liver slices. 1303 67

Hydrogen cyanide is a high volume production chemical that causes severe environmental problems. The toxicity of potassium cyanide (KCN) to basket willow trees (Salix viminalis) was tested. In aqueous solution, 2 mg CN l(-1) as KCN depressed the transpiration after 72 h about 50%. Trees exposed to 0.4 mg CN l(-1) in aqueous solution showed initially a depression of transpiration, but recovered. Doses of 8 and 20 mg CN l(-1) in aqueous solution were quickly mortal to the trees. At the end of the test, almost all cyanide had disappeared from the solutions. Levels of cyanide in plants were related to the toxicity, with no elevated levels of cyanide in plants exposed to 0.4 mg CN l(-1). Willows grown in sand survived 423.5 h irrigation with 20 mg CN l(-1). Willows grown in sand irrigated with 50 mg CN l(-1) died within a few days. The roots of the surviving willows were able to consume about 10 mg CN kg fresh weight(-1)h(-1). Vascular plants possess the enzymes beta-cyanoalanine synthase and beta-cyanoalanine hydrolase, which convert free cyanide to the amino acid asparagine. The in vivo capacity of woody plants (willow, poplar, elder, rose, birch) to remove cyanide was evaluated. Tests were performed with detached leaves and roots in KCN solutions of different concentrations. The highest removal capacity was obtained for basket willow hybrids (Salix viminalis x schwerinii). The Michaelis-Menten kinetics was determined. Realistic values of the half-saturation constant, K(M), were between 0.6 and 1.7 mg CN l(-1); the maximum metabolic capacity, v(max), was around 9.3 mg CN kg fresh weight(-1)h(-1). The removal of cyanide by plants might be useful in phytoremediation and treatment of wastewater from gold mining.
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PMID:Removal of cyanide by woody plants. 1457 45

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