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Results for “Chloride Ion Level”

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PubMedDate not supplied

Investigation of corrosion caused by constituents of refinery wastewater effluent used as circulating cooling water.

The corrosion rate of steel plate using single-factor, multifactor, and complex water systems was investigated via refinery wastewater effluents used as circulating cooling water. The results show that the primary corrosion factors of steel depend on the characteristics of the ions, the formation of the oxidized coating, the diffusion of dissolved oxygen, and other complex factors, although ions such as chloride, calcium, and carbonate play an important role. The corrosion rate of carbon steel exhibits two trends: The corrosion rate is high at low conductivity, increases to a maximum, and then decreases and becomes stable with increasing conductivity, as is the case with chloride, sulfate, nitrate and calcium ions. On the other hand, the corrosion rate is highest at low conductivity and then decreases and becomes stable with increasing conductivity, as is the case with carbonate, silicate, and sodium nitrate ions. Research results indicate that the anticorrosive ability is minimal at low conductivity; but is excellent at high conductivity. Pretreatment of low-conductivity water using air flotation and clarification to decrease the concentrations of chloride, calcium, and carbonate ions to a suitable level to satisfy the anticorrosion requirements is required. However, it is not necessary to significantly reduce the salt concentration or conductivity of the water by osmosis or ion exchange to obtain an anticorrosion effect when reusing wastewater effluents as circulating cooling water.

Carbon↗

PubMed1970

Mechanism of prophylaxis by silver compounds against infection of burns.

To clarify tthe mechanism by which local application of silver compounds protects burns against infection, an ion-specific electrode was used to measùre the concentration of silver ions in solutions. By this method it was shown that in burn dressings silver ions were reduced to a very low level by precipitation as silver chloride. The antibacterial effect was found to depend on the availability of silver ions from solution in contact with precipitate. Between 10(-5) and 10(-6) molar silver nitrate solution in water was rapidly bactericidal. The minimal amount of silver nitrate causing inhibition of respiration of skin in tissue culture was about 25 times the minimal concentration of silver nitrate that inhibited growth of Pseudomonas aeruginosa.

Adsorption↗

PubMed2006

Novel dosage forms and regimens for sevelamer-based phosphate binders.

Sevelamer, a nonabsorbed, calcium- and metal-free dietary phosphate binder, consists of a polyallylamine polymer backbone with a cationic charge that shows a high capacity for binding anionically charged compounds such as phosphate. The currently licensed form of sevelamer, Renagel, exists as sevelamer hydrochloride, which disassociates in the acidic environment of the stomach and early gastrointestinal tract, exchanging the chloride ions attached to the polymer backbone for phosphate ions. The resulting absorption of these chloride ions has been reported to be accompanied by a reduction in serum levels of bicarbonate in some patients. To minimize the possibility of this effect, a new salt form of sevelamer has been developed in which carbonate replaces the chloride counter ion, thereby providing a source of buffer. The majority of phosphate binders exist only in tablet form and are dosed three times per day with meals. Genzyme has developed sevelamer carbonate in tablet form and also as a powder formulation that can be taken after mixing with water. This allows for an alternate and potentially more palatable way of dosing. Preliminary data exist suggesting that once daily dosing with sevelamer hydrochloride tablets provides similar phosphate control to three times daily dosing. By providing novel dosage forms and regimens for sevelamer-based phosphate binders, Genzyme will be providing patients and health care providers additional choices and flexibility in controlling phosphorus levels in chronic kidney disease. This should translate to increased compliance and improved rates of phosphate control.

Animals↗

PubMed2000

The interrelationship between chloride ions and endothelium on alpha(1)-adrenoceptor-mediated contractions in aortic rings from Dahl normotensive and hypertensive rats.

OBJECTIVES: The effects of chloride-free buffer in the absence or presence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), or chloride channel antagonist, indanyloxyacetic acid 94 (IAA-94) on alpha(1)-adrenoceptor mediated contractions were investigated in aortic rings from Dahl salt-resistant normotensive (SRN) and salt-sensitive hypertensive (SSH) rats on a 4% salt diet. METHODS: Systolic and diastolic blood pressure were measured via intra-arterial catheters under halothane anesthesia. Subsequently, the aorta was removed and cirazoline-induced contractions were recorded in normal Krebs and chloride-free buffer using ring preparation. Guanosine 3',5'-cyclic monophosphate (cyclic GMP) content of aortic rings was also determined by scintillation proximity assay kits. RESULTS: Systolic and diastolic blood pressure of SSH (180/130+/-1/1, mean+/-S.E.; n=14) were significantly higher than those of SRN (101/76+/-1/1, mean+/-S.E.; n=14) 7 weeks after they were placed on a salt diet. While the presence of L-NAME failed to have any impact on cirazoline-induced contractions in aortic rings from SSH rats, it significantly accentuated the effects of cirazoline in tissues from SRN rats. On the other hand, IAA-94 was able to inhibit cirazoline-mediated contractions in aortic rings from both SRN and SSH rats. The removal of chloride ions potentiated contractions produced by cirazoline in tissues from SRN but not SSH rats. Moreover, cirazoline-evoked responses in tissues from SRN were not further accentuated by the inclusion of L-NAME in chloride-free buffer. Cirazoline-mediated contractions in tissues from SSH rats were not influenced by absence of chloride ions, and the presence of L-NAME. It was also apparent that the inclusion of IAA-94 in absence of chloride ions did not prevent the potentiation of responses to cirazoline. Removal of chloride ions did not significantly decrease basal cyclic GMP levels in aortic rings from either strain. CONCLUSIONS: Basal release of nitric oxide seems to make a greater contribution in the suppression of cirazoline-evoked contractions in vessels from SRN as opposed to SSH rats. Chloride channels appear to contribute to cirazoline-evoked contractions in normal Krebs but not in chloride-free buffer.

Adrenergic beta-Agonists↗

PubMed2004

Simultaneous determination of fluoride, chloride, nitrite, bromide, nitrate, phosphate and sulfate in aqueous solutions at 10(-9) to 10(-8)% level by ion chromatography.

The method of simultaneous determination of F-, Cl-, NO2-, Br-, NO3-, HPO(4)2-, SO(4)2- ions on trace level by IC using preliminary concentration and water removal from concentrating column was proposed. Detection limits were 10(-9) to 10(-8)% for sample volume 10 ml depending on the anion.

Chromatography, Ion Exchange↗

PubMed1995

A negative anion gap as a clue to diagnose bromide intoxication.

We report on a patient with bromide intoxication, presenting with confusion, disorientation, and auditory and visual hallucinations after taking a sedative medication containing bromide (mixture menopause; 15 ml containing 1 g potassium bromide) for 1 month. Blood chemistry showed a high chloride level (176 mEq/l) and a negative anion gap (-60 mEq/l). The spurious hyperchloremia was due to interference of chloride ion determination by the ion-selective electrode method with a high level of bromide in serum: 352 mg/dl (44 mEq/l). In this case the only striking abnormality which alerted the physician to the possibility of halide intoxication was the negative anion gap. Hence, a negative anion gap is an important clue which leads to the diagnosis of halide intoxication.

Acid-Base Equilibrium↗

PubMed2007

Reusable platinum nanoparticle modified boron doped diamond microelectrodes for oxidative determination of arsenite.

Boron doped diamond (BDD) macro- and microelectrodes were modified by electrodeposition of platinum nanoparticles using a multipotential step electrodeposition technique and used for the oxidative determination of arsenite, As(III). The formation of Pt nanoparticles was evident from cyclic voltammetry measurement, whereas AFM and SEM revealed the size and size distribution of deposited Pt nanoparticles. Raman spectroscopy illustrated a correlation between the typical BDD signature and the number of platinum deposition cycles. Linear sweep voltammetry performed with the modified BDD microelectrode outperformed its macrocounterpart and resulted in very low detecting currents with enhanced signal-to-noise ratios. With linearity up to 100 ppb and a detection limit of 0.5 ppb, the electrochemical system was applicable for processing tap and river water samples. Over 150 repetitive runs could be performed, and electrochemical etching of platinum allowed the reuse of the BDD microelectrode. The presence of copper and chloride ions, the two most severe interferents at levels commonly found in groundwater, did not interfere with the assay.

Arsenites↗

PubMed1994

Bactericidal potency of hydroxyl radical in physiological environments.

Rates of radiolytic inactivation of bacteria suspended in N2O-saturated solutions were dramatically increased over normal background levels when the media contained chloride or bicarbonate ions. The bacteria could be protected from this enhanced toxicity by the addition of free radical scavengers (ethanol, ascorbate, hydrogen peroxide, mannitol, glucose, EDTA, picolinic acid), indicating that the lethal reactions were extracellular in origin. Prior irradiation of chloride-containing solutions led to formation of hypochlorous acid, which was identified by detection of ring-chlorinated products when reacted with fluorescein. Prolonged irradiation of other solutions did not lead to accumulation of bactericidal agents; however, irradiation of bicarbonate-containing solutions in the presence of the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) led to formation of the EPR-detectable DMPO.CO3- adduct. The results are interpreted in terms of formation of secondary radicals, among which the carbonate and chlorine radicals are uniquely toxic to bacteria. From rate comparisons of the solution components, it was concluded that the reactions involving chloride ion are unlikely to be expressed in biological environments, but that the CO3- radical could be an important intermediary oxidant in peroxide-inflicted cellular damage, particularly in spatially confined environments such as the leukocyte phagosome.

Anti-Bacterial Agents↗

PubMed2000

Dexamethasone modulates the activity of the eel branchial Na+/K+ATPase in both chloride and pavement cells.

In fish, gills actively accumulate ions in freshwater (FW) with Na+ absorption taking place at the level of pavement cells, and excrete monovalent ions, mainly Na+ and Cl-, through the chloride cells in sea water (SW). The Na+/K+ATPase plays a crucial role in the functionality of osmoregulatory cells and we showed previously that angiotensin II modulates its activity in the eel gill (1). We here show the effects of synthetic steroid dexamethasone (DEX) on the activity of Na+/K+ATPase in both gill pavement and chloride cells from FW- and SW-adapted animals. Results showed that in the chloride cells 100 nM DEX provoked a significant increment in the activity of Na+/K+ATPase in both SW- and FW-adapted animals. This effect was greatest at 2 hours in SW, and at 6 hours in FW. The increment in the activity of the Na+/K+ATPase was dose-dependent in both environmental adaptations. Conversely, in pavement cells from FW-adapted eels 100 nM DEX decremented the activity of Na+/K+ATPase (4-fold reduction after 6 hour incubations), while in SW, DEX increased the enzyme activity of about 25% at 2 hours, and of about 55% at 6 hours. These results are consistent with the different physiological roles that pavement and chloride cells have in the two different adaptive conditions.

Animals↗

PubMedDate not supplied

[Effect of ammonium chloride on NDP(P)+-dependent glutamate dehydrogenase from bovine liver].

It was shown that NAD(P)(+)-dependent glutamate dehydrogenase from bovine liver (EC 1.4.1.3) was activated under the action of ammonium chloride in concentration which corresponded to the level of ammonium in normal blood (2-10 mM). Ammonium chloride increases the activity of glutamate dehydrogenase 1.8 times. Having enhanced the level of ammonium chloride to the amount which corresponds to the level of ammonium ions in blood during the pathology (10-25 mM), this substance inhibited the enzyme activity of glutamate dehydrogenase. Influence of 20 mM ammonium chloride on IR-spectra of NAD(P)(+)-dependent glutamate dehydrogenase in the deuterium oxide solution leads to the widening of the absorption line at 3300 cm-1 toward the higher energy. It is supposed that inhibition action of ammonium ions on the activity of glutamate dehydrogenase is connected with partial destruction of stereoregular hydrogen bonds in the enzyme molecule.

Ammonium Chloride↗

PubMed2003

Effects of dextroamphetamine, lithium chloride, sodium valproate and carbamazepine on intraplatelet Ca2+ levels.

OBJECTIVE: To explore the possible involvement of second-messenger pathways in the pathophysiology of bipolar disorder and the mechanism of action of mood stabilizers, we investigated the effects of dextroamphetamine (a model for mania) and the most widely used mood stabilizers, lithium chloride, sodium valproate and carbamazepine, on intraplatelet levels of calcium ion ([Ca2+). DESIGN: In the first part of the study, dextroamphetamine was administered in vivo in a double-blind, placebo-controlled, crossover design. In the second part of the study, platelets from untreated subjects were incubated in vitro with dextroamphetamine, lithium chloride, sodium valproate or carbamazepine. PARTICIPANTS: Fifteen healthy men between 18 and 45 years of age. OUTCOME MEASURES: Basal, thrombin-induced and serotonin- (5-HT) induced intraplatelet [Ca2+] determined by means of fura-2 fluorescent intensity. RESULTS: In vivo administration of dextroamphetamine had no effect on basal or agonist-induced intraplatelet [Ca2+]. However, in vitro basal platelet [Ca2+] was significantly higher in samples incubated with dextroamphetamine (86.8 nmol/L [standard error of the mean, SEM, 3.9], p < 0.001), lithium chloride (76.4 nmol/L [SEM 3.1], p < 0.002), sodium valproate (82.7 nmol/L [SEM 3.7], p < 0.001) and carbamazepine (84.8 nmol/L [SEM 3.3], p < 0.001) than in the controls (58.2 nmol/L [SEM 2.3]). Thrombin-induced and 5-HT-induced peak cytosolic [Ca2+] were significantly greater than control levels in samples incubated with carbamazepine (277.1 nmol/L [SEM 19.9] v. 195.8 nmol/L [SEM 12.2], p < 0.002; and 153.0 nmol/L [SEM 8.2] v. 115.4 nmol/L [SEM 5.7], p < 0.003, respectively). CONCLUSIONS: This study does not support the involvement of intraplatelet [Ca2+] in the dextroamphetamine model of mania; however, the modulation of intraplatelet [Ca2+] by the mood stabilizers lithium chloride, sodium valproate and carbamazepine implicates intracellular [Ca2+] in the therapeutic mechanisms of these drugs and the pathophysiological basis of mania.

Adolescent↗

PubMed1996

A demonstration using mouse models that successful gene therapy for cystic fibrosis requires only partial gene correction.

Quantifying the level of transgene expression necessary for phenotypic effect is an important consideration in designing somatic gene therapy protocols. A nonlinear relationship between phenotype and gene activity is predicted by control analysis for any autosomal recessive condition. The unaffected phenotype of heterozygotes for autosomal recessive disorders demonstrates that 50% of the normal level of gene expression is sufficient to prevent disease. By extension, an exaggerated and positive effect on the mutant phenotype is predicted to arise from only a small addition of normal transgene expression delivered by gene therapy. We tested this expectation directly by intercrossing mice carrying different Cftr alleles which modulate Cftr gene expression from 0 to 100%. We demonstrate that 5% of the normal level of Cftr gene expression results in a disproportionately large correction of the chloride ion transport defect (50% of normal) and essentially complete rescue of the intestinal disease (100% survival). It follows that even modest levels of transgene expression and only partial correction of CFTR channel activity may have a significant clinical impact.

Animals↗

PubMedDate not supplied

[Urine viscosity in the evaluation of homeostasis in heart surgery patients in the early postoperative period].

A total of 100 dynamic measurements of the urinary viscosity were carried out in 38 patients subjected to open-heart surgery. Biochemical parameters and levels of electrolytes were measured in the cystic urine. The viscosity of the urine was found to be unchanged from 10 to 300 sec-1. A significant increase of its level was observed only in acute renal failure and led to the development of multiorgan abnormalities. The results indicate that urine viscosity in the early postoperative period was due to pH values (r = 0.47, p < 0.05) and free hemoglobin level (r = -0.52, p < 0.01) in coronary patients and due to concentrations of sodium (r = -0.57, p < 0.01) and chloride ions (r = 0.38, p < 0.01), osmolarity (r = -0.53, p < 0.1), and protein levels (e = -0.37, p < 0.1) in patients with acquired heart diseases. These causal relations were conditioned by the postoperative directions of regular reactions of homeostasis, because in coronary disease it is virtually the same as before surgery. Contrariwise, renal perfusion has a great impact on homeostasis stabilization in new bloodflow state in patients subjected to open-heart surgery for acquired heart diseases. As molecular and cellular disorders anticipate the clinical symptoms, we came to a conclusion that increase of urine viscosity may be an early sign predicting the development of multiorgan abnormalities.

Acute Kidney Injury↗

PubMed1986

Barbiturate and benzodiazepine modulation of GABA receptor binding and function.

The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) acts primarily on receptors that increase chloride permeability in postsynaptic neurons. These receptors are defined by sensitivity to the agonist muscimol and the antagonist bicuculline, and are also subject to indirect allosteric inhibition by picrotoxin-like convulsants and enhancement by the clinically important drugs, the benzodiazepines and the barbiturates. All of these drugs modulate GABA-receptor regulated chloride channels at the cellular level assayed by electrophysiological or radioactive ion tracer techniques. Specific receptor sites for GABA, benzodiazepines, picrotoxin/convulsants, and barbiturates can be assayed in vitro by radioactive ligand binding. Mutual chloride-dependent allosteric interactions between the four receptor sites indicate that they are all coupled in the same membrane macromolecular complex. Indirect effects of barbiturates on the other three binding sites define a pharmacologically specific, stereospecific receptor. All of the activities can be solubilized in the mild detergent 3-[(3-cholamidopropyl)-dimethylammonio]propane sulfonate (CHAPS) and co-purify as a single protein complex.

Allosteric Regulation↗

PubMed1981

Chloride permeability in human red cells: influence of membrane protein rearrangement resulting from ATP depletion and calcium accumulation.

A 15% of band 3 protein, the assumed chloride channel, is associated with spectrin, the major peripheral protein of a lattice located at the red cell membrane-cytosol interface, the present study was undertaken to evaluate whether a rearrangement of the lattice modifies the functional property of band 3 protein. Such a rearrangement was modulated by depletion of cell ATP and/or by accumulation of Ca2+ ions within the cell. ATP depletion induces an inhibition of the electroneutral one-for-one chloride exchanges. Neither the modification of red cell morphology due to ATP depletion (discocyte-echinocyte transformation) nor a direct effect of the decrease in internal ATP level can account for this inhibition. On the other hand, it seems reasonable to consider that inhibition is related to the changes in membrane protein organization (formation of heteropolymers) induced by the decrease in ATP level. But it does not appear that the degree of inhibition is modified when this altered assembly of membrane protein is stabilized by disulfide linkages. Accumulation of Ca2+ ions in the cell at a relatively low concentration (10 micro M range) inhibits chloride exchange without apparent modification of the assembly of membrane proteins. This effect of calcium on chloride exchanges is speculatively denoted as a "direct" effect of calcium. Calcium loading of fresh red cells at higher concentrations (500 to 1000 micro M) obtained by use of the ionophore A23187 induces a very strong inhibition of chloride exchanges. In this case, inhibition can be reasonably accounted for by two simultaneous effects of calcium: a "direct" effect which explains half of the inhibition and an "indirect effect due to the formation of membrane protein complexes stabilized by covalent crosslinkages (activation by Ca2+ ions of a transglutaminase). It is interesting to note that intracellular calcium, whatever the level, inhibits electroneutral exchanges of chloride but increases net chloride movements.

Adenosine Triphosphate↗

PubMed2003

Bromide intoxication by the combination of bromide-containing over-the-counter drug and dextromethorphan hydrobromide.

A 30-year old woman was presented to the emergency room with marked lethargy and fever. Her physical examination showed an acneiform eruption on the face. Blood biochemistry showed a high chloride level and a negative anion gap. High blood bromide level measurements on an ion-selective electrode was noted later to cause spurious hyperchloremia with a negative anion gap. After receiving saline hydration and diuretic treatment, her serum chloride returned to normal range on hospital day nine. Slow resolution of her mental status occurred over 2 months. Her skin lesions disappeared about 5 months later. In conclusion, in face of an unusual high chloride level and a negative anion gap in a patient of long-term use of over-the-counter (OTC) agents, bromide intoxication should be included in the differential diagnosis.

Adult↗

PubMed1991

Chloride ion transport in transformed normal and cystic fibrosis epithelial cells.

The inability of beta-adrenergic agonists (eg. isoproterenol) to activate a specific apical membrane chloride channel in epithelial cells is characteristic of cystic fibrosis (CF). The study of these channels has been facilitated by the transformation of human airway epithelial cells. Clonal populations of SV40 large T-antigen transformed airway epithelial cells from both normal and cystic fibrosis individuals have been established. A limitation in the use of these cell lines has been the loss of the ability to form tight junctions after multiple subcultures. In particular, this loss appears to be associated with cell "crisis". A selection protocol that involves growing cells in medium that is high in Ca2+ and supplemented with fetal bovine serum (FBS) has been employed to facilitate progression through crisis. One cell line (1HAEo-) that has a normal phenotype and retains tight junctions post-crisis has been produced using this protocol. Immunofluorescent staining with a monoclonal antibody to the E-cadherin adhesion molecule shows a characteristic pericellular localization, indicating the presence of the junctional complex. The presence of tight junctions has been confirmed by electron microscopy. These cells produce elevated (greater than 30 fold) levels of cAMP in response to exposure to isoproterenol or forskolin. Chloride ion transport, as measured by 36Cl- efflux, is stimulated greater than 2 fold by these agents. Three post-crisis CF cell lines which grow in serum-containing medium have been established. These do not exhibit tight junctions. Elevated (greater than 25 fold) levels of cAMP are detected in these cells after addition of isoproterenol or forskolin, but this increase in cAMP is not accompanied by an increase in 36Cl-efflux. Both normal (1HAEo-) and CF cells show increased 36Cl-efflux following addition of the calcium ionophore A23187. (ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport, Active↗

PubMed2001

Insecticidal activity of glufosinate through glutamine depletion in a caterpillar.

The herbicide glufosinate-ammonium (GLA) is a competitive inhibitor of glutamine synthetase (GS), an enzyme converting glutamate to glutamine in both plants and animals. Because GS is essential for ammonia detoxification in plants, GLA treatment disrupts photorespiration by causing a build-up of ammonia and a loss of glutamine in plant tissues. This study reports that GLA applied to leaf surfaces is also toxic to 5th-instar caterpillars of the skipper butterfly Calpodes ethlius (LD50 = 400 mg kg-1). After ingesting GLA, caterpillars stopped feeding and became dehydrated through a loss of rectal function. Caterpillars showed symptoms of neurotoxicity, such as proleg tremors, body convulsions and complete paralysis before death. Incubation of several tissues isolated from normal feeding-stage caterpillars with the GS substrates glutamate and ammonium showed that GLA inhibited GS activity in vitro. Within 24 h of ingesting GLA, caterpillars had a greatly reduced glutamine content and the ammonium ion levels had more than doubled. Injection of ammonium chloride into non-GLA-treated caterpillars had no deleterious effect, suggesting that glutamine depletion, and not a rise in body ammonium, was the primary cause of GLA toxicity following GS inhibition. This was supported by the observation that the onset of the symptoms of GLA poisoning could be postponed by giving GLA-fed caterpillars several subsequent daily injections of glutamine. The effective GLA dose fed to 5th-instar caterpillars in this study was comparable to the amount that might realistically by acquired from feeding on GLA-treated crops.

Amino Acids↗