The Experts below are selected from a list of 201 Experts worldwide ranked by ideXlab platform
Robert W. Peoples - One of the best experts on this subject based on the ideXlab platform.
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Differential actions of ethanol and Trichloroethanol at sites in the M3 and M4 domains of the NMDA receptor GluN2A (NR2A) subunit.
British journal of pharmacology, 2009Co-Authors: Abdel Salous, Hong Ren, Ka Lamb, Robert H. Lipsky, Robert W. PeoplesAbstract:Background and purpose: Alcohol produces its behavioural effects in part due to inhibition of N-methyl-d-aspartate (NMDA) receptors in the CNS. Previous studies have identified amino acid residues in membrane-associated domains 3 (M3) and 4 (M4) of the NMDA receptor that influence ethanol sensitivity. In addition, in other alcohol-sensitive ion channels, sedative-hypnotic agents have in some cases been shown to act at sites distinct from the sites of ethanol action. In this study, we compared the influence of mutations at these sites on sensitivity to ethanol and Trichloroethanol, a sedative-hypnotic agent that is a structural analogue of ethanol. Experimental approach: We constructed panels of mutants at ethanol-sensitive positions in the GluN2A (NR2A) NMDA receptor subunit and transiently expressed these mutants in human embryonic kidney 293 cells. We used whole-cell patch-clamp recording to assess the actions of ethanol and Trichloroethanol in these mutant NMDA receptors. Key results: Ethanol sensitivity of mutants at GluN2A(Ala825) was not correlated with any physicochemical measures tested. Trichloroethanol sensitivity was altered in two of three ethanol-insensitive mutant GluN2A subunits: GluN2A(Phe637Trp) in M3 and GluN2A(Ala825Trp) in M4, but not GluN2A(Met823Trp). Trichloroethanol sensitivity decreased with increasing molecular volume at Phe637 or increasing hydrophobicity at Ala825 and was correlated with ethanol sensitivity at both sites. Conclusions and implications: Evidence obtained to date is consistent with a role of GluN2A(Ala825) as a modulatory site for ethanol and Trichloroethanol sensitivity, but not as a binding site. Trichloroethanol appears to inhibit the NMDA receptor in a manner similar, but not identical to, that of ethanol.
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arginine 246 of the pretransmembrane domain 1 region alters 2 2 2 Trichloroethanol action in the 5 hydroxytryptamine3a receptor
Journal of Pharmacology and Experimental Therapeutics, 2008Co-Authors: Robert W. PeoplesAbstract:Ligand-gated ion channels participate in synaptic transmission, and they are involved in neurotransmitter release. The functions of the channels are regulated by a variety of modulators. The interaction of 2,2,2-Trichloroethanol, the active hypnotic metabolite of chloral hydrate, with the 5-hydroxytryptamine (5-HT) (serotonin) type 3 receptor results in a positive allosteric modulation. We have demonstrated previously that arginine 246 (R246) located in the pretransmembrane domain 1 is critical for coupling agonist binding to gating. In this study, we examined the role of R246 in the action of Trichloroethanol with a combination of mutagenesis and whole-cell patch-clamp techniques. The R246A mutation converted the partial agonist dopamine into a full agonist at the 5-HT3A receptor, and it facilitated activation of the mutant receptor by dopamine, suggesting an enhanced gating process due to the mutation. The positive modulation of the 5-HT3A receptor by Trichloroethanol was dramatically reduced by the R246A mutation. Trichloroethanol had little agonist activity in the wild-type receptor (<1% of maximal 5-HT response). However, the R246A mutation significantly increased the direct activation of the receptor by Trichloroethanol in the absence of agonist (∼10% of maximal 5-HT response). The current activated by Trichloroethanol could be blocked by the competitive 5-HT3 receptor antagonist tropanyl 3,5-dichlorobenzoate (MDL 72222), and it had a similar reversal potential to those of current activated by 5-HT. In addition, predesensitization of the mutant receptor by Trichloroethanol prevented 5-HT from activating the receptor. These data suggest that R246 is a crucial site for mediating the actions of both agonists and modulators.
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Arginine 246 of the pretransmembrane domain 1 region alters 2,2,2-Trichloroethanol action in the 5-hydroxytryptamine3A receptor.
The Journal of pharmacology and experimental therapeutics, 2007Co-Authors: Robert W. PeoplesAbstract:Ligand-gated ion channels participate in synaptic transmission, and they are involved in neurotransmitter release. The functions of the channels are regulated by a variety of modulators. The interaction of 2,2,2-Trichloroethanol, the active hypnotic metabolite of chloral hydrate, with the 5-hydroxytryptamine (5-HT) (serotonin) type 3 receptor results in a positive allosteric modulation. We have demonstrated previously that arginine 246 (R246) located in the pretransmembrane domain 1 is critical for coupling agonist binding to gating. In this study, we examined the role of R246 in the action of Trichloroethanol with a combination of mutagenesis and whole-cell patch-clamp techniques. The R246A mutation converted the partial agonist dopamine into a full agonist at the 5-HT3A receptor, and it facilitated activation of the mutant receptor by dopamine, suggesting an enhanced gating process due to the mutation. The positive modulation of the 5-HT3A receptor by Trichloroethanol was dramatically reduced by the R246A mutation. Trichloroethanol had little agonist activity in the wild-type receptor (
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2,2,2-Trichloroethanol Action in the 5-Hydroxytryptamine3A Receptor
2007Co-Authors: Robert W. PeoplesAbstract:Ligand-gated ion channels participate in synaptic transmission, and they are involved in neurotransmitter release. The functions of the channels are regulated by a variety of modulators. The interaction of 2,2,2-Trichloroethanol, the active hypnotic metab-olite of chloral hydrate, with the 5-hydroxytryptamine (5-HT) (serotonin) type 3 receptor results in a positive allosteric mod-ulation. We have demonstrated previously that arginine 246 (R246) located in the pretransmembrane domain 1 is critical for coupling agonist binding to gating. In this study, we examined the role of R246 in the action of Trichloroethanol with a combi-nation of mutagenesis and whole-cell patch-clamp techniques. The R246A mutation converted the partial agonist dopamine into a full agonist at the 5-HT3A receptor, and it facilitated activation of the mutant receptor by dopamine, suggesting a
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Inhibition of excitatory amino acid-activated currents by Trichloroethanol and trifluoroethanol in mouse hippocampal neurones
British journal of pharmacology, 1998Co-Authors: Robert W. Peoples, Forrest F. WeightAbstract:1. The effects of the active metabolite of chloral derivative sedative-hypnotic agents, 2,2,2-Trichloroethanol (Trichloroethanol), and its analog 2,2,2-trifluoroethanol (trifluoroethanol), were studied on ion current activated by the excitatory amino acids N-methyl-D-aspartate (NMDA) and kainate in mouse hippocampal neurones in culture using whole-cell patch-clamp recording. 2. Both Trichloroethanol and trifluoroethanol inhibited excitatory amino acid-activated currents in a concentration-dependent manner. Trichloroethanol inhibited NMDA- and kainate-activated currents with IC50 values of 6.4 and 12 mM, respectively, while trifluoroethanol inhibited NMDA- and kainate-activated currents with IC50 values of 28 and 35 mM, respectively. 3. Both Trichloroethanol and trifluoroethanol appeared to be able to inhibit excitatory amino acid-activated currents by 100 per cent. 4.Concentration-response analysis of NMDA- and kainate-activated current revealed that Trichloroethanol decreased the maximal response to both agonists without significantly affecting their EC50 values. 5. Both Trichloroethanol and trifluoroethanol inhibited excitatory amino acid-activated currents more potently than did ethanol. The inhibitory potency of Trichloroethanol and trifluoroethanol appears to be associated with their increased hydrophobicity. 6. The observation that Trichloroethanol inhibits excitatory amino acid-activated currents at anaesthetic concentrations suggests that inhibition of excitatory amino acid receptors may contribute to the CNS depressant effects of chloral derivative sedative-hypnotic agents.
Richat Abbas - One of the best experts on this subject based on the ideXlab platform.
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A human physiologically based pharmacokinetic model for trichloroethylene and its metabolites, trichloroacetic acid and free Trichloroethanol.
Toxicology and applied pharmacology, 1998Co-Authors: Jeffrey W. Fisher, Deirdre A. Mahle, Richat AbbasAbstract:Nine male and eight female healthy volunteers were exposed to 50 or 100 ppm trichloroethylene vapors for 4 h. Blood, urine, and exhaled breath samples were collected for development of a physiologically based pharmacokinetic (PBPK) model for trichloroethylene and its two major P450-mediated metabolites, trichloroacetic acid and free Trichloroethanol. Blood and urine were analyzed for trichloroethylene, chloral hydrate, free Trichloroethanol and Trichloroethanol glucuronide, and trichloroacetic acid. Plasma was analyzed for dichloroacetic acid. Trichloroethylene was also measured in exhaled breath samples. Trichloroethylene, free Trichloroethanol, and trichloroacetic acid were found in blood samples of all volunteers and only trace amounts of dichloroacetic acid (4–12 ppb) were found in plasma samples from a few volunteers. Trichloroethanol glucuronide and trichloroacetic acid were found in urine of all volunteers. No chloral hydrate was detected in the volunteers. Gender-specific PBPK models were developed with fitted urinary rate constant values for each individual trichloroethylene exposure to describe urinary excretion of Trichloroethanol glucuronide and trichloroacetic acid. Individual urinary excretion rate constants were necessary to account for the variability in the measured cumulative amount of metabolites excreted in the urine. However, the average amount of trichloroacetic acid and Trichloroethanol glucuronide excreted in urine for each gender was predicted using mean urinary excretion rate constant values for each sex. A four-compartment physiological flow model was used for the metabolites (lung, liver, kidney, and body) and a six-compartment physiological flow model was used for trichloroethylene (lung, liver, kidney, fat, and slowly and rapidly perfused tissues). Metabolic capacity (Vmaxc) for oxidation of trichloroethylene was estimated to be 4 mg/kg/h in males and 5 mg/kg/h in females. Metabolized trichloroethylene was assumed to be converted to either free Trichloroethanol (90%) or trichloroacetic acid (10%). Free Trichloroethanol was glucuronidated forming Trichloroethanol glucuronide or converted to trichloroacetic acid via back conversion of Trichloroethanol to chloral (trichloroacetaldehyde). Trichloroethanol glucuronide and trichloroacetic acid were then excreted in urine. Gender-related pharmacokinetic differences in the uptake and metabolism of trichloroethylene were minor, but apparent. In general, the PBPK models for the male and female volunteers provided adequate predictions of the uptake of trichloroethylene and distribution of trichloroethylene and its metabolites, trichloroacetic acid and free Trichloroethanol. The PBPK models for males and females consistently overpredicted exhaled breath concentrations of trichloroethylene immediately following the TCE exposure for a 2- to 4-h period. Further research is needed to better understand the biological determinants responsible for the observed variability in urinary excretion of Trichloroethanol glucuronide and trichloroacetic acid and the metabolic pathway resulting in formation of dichloroacetic acid.
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a physiologically based pharmacokinetic model for trichloroethylene and its metabolites chloral hydrate trichloroacetate dichloroacetate Trichloroethanol and Trichloroethanol glucuronide in b6c3f1 mice
Toxicology and Applied Pharmacology, 1997Co-Authors: Richat Abbas, Jeffrey W. FisherAbstract:A six-compartment physiologically based pharmacokinetic (PBPK) model for the B6C3F1 mouse was developed for trichloroethylene (TCE) and was linked with five metabolite submodels consisting of four compartments each. The PBPK model for TCE and the metabolite submodels described oral uptake and metabolism of TCE to chloral hydrate (CH). CH was further metabolized to Trichloroethanol (TCOH) and trichloroacetic acid (TCA). TCA was excreted in urine and, to a lesser degree, metabolized to dichloroacetic acid (DCA). DCA was further metabolized. The majority of TCOH was glucuronidated (TCOG) and excreted in the urine and feces. TCOH was also excreted in urine or converted back to CH. Partition coefficient (PC) values for TCE were determined by vial equilibrium, and PC values for nonvolatile metabolites were determined by centrifugation. The largest PC values for TCE were the fat/blood (36.4) and the blood/air (15.9) values. Tissue/blood PC values for the water-soluble metabolites were low, with all PC values under 2.0. Mice were given bolus oral doses of 300, 600, 1200, and 2000 mg/kg TCE dissolved in corn oil. At various time points, mice were sacrificed, and blood, liver, lung, fat, and urine were collected and assayed for TCE and metabolites. The 1200 mg/kg dose group was used to calibrate the PBPK model for TCE and its metabolites. Urinary excretion rate constant values were 0.06/hr/kg for CH, 1.14/hr/kg for TCOH, 32.8/hr/kg for TCOG, and 1.55/hr/kg for TCA. A fecal excretion rate constant value for TCOG was 4.61/hr/kg. For oral bolus dosing of TCE with 300, 600, and 2000 mg/kg, model predictions of TCE and several metabolites were in general agreement with observations. This PBPK model for TCE and metabolites is the most comprehensive PBPK model constructed for P450-mediated metabolism of TCE in the B6C3F1 mouse.
Jeffrey W. Fisher - One of the best experts on this subject based on the ideXlab platform.
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A human physiologically based pharmacokinetic model for trichloroethylene and its metabolites, trichloroacetic acid and free Trichloroethanol.
Toxicology and applied pharmacology, 1998Co-Authors: Jeffrey W. Fisher, Deirdre A. Mahle, Richat AbbasAbstract:Nine male and eight female healthy volunteers were exposed to 50 or 100 ppm trichloroethylene vapors for 4 h. Blood, urine, and exhaled breath samples were collected for development of a physiologically based pharmacokinetic (PBPK) model for trichloroethylene and its two major P450-mediated metabolites, trichloroacetic acid and free Trichloroethanol. Blood and urine were analyzed for trichloroethylene, chloral hydrate, free Trichloroethanol and Trichloroethanol glucuronide, and trichloroacetic acid. Plasma was analyzed for dichloroacetic acid. Trichloroethylene was also measured in exhaled breath samples. Trichloroethylene, free Trichloroethanol, and trichloroacetic acid were found in blood samples of all volunteers and only trace amounts of dichloroacetic acid (4–12 ppb) were found in plasma samples from a few volunteers. Trichloroethanol glucuronide and trichloroacetic acid were found in urine of all volunteers. No chloral hydrate was detected in the volunteers. Gender-specific PBPK models were developed with fitted urinary rate constant values for each individual trichloroethylene exposure to describe urinary excretion of Trichloroethanol glucuronide and trichloroacetic acid. Individual urinary excretion rate constants were necessary to account for the variability in the measured cumulative amount of metabolites excreted in the urine. However, the average amount of trichloroacetic acid and Trichloroethanol glucuronide excreted in urine for each gender was predicted using mean urinary excretion rate constant values for each sex. A four-compartment physiological flow model was used for the metabolites (lung, liver, kidney, and body) and a six-compartment physiological flow model was used for trichloroethylene (lung, liver, kidney, fat, and slowly and rapidly perfused tissues). Metabolic capacity (Vmaxc) for oxidation of trichloroethylene was estimated to be 4 mg/kg/h in males and 5 mg/kg/h in females. Metabolized trichloroethylene was assumed to be converted to either free Trichloroethanol (90%) or trichloroacetic acid (10%). Free Trichloroethanol was glucuronidated forming Trichloroethanol glucuronide or converted to trichloroacetic acid via back conversion of Trichloroethanol to chloral (trichloroacetaldehyde). Trichloroethanol glucuronide and trichloroacetic acid were then excreted in urine. Gender-related pharmacokinetic differences in the uptake and metabolism of trichloroethylene were minor, but apparent. In general, the PBPK models for the male and female volunteers provided adequate predictions of the uptake of trichloroethylene and distribution of trichloroethylene and its metabolites, trichloroacetic acid and free Trichloroethanol. The PBPK models for males and females consistently overpredicted exhaled breath concentrations of trichloroethylene immediately following the TCE exposure for a 2- to 4-h period. Further research is needed to better understand the biological determinants responsible for the observed variability in urinary excretion of Trichloroethanol glucuronide and trichloroacetic acid and the metabolic pathway resulting in formation of dichloroacetic acid.
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a physiologically based pharmacokinetic model for trichloroethylene and its metabolites chloral hydrate trichloroacetate dichloroacetate Trichloroethanol and Trichloroethanol glucuronide in b6c3f1 mice
Toxicology and Applied Pharmacology, 1997Co-Authors: Richat Abbas, Jeffrey W. FisherAbstract:A six-compartment physiologically based pharmacokinetic (PBPK) model for the B6C3F1 mouse was developed for trichloroethylene (TCE) and was linked with five metabolite submodels consisting of four compartments each. The PBPK model for TCE and the metabolite submodels described oral uptake and metabolism of TCE to chloral hydrate (CH). CH was further metabolized to Trichloroethanol (TCOH) and trichloroacetic acid (TCA). TCA was excreted in urine and, to a lesser degree, metabolized to dichloroacetic acid (DCA). DCA was further metabolized. The majority of TCOH was glucuronidated (TCOG) and excreted in the urine and feces. TCOH was also excreted in urine or converted back to CH. Partition coefficient (PC) values for TCE were determined by vial equilibrium, and PC values for nonvolatile metabolites were determined by centrifugation. The largest PC values for TCE were the fat/blood (36.4) and the blood/air (15.9) values. Tissue/blood PC values for the water-soluble metabolites were low, with all PC values under 2.0. Mice were given bolus oral doses of 300, 600, 1200, and 2000 mg/kg TCE dissolved in corn oil. At various time points, mice were sacrificed, and blood, liver, lung, fat, and urine were collected and assayed for TCE and metabolites. The 1200 mg/kg dose group was used to calibrate the PBPK model for TCE and its metabolites. Urinary excretion rate constant values were 0.06/hr/kg for CH, 1.14/hr/kg for TCOH, 32.8/hr/kg for TCOG, and 1.55/hr/kg for TCA. A fecal excretion rate constant value for TCOG was 4.61/hr/kg. For oral bolus dosing of TCE with 300, 600, and 2000 mg/kg, model predictions of TCE and several metabolites were in general agreement with observations. This PBPK model for TCE and metabolites is the most comprehensive PBPK model constructed for P450-mediated metabolism of TCE in the B6C3F1 mouse.
Forrest F. Weight - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of excitatory amino acid-activated currents by Trichloroethanol and trifluoroethanol in mouse hippocampal neurones
British journal of pharmacology, 1998Co-Authors: Robert W. Peoples, Forrest F. WeightAbstract:1. The effects of the active metabolite of chloral derivative sedative-hypnotic agents, 2,2,2-Trichloroethanol (Trichloroethanol), and its analog 2,2,2-trifluoroethanol (trifluoroethanol), were studied on ion current activated by the excitatory amino acids N-methyl-D-aspartate (NMDA) and kainate in mouse hippocampal neurones in culture using whole-cell patch-clamp recording. 2. Both Trichloroethanol and trifluoroethanol inhibited excitatory amino acid-activated currents in a concentration-dependent manner. Trichloroethanol inhibited NMDA- and kainate-activated currents with IC50 values of 6.4 and 12 mM, respectively, while trifluoroethanol inhibited NMDA- and kainate-activated currents with IC50 values of 28 and 35 mM, respectively. 3. Both Trichloroethanol and trifluoroethanol appeared to be able to inhibit excitatory amino acid-activated currents by 100 per cent. 4.Concentration-response analysis of NMDA- and kainate-activated current revealed that Trichloroethanol decreased the maximal response to both agonists without significantly affecting their EC50 values. 5. Both Trichloroethanol and trifluoroethanol inhibited excitatory amino acid-activated currents more potently than did ethanol. The inhibitory potency of Trichloroethanol and trifluoroethanol appears to be associated with their increased hydrophobicity. 6. The observation that Trichloroethanol inhibits excitatory amino acid-activated currents at anaesthetic concentrations suggests that inhibition of excitatory amino acid receptors may contribute to the CNS depressant effects of chloral derivative sedative-hypnotic agents.
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Trichloroethanol potentiation of γ aminobutyric acid activated chloride current in mouse hippocampal neurones
British Journal of Pharmacology, 1994Co-Authors: Robert W. Peoples, Forrest F. WeightAbstract:1. The action of 2,2,2-Trichloroethanol on gamma-aminobutyric acid (GABA)-activated Cl- current was studied in mouse hippocampal neurones in tissue culture by use of whole-cell patch-clamp recording. 2. Trichloroethanol increased the amplitude of currents activated by 1 microM GABA or 0.1 microM muscimol. Trichloroethanol, 1-25 mM, potentiated current activated by 1 microM GABA in a concentration-dependent manner with an EC50 of 3.0 +/- 1.4 mM and a maximal response (Emax) of 576 +/- 72% of control. 3. Trichloroethanol potentiated currents activated by GABA concentrations or = 10 microM. Despite marked potentiation of currents activated by low concentrations of GABA, Trichloroethanol did not significantly alter the EC50, slope, or Emax of the GABA concentration-response curve. 4. Trichloroethanol, 5 mM, potentiated GABA-activated current in neurones in which ethanol, 10-500 mM, did not. The effect of Trichloroethanol was not altered by the putative ethanol antagonist, Ro 15-4513. Trichloroethanol did not potentiate currents activated by pentobarbitone. 5. In the absence of exogenous GABA, Trichloroethanol at concentrations > or = 2.5 mM activated a current that appeared to be carried by Cl- as its reversal potential changed with changes in the Cl- gradient and as it was inhibited by the GABAA antagonists, bicuculline methiodide and picrotoxin. 6. Since Trichloroethanol is thought to be the active metabolite of chloral hydrate and other chloral derivative anaesthetics, potentiation of the GABA-activated current in central nervous system neurones by Trichloroethanol may contribute to the sedative/hypnotic effects of these agents.
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Trichloroethanol potentiation of γ‐aminobutyric acid‐activated chloride current in mouse hippocampal neurones
British journal of pharmacology, 1994Co-Authors: Robert W. Peoples, Forrest F. WeightAbstract:1. The action of 2,2,2-Trichloroethanol on gamma-aminobutyric acid (GABA)-activated Cl- current was studied in mouse hippocampal neurones in tissue culture by use of whole-cell patch-clamp recording. 2. Trichloroethanol increased the amplitude of currents activated by 1 microM GABA or 0.1 microM muscimol. Trichloroethanol, 1-25 mM, potentiated current activated by 1 microM GABA in a concentration-dependent manner with an EC50 of 3.0 +/- 1.4 mM and a maximal response (Emax) of 576 +/- 72% of control. 3. Trichloroethanol potentiated currents activated by GABA concentrations or = 10 microM. Despite marked potentiation of currents activated by low concentrations of GABA, Trichloroethanol did not significantly alter the EC50, slope, or Emax of the GABA concentration-response curve. 4. Trichloroethanol, 5 mM, potentiated GABA-activated current in neurones in which ethanol, 10-500 mM, did not. The effect of Trichloroethanol was not altered by the putative ethanol antagonist, Ro 15-4513. Trichloroethanol did not potentiate currents activated by pentobarbitone. 5. In the absence of exogenous GABA, Trichloroethanol at concentrations > or = 2.5 mM activated a current that appeared to be carried by Cl- as its reversal potential changed with changes in the Cl- gradient and as it was inhibited by the GABAA antagonists, bicuculline methiodide and picrotoxin. 6. Since Trichloroethanol is thought to be the active metabolite of chloral hydrate and other chloral derivative anaesthetics, potentiation of the GABA-activated current in central nervous system neurones by Trichloroethanol may contribute to the sedative/hypnotic effects of these agents.
Barbara Gzyl - One of the best experts on this subject based on the ideXlab platform.
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properties of mixed adsorption films of 2 2 2 Trichloroethanol ethanol at the water air interface
Joint International Conference on Information Sciences, 1996Co-Authors: Maria Paluch, Barbara GzylAbstract:Abstract The properties of aqueous 2,2,2-Trichloroethanol–ethanol mixtures were studied by surface potential and surface tension measurements. Based on the Gibbs equation and Motomura's method the relative surface excesses of adsorbed substances, molar fractions of solutes, surface orientation angles of molecules at the interface, and miscibility of adsorbed films were determined. The effective dipole moment of 2,2,2-Trichloroethanol was obtained on the basis of surface excess values and surface potential changes, using the Helmholtz equation.
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Properties of mixed adsorption films of 2,2,2-Trichloroethanol-ethanol at the water/air interface
Journal of Colloid and Interface Science, 1996Co-Authors: Maria Paluch, Barbara GzylAbstract:Abstract The properties of aqueous 2,2,2-Trichloroethanol–ethanol mixtures were studied by surface potential and surface tension measurements. Based on the Gibbs equation and Motomura's method the relative surface excesses of adsorbed substances, molar fractions of solutes, surface orientation angles of molecules at the interface, and miscibility of adsorbed films were determined. The effective dipole moment of 2,2,2-Trichloroethanol was obtained on the basis of surface excess values and surface potential changes, using the Helmholtz equation.
