PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Isethionic Acid”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1986

Role of the decrease in ionized calcium in the inhibition of insulin release by chloride-free solutions.

Replacement of extracellular Cl- by isethionate or sulfate during stimulation with glucose or tolbutamide reversibly inhibited insulin release by perifused mouse islets. The concentration of ionized Ca2+ was decreased by 30 and 55% in isethionate and sulfate solutions, respectively. If this fall was prevented, the inhibition of release was only slightly affected (isethionate) or substantially attenuated (sulfate). In conclusion, the inhibition of insulin release occurring in Cl(-)-free solutions cannot be completely ascribed to a decrease in ionized Ca2+ in the medium. The contribution of this latter depends on the Cl- substitute.

Animals↗
PubMed1981

Permeant anions are not required for norepinephrine secretion from pheochromocytoma cells.

The 'chemiosmotic' model for secretion proposed by Pollard and his colleagues (Int. Rev. Cytol. 58, 159-197, 1979) was tested with pheochromocytoma cells. Contrary to the prediction of this model, norepinephrine secretion did not require the presence of a permeant anion in the medium. Secretion was not blocked by replacing much of the Cl- of the medium with isethionate or by replacing all of the Cl- salts of the medium with isotonic sucrose. Biochemical evidence is presented to indicate that the cells secreted by the normal exocytotic mechanism in the sucrose medium. Making the normal bathing medium hypertonic with 300 mM sucrose increased the basal level of norepinephrine release, but also suppressed secretion in response to a strong secretagogue (1 mM Ba2+). The data indicate that the Pollard model does not apply to pheochromocytoma cells, but suggest the possible involvement of osmotic pressure in exocytosis.

Adrenal Gland Neoplasms↗
PubMed1983

Characterization of a DFP-hydrolyzing enzyme in squid posterior salivary gland by use of Soman, DFP and manganous ion.

1. A phosphorus-fluorine splitting enzyme (DFPase) from squid nerve hydrolyzes DFP 5-10 times faster than it hydrolyzes another P-F compound, Soman, whereas a superficially similar enzyme from rat kidney hydrolyzes Soman 20-40 times faster than it hydrolyzes DFP, all under comparable conditions. 2. The DFPase from rat kidney is stimulated 2- to 3-fold by 4 X 10(-4) M Mn2+, whereas the DFPase from squid nerve is unaffected or slightly inhibited by 4 X 10(-4) M Mn2+. 3. These observations form the basis for distinguishing between a squid type DFPase and a mammalian DFPase, the names not being rigorously indicative of enzyme source or substrate. 4. When these criteria are applied to a P-F splitting enzyme found in squid saliva, the enzyme is identifiable as squid type DFPase. There is a significantly higher level of this enzyme in whole saliva from female squids than in whole saliva from male squids. This squid type DFPase is different from the proteinous toxin also found in squid saliva.

Animals↗
PubMed1988

Localisation of the insulin-sensitive phosphatidylinositol glycan at the outer surface of the cell membrane.

A phosphatidylinositol-glycan has been implicated in the mechanism of action of insulin. Some of the actions of insulin may be mediated by the generation of the polar head group of this phosphatidylinositol-glycan. Localisation of the insulin-sensitive phosphatidylinositol-glycan was investigated by reacting the glycophospholipid with the imidoester [1-14C]-isethionyl acetimidate. The present results indicate that most of the insulin-sensitive phosphatidylinositol-glycan is localized at the plasma membrane of rat liver, being 85% of the glycophospholipid present at the outer surface of the cell. These results suggest a paracrine action of insulin.

Animals↗
PubMed1986

Potassium loss from rabbit myocardium during hypoxia: evidence for passive efflux linked to anion extrusion.

To determine the effects of permeant and impermeant anions and of osmolarity on potassium (K+) exchange, the net uptake and efflux of 42K+ were recorded in the isolated arterially perfused rabbit septum. Perfusion with solution made hyperosmolar by adding NaCl (30 mM) or sucrose (60 mM) caused similar increases of 42K+ uptake which were reversible on returning to the control solution. Washout experiments showed that the loss of K+ on returning to the control perfusate was due to a decreased influx probably mediated by inhibition of the sodium pump. The effects of anions were studied by replacing chloride in the control solution with the inert and impermeant substitute isethionate (114 mM) or by loading the myocardium with sodium dimethyloxazeolidinedione (NaDMO, 30 mM) under isosmotic condition and switching to a perfusate containing sodium isethionate (30 mM). In both these conditions a reduction of 42K content could be detected and was attributable to an increased efflux. During hypoxic substrate free perfusion K+ loss was due to an increased efflux with no evidence for altered influx of potassium. The extrusion of accumulated anions from the myocardium could be the major determinant of the early potassium loss during hypoxia and ischaemia.

Animals↗
PubMed1982

Relationship between tubulo-glomerular feedback responses and perfusate hypotonicity.

Previous studies have established that during orthograde perfusion from a late proximal tubule site, there is a direct relationship between the magnitude of the feedback response and the level of distal tubular fluid sodium chloride concentration. The present study was conducted in the rat to extend this observation by assessing stop flow pressure (SFP) feedback responses during retrograde perfusion into the early distal tubule with solutions varying in total solute concentration and in the anionic constituent. SFP was measured after blockade of the intermediate proximal and late distal tubular segments with wax. Retrograde perfusion was initiated from an early distal tubular site at 15 nl/min. All solutions contained a 38 mOsm/kg matrix base, and the total solute concentration was increased with either sodium chloride or sodium isethionate to achieve osmolalities of 68, 85, and 120 mOsm/kg. For comparison, feedback responses during perfusion with a 120 mOsm/kg choline chloride solution were evaluated. During perfusion with the 120 mOsm/kg solutions, SFP decreased by 13 +/- 1.3 mm Hg with the sodium chloride solution, 12 +/- 1.5 mm Hg with the sodium isethionate solution, and 12 +/- 1.3 mm Hg with the choline chloride solution. During perfusion with solutions having an osmolality of 85 mOsm/kg, SFP decreased by 8 +/- 1.3 mm Hg with sodium chloride and 8 +/- 0.8 mm Hg with sodium isethionate. The 68 mOsm/kg solutions elicited decreases in SFP of 4.4 +/- 0.4 mm Hg and 5 +/- 0.5 mm Hg. During perfusion with the 38 mOsm/kg matrix solution, SFP decreased by an average of 1.4 +/- 0.9 mm Hg. Linear regression analysis revealed a 1 mm Hg decrease in SFP for every 7.7 mOsm/kg decrease in perfusate osmolality below 120 mOsm/kg. These results confirm previous findings that the magnitude of the feedback response is associated closely with the concentration of the perfusate over a narrow range from 38 to 120 mOsm/kg. Since the responses with sodium isethionate solutions were similar to the responses obtained with sodium chloride containing solutions, these studies provide evidence that the magnitude of the feedback responses are not specifically dependent on alterations in chloride concentration.

Animals↗
PubMed1977

Oxidative phosphorylation. Halide-dependent and halide-independent effects of triorganotin and trioganolead compounds on mitochondrial functions.

1. Each of five triorganotin and five triorganolead compounds was shown to perturb mithochondrial functions in three different ways. One is dependent and two are independent of Cl- in the medium. 2. Structure-activity relationships for the three interactions are described, and compounds suitable as tools for the separate study of each process are defined. 3. In a Cl- -containing medium trimethyltin, triethyltin, trimethyl-lead, triethyl-lead and tri-n-propyl-lead all produce the same maximum rate of ATP hydrolysis and O2 uptake; this rate is much less than that produced by uncoupling agents such as 2,4-dinitrophenol. 4. Increase in ATP hydrolysis and O2 uptake are measures on energy ultilization when triogranotin and triorganolead compounds bring about an exchange of external C1- for intramitochondrial OH- ions. Possible rate-limiting steps in this process are discussed. 5. In a C1- -containing medium ATP synthesis linked to the oxidation of beta-hydroxybutyrate or reduced cytochrone c is less inhibited by triethyltin or triethyl-lead than is ATP synthesis linked to the oxidation of succinate, pyruvate or L-glutamate. 6. The inhibition of ATP synthesis linked to the oxidation of both beta-hydroxybutyrate and reduced cytochrome c consists of two processes: one is a limited uncoupling and is C1- -dependent and the other is a C1- -independent inhibition of the energy-conservation system. 7. The different sensitivities to inhibition by triethyltin of mitochondrial functions involving the oxidation of beta-hydroxybutyrate and succinate are compared and discussed.

Adenosine Triphosphate↗
PubMed1983

Differential control of insulin secretion and somatostatin-receptor recruitment in isolated pancreatic islets.

Somatostatin receptors appear to be localized to secretory granules in pancreatic islet homogenates. Recruitment of these receptors to the islet-cell surfaces may mark the contact event between secretory granules and plasma membranes before release of insulin by fission. Isethionate, an impermeant anionic replacement for chloride, blocks the release step but does not affect receptor recruitment. By contrast, low concentrations of phenothiazine drugs, such as trifluoperazine and promethazine, inhibit both receptor recruitment and secretion. Scatchard analysis of phenothiazine effects on somatostatin receptors reveals that these drugs reduce the number of receptors but do not affect the affinity of the receptor for somatostatin. These data indicate that membrane contact and fission steps during exocytosis can be biochemically separated.

Animals↗
PubMed1993

On the mechanism of rectification of the isoproterenol-activated chloride current in guinea-pig ventricular myocytes.

The whole cell configuration of the patch clamp technique was used to investigate the mechanism underlying rectification of the isoproterenol-activated chloride (Cl-) current in isolated guinea pig ventricular myocytes. When extracellular Cl- was replaced with either bromide (Br-), glutamate (Glut), iodide (I-), isethionate (Iseth), or nitrate (NO3-), the magnitude of the shift in reversal potential of the macroscopic current suggested the following selectivity sequence: NO3- > Br- > or = Cl- > or = I- > Iseth > or = Glut. This information was used to investigate the role of permeant ions in rectification of this current. Consistent with previous observations, when the concentration of intracellular Cl- (Cli-) was less than the concentration of extracellular Cl- (Clo-) (40 mM Cli-/150 mM Clo-) the current exhibited outward rectification, but when Cli- was increased to equal that outside (150 Cli-/150 Clo-), the current no longer rectified. Rectification in the presence of asymmetrical concentrations of permeant ions on either side of the membrane is predicted by constant field theory, as described by the Goldman-Hodgkin-Katz current equation. However, when the Cl- gradient was reversed (150 Cli-/40 Clo-) the current did not rectify in the opposite direction, and in the presence of lower symmetrical concentrations of Cl- inside and out (40 Cli-/40 Clo-), outward rectification did not disappear. Reducing Cli- by equimolar replacement with glutamate caused a concentration dependent increase in the degree of rectification. However, when Cli- was replaced with more permeant anions (NO3- and Br-), rectification was not observed. These results can be explained by a single binding site model based on Eyring rate theory, indicating that rectification is a function of the concentration and the permeability of the anions in the intracellular solution.

Animals↗
PubMed1975

A component of fluid absorption linked to passive ion flows in the superficial pars recta.

We studied salt and water absorption in isolated rabbit superficial proximal straight tubules perfused and bathed with solutions providing oppositely directed transepithelial anion gradients similar to those which might obtain in vivo. The perfusing solution contained 138.6 mM Cl- 3.8 mM HCO-3 (pH 6.6) while the bathing solution contained 113.6 mM Cl- and 25 mM HCO-3 (pH 7.4); the system was bubbled with 95% O2-5% CO2. At 37 degrees C, net volume absorption (Jv nl min-1 mm-1) was 0.32 +/- 0.03 (SEM); Ve, the transepithelial voltage (millivolts; lumen to bath), was +3.1 +/- 0.2. At 21 degrees C, Ve rose to +3.7 +/- 0.1 and Jv fell to 0.13 +/- 0.01 (significantly different from zero at P less than 0.001); in the presence of 10(-4)M ouabain at 37 degrees C, Ve rose to +3.8 +/- 0.1 and Jv fell to 0.16 +/- 0.01 (P less than 0.001 with respect to zero). In paired experiments, the ouabain- and temperature-insensitive moieties of Jv and Ve became zero when transepithelial anion concentration gradients were abolished. Titrametric determinations net chloride flux at 21 degrees C or at 37 degrees C with 10(-4) M ouabain showed that chloride was the sole anion in an isotonic absorbate. And, combined electrical and tracer flux data indicated that the tubular epithelium was approximately 18 times more permeable to Cl- than to HCO-3. We interpret these results to indicate that, in these tubules, NaCl absorption depends in part on transepithelial anion concentration gradients similar to those generated in vivo and in vitro by active Na+ absorption associated with absorption to anions other than chloride. A quantitative analysis of passive solute and solvent flows in lateral intercellular spaces indicated that fluid absorption occurred across junctional complexes when the osmolality of the lateral intercellular spaces was equal to or slightly less than that of the perfusing and bathing solutions; the driving force for volume flow under these conditions depended on the fact that sigmaHCO3 exceeded sigmaCl.

Absorption↗
PubMed1977

Enzymatic oxidation of isethionate to sulfoacetaldehyde in bacterial extract.

Isethionate degradation in a bacterial extract was shown by the isolation of enzymes and by identification of an intermediate to take place in two steps; dehydrogenation to sulfoacetaldehyde and desulfonation leading to the formation of sulfite and acetate. The enzyme responsible for isethionate oxidation in the presence of FAD was particulate in nature and a solubilized preparation obtained by extraction with buffer of low ionic strength had oxidizing activities against only isethionate and n-butanol among compounds tested. The enzyme was inhibited by thiol and carbonyl reagents.

Acetaldehyde↗
PubMed1993

Isolation of a glycosyl-phosphatidylinositol (GPI) from rat brain.

Brain lipids were labelled with [1-14C]-isethionyl acetimidate and purified by sequential thin layer chromatography. Four labelled peaks were obtained, the first ones migrating with the same Rf as glycosyl-phosphatidylinositol (GPI). Further proof of the isolation of GPI was obtained by the observations that 44.8% of the radioactivity associated with the lipid in peak I was converted to the water phase by the effect of a PI-specific phospholipase C, and that the soluble material so obtained produced a dose-dependent inhibition of cAMP-dependent protein kinase activity. These findings indicate a biological equivalence between GPI and its polar head group from rat brain and those described in other cell types, and are consistent with the proposed role of these molecules in cellular signalling.

Animals↗
PubMed1990

Asymmetric distribution of the phosphatidylinositol-linked phospho-oligosaccharide that mimics insulin action in the plasma membrane.

We have investigated the topography of a glycosyl-phosphatidylinositol implicated in insulin action by a combination of two complementary methods: (a) chemical labelling with a non-permeable (isethionyl acetimidate) and a permeable (ethyl acetimidate) probe; and (b) enzymatic modifications with beta-galactosidase (EC 3.2.1.23) or phosphatidylinositol-specific phospholipase C (EC 3.1.4.3). Using the first approach the majority of the glycosyl-phosphatidylinositol is found in the outer surface of intact hepatocytes, adipocytes, fibroblasts and lymphocytes, but not in erythrocytes which presented only a 20% of the total labelled glycosyl-phosphatidylinositol to the exterior. Upon insulin addition (10 nM), about 60% of the total glycosyl-phosphatidylinositol was hydrolysed in both hepatocytes and adipocytes but not in erythrocytes. In agreement with the extracellular localization in hepatocytes and with the proposed role of this glycolipid in insulin action, treatment of rat hepatocytes with beta-galactosidase from Escherichia coli, an enzyme that hydrolyses the oligosaccharide moiety of the glycosyl-phosphatidylinositol, cleaved 65% of the total glycophospholipid and blocked the effect of insulin (but not of glucagon) on pyruvate kinase (EC 2.7.1.40). Similar treatment with phosphatidylinositol-specific phospholipase C from Bacillus cereus hydrolysed 62% of the total glycosyl-phosphatidylinositol. From the various approaches used it is concluded that the majority of this glycophospholipid is at the outer surface in a variety of insulin-sensitive cells.

Animals↗