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PubMed1989

Sodium phenobarbitone reverses the anxiogenic effects of compounds acting at three different central sites.

Sodium phenobarbitone was tested for its ability to antagonise the anxiogenic effects of compounds acting at three different central sites. These compounds were: FG 7142, a beta-carboline which acts at the benzodiazepine binding site on the GABA-benzodiazepine receptor complex; pentylenetetrazole, which acts at the picrotoxinin site on the GABA-benzodiazepine receptor complex; and yohimbine which is an antagonist at the alpha 2-adrenoceptor. The experiments were carried out in two tests of anxiety using rats. In the social interaction test (the test arena was familiar and dimly lit), FG 7142 (5 mg/kg) and pentylenetetrazole (15 mg/kg) reduced the time spent in social interaction (indicating anxiogenic activity); these effects were reversed by sodium phenobarbitone (35 mg/kg). Sodium phenobarbitone (35 mg/kg) alone decreased locomotor activity as measured in the social interaction test, which was reversed by pentylenetetrazole (15 mg/kg). In the elevated plus-maze, FG 7142 (6.7 mg/kg) pentylenetetrazole (20 mg/kg) and yohimbine (4 mg/kg) reduced the percentage of open-arm entries and the percentage of time spent on the open arms (indicating anxiogenic activity); these effects were reversed by sodium phenobarbitone (35 mg/kg). Sodium phenobarbitone (35 mg/kg) alone significantly increased the percentage of open-arm entries and the percentage of time spent on the open arms (indicating anxiolytic activity). This study, together with previous studies using other clinically-effective anxiolytic drugs, suggests that the ability of a compound to antagonise the effects of anxiogenic agents may be a useful indirect means of predicting anxiolytic activity.

Animals↗
PubMed1986

Na-Ca exchange in renal tubular basolateral membranes.

We investigated the Na-dependent Ca transport in purified bovine luminal and basolateral renal tubular membranes. Na-dependent Ca uptake was observed in basolateral but not in luminal kidney tubular membranes. 45Ca uptake in basolateral membrane vesicles loaded with Na and suspended in K buffer was significantly greater than that observed in vesicles loaded with Na and suspended in Na buffer. The Na ionophore ETH-227 inhibited Na-dependent Ca uptake indicating that the Ca uptake was dependent on Na gradient. The Ca taken up in the presence of Na gradient could be released by the Ca ionophore A-23187 suggesting that Ca was accumulated inside the vesicles. In vesicles loaded with 45Ca, addition of Na to the media promoted Ca efflux. Methyl triphenylphosponium uptake and Ca uptake were significantly higher in the presence of a Na gradient as compared to those observed in the presence of other monovalent cation gradients, indicating the specificity for Na gradient and arguing against a calcium-activated sodium conductance pathway. The Na-dependent Ca uptake varied with intravesicular Na concentration with an apparent Km of 20-40 mM. The Km for Ca of the Na-dependent Ca uptake was 50 microM and the Vmax was 0.2 nmol/mg protein/min. The Na-dependent Ca uptake was inhibited by LaCl3, tetracaine and verapamil, unaffected by quinidine and amiloride, and slightly stimulated by chymotrypsin. These data demonstrate that the Na-dependent Ca transport by renal basolateral membranes is mediated by a Na-Ca exchange system and not by a calcium-activated sodium conductance pathway.

Acetamides↗
PubMed2001

Iodide transport in lactating rat mammary tissue via a pathway independent from the Na+/I- cotransporter: evidence for sulfate/iodide exchange.

Although it is beyond doubt that mammary cells accumulate iodide via a Na+-dependent transport mechanism, it is not clear if this is the only pathway for iodide transport in mammary tissue. In view of this, experiments were designed to test for the presence of an anion-exchange pathway which could mediate the transport of iodide into mammary cells; thus, the effect of external iodide on sulfate efflux from rat mammary tissue has been investigated. Iodide trans-stimulated sulfate efflux from mammary tissue explants in a dose-dependent manner: 0.1, 1.0 and 10.0 mM iodide stimulated the fractional release of iodide by 56 +/- 2.2, 166.5 +/- 17.5, and 302.9 +/- 29.8%, respectively. The stimulation of sulfate efflux by external iodide was completely inhibited by DIDS (4.4'-diisothiocyanatostilbene 2,2'-disulfonic acid). Perchlorate (1 mM) also trans-stimulated sulfate efflux in a manner that was inhibited by DIDS. Furthermore, iodide trans-accelerated sulfate efflux from rat mammary acini via a DIDS-sensitive mechanism. The results are consistent with the presence of a DIDS-sensitive anion-exchange mechanism which can accept iodide as a substrate. It appears that the iodide-sulfate exchange mechanism is independent from the sodium-dependent iodide transporter given that sulfate is not a substrate of the latter system. The iodide-sulfate exchanger may operate in parallel with the sodium-dependent iodide transporter to mediate iodide uptake into mammary cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1950

Accumulation of potassium by human red cells.

1. A method is described for measuring the accumulation of K at 37 degrees C. by washed human red cells in glucose-containing systems in which the pH is kept constant, the K content of the cells being compared with that of the cells of systems which contain no added glucose but which are otherwise treated similarly. 2. In systems containing added glucose, the accumulation of K begins shortly after the cells have been warmed to 37 degrees C., proceeds to a maximum which is reached after about 10 hours, and then falls exponentially. The maximum rate of accumulation is found during the first 3 hours. In systems which contain no added glucose, the K content of the cells appears to decrease exponentially with time for about 18 to 24 hours; thereafter the K content of the cells may decrease rapidly and the systems may show considerable hemolysis. Sometimes a small accumulation effect is observed during the first 2 to 3 hours; this may be the result of the washed cells not having been completely freed of glucose. 3. The accumulation process proceeds at its maximum rate at pH 7.4 to 7.6, which is also the pH at which the K loss from the red cells is at a minimum in systems containing no added glucose. 4. When red cells are stored at 4 degrees C. for increasing lengths of time, the storage is accompanied by increasing K loss and the maximum rate of accumulation observed when the cells are warmed to 37 degrees C. at first becomes greater. If the storage at 4 degrees C. is continued for more than 3 to 4 days, the rate of the accumulation which occurs at 37 degrees C decreases again, the accumulation mechanism showing progressive deterioration with time even at low temperatures. This deterioration has a counterpart in the progressive deterioration (deduced from the analysis of the curves relating K content and time) of the accumulation mechanism with time at 37 degrees C. 5. The accumulation of K occurs at a maximum rate when the concentration of glucose in the system is between 50 and 200 mg./100 ml. Its temperature coefficient over the range 27-37 degrees C. is 2.4. In the presence of glucose and at pH 7.6, accumulation of K takes place from isotonic mixtures of KCl and LiCl or of KCl and CsCl only a little less actively than from mixtures of KCl and NaCl; i.e., the accumulation of K under optimum conditions seems to be an active process which is at least partly independent of the excretion of Na.

Biological Transport↗
PubMed2005

Electron atomic scattering factors, Debye-Waller factors and the optical potential for high-energy electron diffraction.

High-energy electrons may be elastically and inelastically scattered by a solid. To a good approximation the effect of inelastic scattering on the elastically scattered electrons may be taken into account using the concept of the complex optical potential. The optical potential may be calculated using electron atomic scattering factors and Debye-Waller factors, which in turn can be evaluated numerically using Hartree Fock atomic wave functions and shell models of lattice dynamics. The numerical electron atomic scattering factors have been parameterized using five Gaussian functions for all the neutral atoms of the periodic table and for 106 important ions, and the temperature-dependent Debye-Waller B-factors have been fitted by using fourth degree polynomial regression fitting for 19 compounds with the sodium chloride structure, 5 compounds with the cesium chloride structure, 17 compounds with the zinc-blend structure and 68 elemental crystals.

Journal Article↗
PubMed2003

Predicting neonatal perchlorate dose and inhibition of iodide uptake in the rat during lactation using physiologically-based pharmacokinetic modeling.

Perchlorate (ClO4-), a contaminant in drinking water, competitively inhibits active uptake of iodide (I-) into various tissues, including mammary tissue. During postnatal development, inhibition of I- uptake in the mammary gland and neonatal thyroid and the active concentration ClO4- in milk indicate a potentially increased susceptibility of neonates to endocrine disruption. A physiologically based pharmacokinetic (PBPK) model was developed to reproduce measured ClO4- distribution in the lactating and neonatal rat and predict resulting effects on I- kinetics from competitive inhibition at the sodium iodide symporter (NIS). Kinetic I- and ClO4- behavior in tissues with NIS (thyroid, stomach, mammary gland, and skin) was simulated with multiple subcompartments, Michaelis-Menten (M-M) kinetics and competitive inhibition. Physiological and kinetic parameters were obtained from literature and experiment. Systemic clearance and M-M parameters were estimated by fitting simulations to tissue and serum data. The model successfully describes maternal and neonatal thyroid, stomach, skin, and plasma, as well as maternal mammary gland and milk data after ClO4- exposure (from 0.01 to 10 mg/kg-day ClO4-) and acute radioiodide (2.1 to 33,000 ng/kg I-) dosing. The model also predicts I- uptake inhibition in the maternal thyroid, mammary gland, and milk. Model simulations predict a significant transfer of ClO4- through milk after maternal exposure; approximately 50% to 6% of the daily maternal dose at doses ranging from 0.01 to 10.0 mg ClO4-/kg-day, respectively. Comparison of predicted dosimetrics across life-stages in the rat indicates that neonatal thyroid I- uptake inhibition is similar to the adult and approximately tenfold less than the fetus.

Animals↗
PubMed1993

Comparison of three short-term assays: results on seven chemicals. Potential contribution to the control of water genotoxicity.

Three short-term assays (the SOS chromotest, the Ames fluctuation test and the newt micronucleus test) were used to evaluate the genotoxicity of seven chemicals (4-nitroquinoline 1-oxide, potassium dichromate, formaldehyde, sodium hypochlorite, benzo[a]pyrene, cyclophosphamide and 2-naphthylamine). In the SOS chromotest, all seven compounds except sodium hypochlorite and cyclophosphamide were found to induce primary DNA damage in E. coli. With the Ames fluctuation test, all seven chemicals except sodium hypochlorite showed mutagenic activity on Salmonella typhimurium TA100, TA102 or TA98. The newt micronucleus assay detected a clastogenic effect of all seven compounds except formaldehyde on the peripheral blood erythrocytes of Pleurodeles waltl larvae. For each compound, the sensitivity of the tests was compared; (1) the SOS chromotest is the least sensitive assay in every case, (2) the Ames fluctuation test is the most sensitive assay for studied chemicals with direct genotoxic effect and (3) the newt micronucleus assay is the most sensitive test for tested compounds with indirect genotoxic activity. The potential contribution of these three tests in the monitoring of water genotoxicity is discussed.

2-Naphthylamine↗
PubMed2006

Seleno-enzymes and seleno-compounds: the two faces of selenium.

Selenium protects cells and inhibits many inflammatory cell mechanisms through antioxidant seleno-enzymes. Immunity improvement is illustrated by the study of Berger and colleagues, with reduction of nosocomial pneumonia in burnt patients under multi-trace-element supplementation. As seleno-compounds (especially sodium selenite) are pro-oxidant, however, administration above 800 microg/day may be dangerous in septic shock. Paradoxically, direct reversible pro-oxidative effects of seleno-compounds may also be beneficial for reduction of inflammation (genomic action, apoptosis), and may even be bactericidal or virucidal. These facts need to be further examined, as well as the possible dramatic drop of plasma selenoprotein P in septic shock and its role in endothelium protection.

Apoptosis↗