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PubMed1994

Sodium, large arteries, and diuretic compounds in hypertension.

Clinical and experimental data have shown that antihypertensive drugs do not cause the same change in arterial compliance for an equipotent blood pressure reduction. However, there is not clear data on the effect of sodium and diuretics on the visco-elastic properties of the hypertensive arterial wall. Cross-sectional epidemiologic studies suggest that, at any given value of age and blood pressure, pulse wave velocity is lower in the presence of decreased sodium intake. Longitudinal studies indicate that, in hypertensive subjects, low sodium intake is associated with a larger brachial artery diameter than is high sodium intake. In hypertension in the elderly and in severe hypertension with end-stage renal disease, sodium overload causes a reduction in arterial compliance and distensibility unrelated to blood pressure changes. In animal studies, the diuretic compounds cycletanine and indapamide were shown to increase systemic and carotid compliance independently of blood pressure changes. In contrast, a crossover study of hypertensive subjects showed that the diuretic agent hydrochlorothiazide did not change arterial compliance and pulse wave velocity, whereas the calcium entry blocker, felodipine, improved these parameters. Nevertheless, indapamide decreased the pulse pressure on stroke volume ratio, a parameter used as a marker of aortic distensibility. Taken together, such studies indicate that sodium may act on the arterial wall independently of blood pressure changes. The contribution of counter regulatory mechanisms, possibly related to the renin-angiotensin and sympathetic nervous systems, might explain the differences between the clinical and experimental changes observed with diuretic compounds. Of the various antihypertensive agents, diuretics seem to have the least effect on the arterial system.

Animals↗
PubMed1997

Lipid peroxidation in linoleic acid micelles caused by H2O2 in the presence of myoglobin.

We investigated the lipid peroxidation in linoleic acid micells caused by H2O2 in the presence of metmyoglobin by monitoring the oxygen consumption. O2 consumption usually consisted of two phases. In the first phase, it occurred slowly and linearly until the concentration of linoleic acid hydroperoxide reached a certain value, rapid consumption, presumably by a chain reaction, then followed in the second phase. No effects of diethylenetriaminepentaacetic acid (DTPA) on the induction period (the period during the first phase) and the maximum oxygen consumption rate (MOCR) in the second phase indicate that free ferric ions liberated from myoglobin had no role in any phases during the lipid peroxidation. The differing dose effects of ascorbic acid, alpha-tocopherol, and sodium nitrite on the induction period and MOCR reflect their respective antioxidative mechanisms during lipid peroxidation.

Antioxidants↗
PubMed2001

Design of semicarbazones and their bio-isosteric analogues as potential anticonvulsants.

A series of semicarbazones and hydrazones were prepared and evaluated for anticonvulsant activity. Some compounds provided significant protection against maximal electroshock (MES) and subcutaneous strychnine induced seizures (ScSty). Compound 2a emerged as the most active compound at a dose of 30 mg/kg in ScSty test. The compounds 1a, 1g and 2a-e showed significant potentiation of sedative and hypnotic activity of pentobarbitone sodium. Thus compound 2a could serve as a prototype for future developments.

Animals↗
PubMed1980

Absence of arsenite mutagenicity in E coli and Chinese hamster cells.

Because exposure to compounds of arsenic has been implicated as a cause of cancer, an investigation of the mutagenicity of sodium aresenite in E coli and in Chinese hamster cells was performed. In the E coli system, Trp + revertants were not induced by arsenite in a variety of experimental protocols including spot tests, treat and plate protocols, and fluctuation tests. The mutator effect of a tif-1 strain was partially blocked by arsenite. Arsenite did not cause the induction of lambda prophage. In Chinese hamster cells, arsenite did not induce ouabain-resistant mutants or thioguanine-resistant mutants. We conclude that arsenite is not mutagenic to E coli or to Chinese hamster cells. When added to the plating medium, arsenite can act as an anti-mutagen by inhibition of induction of the error-prone SOS repair system in E coli.

Animals↗
PubMed1969

Schiff bases formed from retinal and phosphatidylethanolamine, phosphatidylserine, ethanolamine or serine.

1. Conditions were established for the reaction of retinal with phosphatidylethanolamine, phosphatidylserine, ethanolamine and serine in chloroform, ethanol or ethanol-water solutions to form retinylidene compounds, or Schiff bases. 2. The Schiff bases were reduced to retinyl compounds with sodium borohydride. 3. Absorption maxima and molar extinction coefficients were determined for the various retinylidene and retinyl compounds and for the corresponding coloured products formed by their reaction with antimony trichloride.

Amino Alcohols↗
PubMed1977

The interaction of phospholipid membranes and detergents with glutamate dehydrogenase.

1. Both the anionic detergent sodium dodecylsulphate and the cationic detergent cetyltrimethylammonium bromide quenched the protein fluorescence of glutamate dehydrogenase. The anionic compound was more effective and brought about 50% quenching at a detergent concentration of 0.4 mM. The zwitterionic amphiphile, lysolecithin, did not quench the protein fluorescence and neither did the short-chain detergent n-hexylsulphonate, which under the range of concentrations examined (less than 1 mM) does not form micelles. 2. The zwitterionic phospholipid, phosphatidylcholine, did not quench the protein fluorescence but the anionic phospholipids, phosphatidylserine and cardiolipin, induced a reversible quenching of the enzyme fluorescence. These observations confirm the specificity of the phospholipid-enzyme interactions as deduced from the kinetic studies of the preceding paper. The degree of quenching brought about by the phospholipids decreased with increasing ionic strength and increasing pH and could be substantially reduced by basic proteins. An electrostatic contribution to the interaction is inferred from these results. 3. The binding of the anionic phospholipids to the enzyme is manifested in a further enhancement of the fluorescence of a 1-anilinonaphthalene-8-sulphonate-enzyme complex. The presence of substrates and allosteric effectors affect the interaction of the lipids with the enzyme as indicated by the magnitude of this increase in fluorescence. The enhancement of fluorescence of NADH when bound to the enzyme was not affected by the binding of the lipids. 4. The complex formed between the enzyme and phosphatidylserine/phosphatidylcholine can be solubilized in isooctane. The photolability of the aqueous protein when subjected to irradiation at 280 nm is suppressed in the isooctane-soluble complex. 5. Phosphatidylserine brings about a rapid (t 1/2 is about 150 ms at a lipid concentration of 0.75 mM) dissociation of the linear aggregates formed between the enzyme oligomers. 6. A model of the enzyme-lipid-membrane complex, consistent with these results, is proposed. It is suggested that the enzyme is an allotopic protein and that the dissociation of the enzyme in vitro may involve binding sites on the protein which are designed for interaction with the cardiolipin of the inner mitochondrial membrane, when the enzyme is in the mitochondrial matrix.

Ammonium Chloride↗
PubMed1988

Pyrethroid insecticides and DDT modify alkaloid-dependent sodium channel activation and its enhancement by sea anemone toxin.

The effects of saturating concentrations of DDT [1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane] and the pyrethroid insecticides cismethrin and deltamethrin on alkaloid-dependent activation of the voltage-sensitive sodium channel were studied using measurements of 22Na+ uptake into mouse brain synaptosomes. In survey experiments, these compounds enhanced sodium uptake stimulated by veratridine and batrachotoxin, but inhibited uptake stimulated by aconitine. Concentration response curves for aconitine run in the absence and presence of 10 microM cismethrin demonstrated that the inhibition was noncompetitive. This unanticipated inhibitory effect of insecticides on aconitine-dependent sodium uptake suggests a possible overlap or negative allosteric coupling between the binding sites for insecticides and aconitine and reveals unique characteristics of the action of aconitine that are not shared by veratridine and batrachotoxin. More detailed studies of the effects of insecticides on veratridine- or batrachotoxin-stimulated uptake found small insecticide-dependent increases in the potency of these activators. In addition to this effect, DDT and deltamethrin also enhanced maximal uptake stimulated by veratridine. Possible mechanisms underlying these effects of insecticides on alkaloid-dependent uptake are discussed in light of a qualitative model formulated from these results and previous biochemical and electrophysiological studies. Additional experiments were designed to assess the interactions of insecticides and toxin II of the sea anemone Anemonia sulcata (ATX II) as modifiers of alkaloid-dependent uptake. DDT and ATX II acted synergistically to increase uptake stimulated by veratridine. Moreover, DDT shifted the potency of ATX II for enhancing veratridine-dependent uptake to 5-fold lower concentrations. In contrast, DDT and subsaturating concentrations of ATX II acted independently in their enhancement of sodium channel activation by batrachotoxin. Mutually exclusive effects on veratridine-dependent uptake were observed when cismethrin was co-applied with ATX II. However, independent effects of cismethrin and ATX II were found with aconitine-modified channels, in that cismethrin was able to inhibit ATX II-enhanced aconitine-dependent sodium flux. Thus, the interactions between insecticides and ATX II as modifiers of alkaloid-dependent uptake are complex and depend on the insecticide-activator combination under study.

Aconitine↗
PubMed2005

Preparation and characterization of NaCS-CMC/PDMDAAC capsules.

A novel capsule system composed of sodium cellulose sulfate (NaCS), carboxymethyl cellulose (CMC) and poly[dimethyl(diallyl)ammonium chloride] (PDMDAAC) was prepared for improving the properties of NaCS/PDMDAAC capsules. The process parameters, such as CMC concentration (0, 2, 4, 6 and 8 g/L), NaCS concentration (20, 25, 30, 35 and 40 g/L), PDMDAAC concentration (20, 30, 40, 50, 60, 70 and 80 g/L), reaction time and temperature were investigated to understand their effects on the diameter, membrane thickness and mechanical strength of capsules. The optimum operation conditions for preparing NaCS-CMC/PDMDAAC capsules were determined as 6-8 g/L CMC, 35-40 g/L NaCS, 60 g/L PDMDAAC and polymerization for 30-40 min. Diffusion of substances with low molecular weight into capsules was investigated, and diffusion coefficients were calculated according to the developed model. The yeast of Candida krusei was chosen as representative cell to evaluate the effects of different cell loading on capsule mechanical strength. Meanwhile the encapsulated osmophilic C. krusei cells were cultured in 250 mL shaking flasks for 72 h to determine the cell leaking properties in short and long term.

Capsules↗
PubMed1997

Moderate doses of iodide in vivo inhibit cell proliferation and the expression of thyroperoxidase and Na+/I- symporter mRNAs in dog thyroid.

The function and the growth of adult thyroid gland is controlled by the opposite actions of thyrotropin (TSH) and iodide, the main substrate of the gland. Iodide deprivation leads to stimulation of the thyroid, improving the efficiency of iodide transport for hormone biosynthesis. We have investigated cell proliferation and thyroid specific gene expression 24 and 48 h after administering KI to dogs previously treated with goitrogens and perchlorate. In the hypothyroid dogs T3 and T4 serum levels decreased from 53 +/- 4 to < 30 ng/dl and from 1.6 +/- 0.6 to < 1 microg/dl respectively; TSH concentration increased from 0.16 +/- 0.02 to 2.7 +/- 0.4 ng/ml. After a 24 h moderate KI treatment (300 microg KI/dog of +/- 10 kg) serum T3 concentrations rose higher than the initial normal values, while T4 concentrations increased to reach values equivalent to the normal level. The high TSH concentration did not change significantly. The hyperplasia of the chronically stimulated thyroid resulting from goitrogens/NaClO4 treatment was not modified by this short term treatment with KI. In contrast, KI decreased the weight of the total gland and the level of cell proliferation, as determined by the fraction of cells incorporating BrdU. The effect of acute administration of KI on the expression of four major thyroid genes, the TSH receptor (TSHr), thyroglobulin (Tg), thyroperoxidase (TPO), and Na+/I- symporter (NIS) was analyzed by Northern blot. Tg, TPO and NIS mRNA expressions were up-regulated by chronic stimulation. The expression of the mRNAs of TSHr and Tg did not significantly differ between hyperstimulated and KI-treated dogs while TPO and NIS mRNA expression decreased after a 48 h KI treatment. TPO and NIS are therefore the only of these four genes whose expression is acutely modulated by iodide in vivo. Under TSH stimulation low doses of iodide resulted in: (1) decreased cell proliferation, (2) reestablished synthesis and secretion of thyroid hormones, (3) diminished TPO and NIS mRNA expression. Notably low doses of iodide under the same conditions had no effect on Tg and TSHr mRNA expression.

Animals↗
PubMed2000

Stability studies on (99m)technetium(III) complexes with tridentate/monodentate thiol ligands and phosphine ('3 + 1 + 1' complexes).

The preparation and characterisation of 3 + 1 + 1 technetium complexes of the general formula [Tc(SES)(RS)(PMe2Ph)] (SES = tridentate dithiol ligand, E = S, O, NMe; RSH = monothiol ligand) at the n.c.a. level is described. The Tc(III) complexes are prepared in a one-step procedure starting from pertechnetate in yields of 85-95% of radiochemical purity. A comparison of their chromatographic data with the fully characterised 99Tc complexes indicate the identity of the investigated compounds. Stability studies show that the 99mTc complexes undergo some alteration in solution. They are oxidised to the 3 + 1 oxotechnetium (V) complexes and/or decompose in aqueous solution. In challenge experiments performed with glutathione, exchange of the monothiolato ligand occurs in the same manner as known for the 3 + 1 complexes.

Chromatography, High Pressure Liquid↗