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At least 649 records · Page 36Linked to original sources
PubMed1986

Effect of in vitro inorganic lead on dopamine release from superfused rat striatal synaptosomes.

The effect of inorganic lead in vitro in several aspects of [3H]dopamine release from superfused rat striatal synaptosomes was examined. Under conditions of spontaneous release, lead (1-30 microM) induced dopamine release in a concentration-dependent manner. The onset of the lead-induced release was delayed by approximately 15-30 sec. The magnitude of dopamine release induced by lead was increased when calcium was removed from the superfusing buffer. Lead-induced release was unaffected in the presence of putative calcium, sodium, and/or potassium channel blockers (nickel, tetrodotoxin, tetraethylammonium, respectively). Depolarization-evoked dopamine release, produced by a 1-sec exposure to 61 mM potassium, was diminished at calcium concentrations below 0.254 mM. The onset of depolarization-evoked release was essentially immediate following exposure of the synaptosomes to high potassium. The combination of lead (3 or 10 microM) with high potassium reduced the magnitude of depolarization-evoked dopamine release. This depression of depolarization-evoked release by lead was greater in the presence of 0.25 mM than 2.54 mM calcium in the superfusing buffer. These findings demonstrate multiple actions of lead on synaptosomal dopamine release. Lead can induce dopamine release by yet unidentified neuronal mechanisms independent of external calcium. Lead can also reduce depolarization-evoked dopamine release by apparent competition with calcium influx at the neuronal membrane calcium channel.

Animals↗
PubMed1982

Lactate efflux-induced electrical potential in membrane vesicles of Streptococcus cremoris.

We developed a procedure for isolating membrane vesicles from the homolactic fermentative bacterium Streptococcus cremoris. The membrane vesicles were shown to have a right-side-out orientation by freeze-etch electron microscopy and to be free of cytoplasmic constituents. The membrane vesicles retained their functional properties and accumulated the amino acids L-leucine, L-histidine, and L-alanine in response to a valinomycin-induced potassium diffusion gradient. Studies with these membrane vesicles strongly supported the possibility that there was a proton motive force-generating mechanism by end product efflux (Michels et al., FEMS Lett. 5:357-364, 1979). Lactate efflux from membrane vesicles which were loaded with L-lactate and diluted in a lactate-free medium led to the generation of an electrical potential across the membrane. The results indicate that lactate efflux is an electrogenic process by which L-lactate is translocated with more than one proton.

Amino Acids↗
PubMed2000

Use of 15N reverse gradient two-dimensional nuclear magnetic resonance spectroscopy to follow metabolic activity in Nicotiana plumbaginifolia cell-suspension cultures.

Nitrogen metabolism was monitored in suspension cultured cells of Nicotiana plumbaginifolia Viv. using nuclear magnetic resonance (NMR) spectroscopy following the feeding of (15NH4)2SO4 and K15NO3. By using two-dimensional 15N-1H NMR with heteronuclear single-quantum-coherence spectroscopy and heteronuclear multiple-bond-coherence spectroscopy sequences, an enhanced resolution of the incorporation of 15N label into a range of compounds could be detected. Thus, in addition to the amino acids normally observed in one-dimensional 15N NMR (glutamine, aspartate, alanine), several other amino acids could be resolved, notably serine, glycine and proline. Furthermore, it was found that the peak normally assigned to the non-protein amino-acid gamma-aminobutyric acid in the one-dimensional 15N NMR spectrum was resolved into a several components. A peak of N-acetylated compounds was resolved, probably composed of the intermediates in arginine biosynthesis, N-acetylglutamate and N-acetylornithine and, possibly, the intermediate of putrescine degradation into gamma-aminobutyric acid, N-acetylputrescine. The occurrence of 15N-label in agmatine and the low detection of labelled putrescine indicate that crucial intermediates of the pathway from glutamate to polyamines and/or the tobacco alkaloids could be monitored. For the first time, labelling of the peptide glutathione and of the nucleotide uridine could be seen.

Amino Acids↗
PubMed2003

Epinephrine reduces the nerve conduction blockage induced by high-potassium in mammalian sciatic nerve.

We investigated the effects of epinephrine on the reversible nerve conduction block induced by high [K(+)](o) using electrophysiological extracellular recordings in the isolated rat sciatic nerve in vitro. Bath application of 400 micro M epinephrine (EN) or norepinephrine (NE) reduced the high-potassium-induced compound action potentials (CAPs) blockage in both sensory and motor fibers. The beta-adrenoreceptor agonist isoproterenol mimicked the EN effect while the alpha-adrenoreceptor agonists phenylephrine and guanfacine did not affect the CAPs reduction. Addition of EN to normal ACSF partially reversed the nerve conduction blockage induced by high frequency stimulation. These results suggest that EN and NE modulate the electrophysiological properties of both sensory and motor axons, and they improve the nerve conduction under high [K(+)](o) by modulating nerve excitability.

Action Potentials↗
PubMed1991

Effects of dopamine agonists on dopamine secretion from PC12 cells: lack of functional autoreceptor activity.

In an effort to determine if PC12 cells have functional dopamine autoreceptors we found that carbachol-stimulated release of dopamine from undifferentiated PC12 cells was inhibited by the dopamine autoreceptor agonists apomorphine and U-68553B. Studies were conducted to determine the mechanism of this effect. The inhibition of dopamine release by apomorphine or U-68553B did not appear to result from effects on dopamine metabolism. When cells were exposed to the dopamine agonists for 2 minutes no changes in dopa, DOPAC or dopamine were observed. Over this same time interval, apomorphine and U68553B at 10 microM inhibited carbachol-stimulated dopamine release by 45.6% and 57.4% respectively. However, these drugs failed to inhibit the potassium dependent release of dopamine from cells suggesting no direct involvement with ion fluxes. Furthermore, haloperidol did not block the inhibitory effects of U-68553B on PC12 cells. This would appear to preclude activation of a dopamine autoreceptor as a possible mechanism. Kinetic analysis revealed that U-68553B is most likely a non-competitive inhibitor (Ki = 2 microM) of the nicotinic acetylcholine receptor. These data do not provide evidence for functional dopamine autoreceptors on undifferentiated PC12 cells but rather indicate that dopamine agonists may alter dopamine release by alternative mechanisms.

Animals↗
PubMed1995

[Studies on inhibitive effects of organic selenium on cell damage caused by SiO2].

Changes in potassium content of macrophage in guinea pigs and in membrane protein of erythrocytes in rats caused by quartz dust, and the effects of selenium-protein and selenium-containing polysaccharide of cell membrane on them were determined with atomic absorption spectrometry and electronic spin label. Results showed quartz could significantly decrease potassium content of macrophage with a dose-effect relationship. Potassium content in the exposed group could return to normal level as the control group by adding Se-protein into quartz dust. Rotational correlation times of the membrane protein in erythrocytes could be decreased by quartz dust, and Se-protein and Se-containing polysaccharide could make them normal. It suggested quartz could cause cell permeability significantly increased, cleavage of peptide-chain of membrane protein, degradation and cross-linkage of protein, and cell damage, but organic selenium could decrease cytotoxicity caused by quartz dust and protect cells from the damage.

Animals↗
PubMed2003

Thyroperoxidase gene mutations in congenital goitrous hypothyroidism with total and partial iodide organification defect.

Mutations of the thyroperoxidase (TPO) gene have been reported as being the most severe and frequent abnormality in thyroid iodide organification defect (IOD) causing goitrous congenital hypothyroidism. The objective of this study was to screen and subsequently identify TPO gene mutations in patients with congenital hypothyroidism with evidence of total iodine organification defects (TIOD) or partial iodine organification defect (PIOD) as defined by the perchlorate discharge test. Seven goitrous patients with TIOD and seven patients with PIOD, from three and five unrelated families, respectively, were studied. We were able to detect different TPO genes mutations in patients with TIOD and PIOD. In TIOD families the results were as follows: (1) a homozygous GGCC insertion at exon 8, position 1277 (family 1); (2) compound heterozygosity with a GGCC insertion at exon 8 (1277) and a nucleotide substitution in exon 11 (2068G>C) (family 2); (3) compound heterozygosity with the mutation 2068G>C in exon 11 and a C insertion in exon 14 between positions 2505-2511 (family 3). In patients with PIOD we have detected: (1) only one heterozygous mutation in two families (4 and 5), in exons 11 and 10 (2084G>A and 1780C>A); (2) a compound heterozygous condition in one family (family 6), with mutations, respectively in exons 8 and 10 (1242G>T and 1780C>A); (3) only polymorphisms (family VII) and (4) a heterozygous mutation in the first base of the border exon/intron 9 +1G>T (family VIII). We did not detect inactivating mutations in exons 11, 16, and 21 of the THOX2 gene where mutations have been previously described. We concluded that homozygous and compound heterozygous mutations found in TIOD characterized the autosomal recessive mode of inheritance and will translate a nonfunctional protein or a protein that may not reach the apical membrane. As for PIOD, the majority of the studied kindreds had only heterozygous mutations and/or polymorphisms. It is conceivable that these TPO gene sequence alterations may partially affect the functional state of the translated protein or affect its transport to the apical membrane.

Adolescent↗
PubMed1993

The application of the AMB protective group in the solid-phase synthesis of methylphosphonate DNA analogues.

Partially methylphosphonate-modified oligodeoxynucleotides were synthesized on solid-phase by employing the easily removable 2-(acetoxymethyl)benzoyl (AMB) group as base-protecting group. Although a rapid AMB deprotection can be accomplished in methanolic potassium carbonate, the lability of the methylphosphonate linkage towards potassium carbonate/methanol excludes the use of this deprotection reagent. Thus, saturated ammonia solution in methanol was investigated as an alternative reagent for AMB removal. It is demonstrated that the combination of the AMB protective group and ammonia/methanol as deprotection reagent significantly improves the synthesis of methylphosphonate-modified DNA fragments. A mild overnight treatment at room temperature is sufficient for complete removal of the AMB group, whereas deprotection of conventionally protected oligonucleotides requires much longer exposure to basic conditions at elevated temperatures.

Acetates↗
PubMed1992

Angiotensin-converting enzyme inhibition, angiotensin, and cognition.

In these studies, we have investigated possible cognition-enhancing effects of angiotensin-converting enzyme (ACE) inhibition, and putative neurochemical correlates for these actions. In a mouse habituation model, ACE inhibitors improved basal performance and antagonized scopolamine-induced deficits. The performance of aged mice and those with lesions of the nucleus basalis was also improved. ACE inhibition also improved scopolamine-impaired performance of rats in a swim-maze model. Neurochemical studies showed that a low dose (10 micrograms/kg i.p.) of ceranapril caused significant alterations in ex vivo rat brain catecholamine levels in the nucleus accumbens, amygdala, and septum. In further studies, angiotensin II (Ang II) was shown to decrease potassium-stimulated [3H] acetylcholine release from slices of rat entorhinal and human temporal cortex, an effect that could be antagonized by the angiotensin receptor antagonist [1-sar,8-thr]Ang II. It is concluded that ACE inhibition can improve both basal and impaired performance in animal models of learning, and that this improvement may be in part a consequence of the removal by ACE inhibition of an inhibitory tone on central acetylcholine release, and/or an effect on central catecholaminergic function.

Acetylcholine↗
PubMed1994

Involvement of nitric oxide and nitrosothiols in relaxation of pulmonary arteries to peroxynitrite.

Peroxynitrite (ONOO-) is an inflammatory cell-derived oxidant, formed by the reaction of superoxide anion (O2-) with nitric oxide (NO), which was recently reported to relax vascular tissues. In the present study, the potential role of NO in the mechanism of relaxation in isolated bovine endothelium-denuded pulmonary arterial smooth muscle rings to ONOO- was evaluated. Potassium-preconstricted pulmonary arterial rings rapidly relaxed for a prolonged period of time on exposure to ONOO- (0.01-0.1 mM). The relaxation after 1 min of exposure to ONOO- (0.1 mM) was reduced 49 and 87%, respectively, by inhibitors of the stimulation of soluble guanylate cyclase, methylene blue, and LY-83583. In contrast, a scavenger of hydroxyl radicals, dimethyl sulfoxide, did not alter this response. Decomposed 0.1 mM ONOO- (which is primarily nitrite) and 0.1 mM nitrite caused a relaxation of pulmonary artery, which slowly developed over 15 min. Small quantities of NO were detected by chemiluminescence quantification methods when ONOO- was added to buffer. Exposure of pulmonary arterial tissue or buffer containing glutathione (GSH) to ONOO- caused a time-dependent increase in the observed generation of NO, whereas decomposed ONOO- produced 10% of the NO generated by ONOO- on incubation with pulmonary arterial tissue. Treatment with diethyl maleate, an agent that depletes tissue GSH, reduced both the relaxation and the formation of NO detected from pulmonary artery on exposure to ONOO-. GSH solutions treated with ONOO- appear to have generated a nitrosothiol-like vascular relaxant compound. Thus ONOO- appears to relax vascular tissue, in part, by nitrosylating tissue GSH (or other thiols), which subsequently releases NO over prolonged time periods.

Aminoquinolines↗
PubMed1989

Prolonged exposure to a K-rich medium makes the rat mast cell membrane permeable to external calcium ions.

Rat mast cells, pretreated with a Ca-free, high KCl medium for more than 30 min, released histamine when subsequently exposed to a medium containing 0.1-2 mM Ca, despite the absence of voltage-dependent Ca channels. Morphological studies showed that high KCl-treated cells became swollen and that the addition of Ca caused degranulation (exocytosis). Ca-stimulated histamine release was inhibited when the high KCl treatment medium contained dinitrophenol and 2-deoxyglucose. The response to Ca was also observed when KCl in the treatment medium was replaced by RbCl, CsCl, KBr or KNO3. When the high K-treated cells were incubated with 0.5 mM 45Ca at 0-1 degree C, 45Ca uptake by these cells was much larger than that by untreated cells, suggesting that the membrane permeability to Ca of these cells is increased. Although prolonged (90 min) incubation of the cells with an isotonic KCl medium increased the rate of leakage of lactate dehydrogenase possibly reflecting extensive cell swelling, most cells recovered the ability of responding to stimulation with compound 48/80 or with simultaneous removal of Na and Ca when subsequently incubated with a Na-based medium containing Ca. Raising the KCl concentration above normal osmolarity in the treatment medium reduced the extents of cell swelling, without reducing the response to Ca addition. Under various other experimental conditions, a poor correlation was also found between the extents of swelling and the magnitude of the response to Ca. These results raised the possibility that intracellular accumulation of a particular species of anions increased membrane permeability to Ca.

Animals↗
PubMed2006

Multi-criteria decision making approach and experimental design as chemometric tools to optimize HPLC separation of domperidone and pantoprazole.

This paper deals with multiple response simultaneous optimization using the Derringer's desirability function for the development of a reversed-phase HPLC method for the simultaneous determination of domperidone and pantoprazole in commercial pharmaceutical preparations. Twenty experiments, taking the retention factor of the first peak, the two resolutions, and three retention times as the responses with three important factors, mobile phase composition, buffer molarity and flow rate, were used to design mathematical models. The experimental responses were fitted into a second order polynomial and the six responses simultaneously optimized to predict the optimum conditions for the effective separation of the studied compounds. The optimum assay conditions were: methanol-acetonitrile-dipotassium hydrogen phosphate (pH 7.0; 15.3 mM) (20:33:47, v/v/v) as the mobile phase and at a flow rate of 1.19 ml/min. While using this optimum condition, baseline separation with a minimum resolution of 2.0 and a run time of less than 6 min were achieved. The method showed good agreement between the experimental data and predictive value throughout the studied parameter space. The optimized assay condition was validated according to ICH guidelines to confirm specificity, linearity, accuracy and precision.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1994

Diphenyleneiodonium inhibits both potassium and calcium currents in isolated pulmonary artery smooth muscle cells.

Diphenyleneiodonium (DPI) blocks hypoxic vasoconstriction in the pulmonary vasculature. Because one of the actions of DPI is the inhibition of NADPH oxidase, this has led to the suggestion that NADPH oxidase acts as an oxygen tension sensor in pulmonary smooth muscle cells. We investigated the effects of DPI on potassium and calcium currents in freshly isolated pulmonary artery smooth muscle cells by using whole cell patch-clamp recordings, since these ionic currents are known to be involved in hypoxic pulmonary vasoconstriction. DPI (3 and 10 microM) reversibly inhibited potassium currents, and in its presence, residual currents appeared markedly more transient than under control conditions. The actions of DPI could not be reversed by 4.4 mM hydrogen peroxide, the product of NADPH oxidase. Calcium channel currents were also reversibly inhibited by 3 microM DPI. Thus DPI is a nonselective blocker of ionic channels in pulmonary smooth muscle cells, and its mechanism of action does not appear to involve inhibition of hydrogen peroxide formation. The ability of DPI to block calcium currents can explain its inhibition of hypoxic pulmonary vasoconstriction.

Animals↗
PubMed2001

Kinetics of chemical degradation of isoxaflutole: influence of the nature of aqueous buffers (alkanoic acid/sodium salt vs phosphate).

A kinetic study of the chemical degradation of isoxaflutole (5-cyclopropyl-1,2-oxazol-4-yl alpha alpha alpha-trifluoro-2-mesyl-p-tolyl ketone) into its diketonitrile derivative (DKN), which is its active herbicide principle, in organic buffers at different pH values was carried out using a HPLC/UV detection method. The values of the pseudo-first-order rate constants Kobs for the reaction were calculated and compared with those previously obtained in inorganic buffers. In both cases, Kobs was found to be dependent on pH and temperature, but at pH 5.2 the degradation of isoxaflutole in CH3COOH/CH3COONa buffers was considerably faster than in KH2PO4/Na2HPO4 buffers, indicating that the compound was sensitive to the nature of the reagents used to prepare buffered solutions. The influence of phosphate and acetate concentrations and the influence of the R-substituent in RCOOH/RCOONa buffers were investigated. For the HA/A- buffers studied, the values of Kobs were linearly dependent on HA and A- concentrations, which meant that the degradation of isoxaflutole was subject to general catalysis. The values of Kobs were also found to be dependent on the number and the position of the CH3 groups of the R-substituent. The known degradation product of DKN (a benzoic acid derivative) was not detected throughout this study.

Biodegradation, Environmental↗
PubMed1977

Cation permeability ratios of sodium channels in normal and grayanotoxin-treated squid axon membranes.

Permeabilities of squid axon membranes to various cations at rest and during activity have been measured by voltage clamp before and during internal perfusion of 4 X 10(-5) M grayanotoxin I. The resting sodium and potassium permeabilities were estimated to be 6.85 X 10(-8) cm/sec and 2.84 X 10(-6) cm/sec, respectively. Grayanotoxin I increased the resting sodium permeability to 7.38 10(-7) cm/sec representing an 11-fold increase. The potassium permeability was increased only by a factor of 1.24. The resting permeability ratios as estimated by the voltage clamp method before application of grayanotoxin I were Na (1): Li (0.83): formamidine (1.34): guanidine (1.49): Cs (0.87): methylguanidine (0.86): methylamine (0.78). Grayanotoxin I did not drastically the resting permeability ratios with a result of Na (1): Li (0.95): formamidine (1.27): guanidine (1.16): Cs (0.47): methylguanidine (0.72): methylamine (0.46). The membrane potential method gave essentially the same resting permability ratios before and during application of grayanotoxin I if corrections were made for permeability to choline as the cation substitute and for changes in potassium permeability caused by test cations. The permeability ration choline/Na was estimated to be 0.72 by the voltage clamp method and 0.65 by the membrane potential method. Grayanotoxin I decreased the ration to 0.43. The permeability ratios during peak transient current were estimated to be Na (1): Li (1.12): formamidine (0.20): guanidine (0.20): Cs (0.085): methylguanidine (0.061): methylamine (0.036). Thus the sodium channels for the peak current are much more selective to cation than the resting sodium channels. It appears that the resting sodium channels in normal and grayanotoixn I-treated axons are operationally different from the sodium channels that undergo a conductance increase upon stimulation.

Animals↗
PubMed1992

Nicotine-induced depolarization of cerebral cortical synaptosomes is dependent upon sodium.

Earlier studies from this laboratory demonstrated that activation of nicotinic cholinergic receptors of cerebral cortical synaptosomes of the rat produced a decrease in the accumulation of [3H]tetraphenylphosphonium ([3H]TPP+) as a result of a decreased synaptosomal membrane potential. In the present study, the role of sodium in the effect of nicotine on the accumulation of [3H]TPP+ and the estimated potential difference was explored. Replacement of buffer sodium with either sucrose or N-methyl-D-glucamine (NMDG), attenuated the depolarization produced by the sodium channel activator, veratridine and had no effect on potassium-induced depolarization. The effect of nicotine on accumulation of [3H]TPP+ into cerebral cortical synaptosomes was abolished in sucrose buffer and attenuated in NMDG buffer. 1,1-Dimethyl-4-phenylpiperazinium iodide (DMP; 30 microM) produced a small increase in the influx of 22Na+ into cerebral cortical synaptosomes. The effect of DMPP on the influx of 22 Na+ was not blocked by tetrodotoxin. These results support the hypothesis that the nicotinic cholinergic receptor in the brain, functions as a sodium ionophore and further demonstrate that accumulation of synaptosomal [3H]TPP+ provides a simple tool with which to assess the effect of nicotine on sodium permeability through open nicotinic cholinergic receptor ionophores.

Animals↗
PubMed1985

Subsynaptosomal distribution of calcium during aging and 3,4-diaminopyridine treatment.

Since previous studies showed that calcium uptake by synaptosomes from rodents declines with aging, the subsynaptosomal distribution of calcium was determined with the disruption method of Scott et al. Calcium uptake by the mitochondrial (digitonin-resistant) and non-mitochondrial (digitonin-labile) compartments, as well as total uptake, were determined at 2, 5 and 10 min. After a 10 min incubation under resting conditions (5 mM-KCl), total calcium uptake decreased at 10 months (-14.6%) and 30 months (-33.0%) of age; mitochondrial calcium uptake increased by 10 months (+ 11.2%) but declined by 30 months (-17.5%); the non-mitochondrial calcium compartment declined at 10 (-34.7%) and 30 (-43.4%) months when compared to the 3 month old control. With potassium depolarization (31 mM-KCl), total calcium uptake declined from 100% (3 months) to 73.8% (10 months) or 53.0% (30 months); mitochondrial calcium uptake declined from 100% (3 months) to 85.6% (10 months) or 68.4% (30 months); non-mitochondrial calcium uptake decreased at 10 (-34.3%) and 30 (-57.7%) months of age when compared to 3 months (100%). The deficits in calcium homeostasis are not due to changes in synaptosomal volumes or to diminished membrane potentials, as assessed by tetraphenylphosphonium ion accumulation. 3,4-Diaminopyridine partially reversed the alterations in total, mitochondrial and non-mitochondrial calcium uptake by synaptosomes from aged mice.

4-Aminopyridine↗
PubMed2005

[Effects of different nitrogenous compounds on growth and nodulation of Abrus cantoniensis].

OBJECTIVE: The research aimed at the effects of different nitrogenous compounds on growth and nodulation of Abrus cantoniensis. METHOD: After the seedlings of the herb were inoculated with rhizobia in potted culture, they were supplied with nutrition solutions which contained the three nitrogenous compounds, KNO3, NH4NO3, (NH4)2SO4 of different nitrogen concentration. The growth and nodulation of seedlings was determined after 70 days. RESULT: Different nitrogenous compounds were able to enhance the vegetable growth of seedlings variously. The effect of (NH4)2SO4 and NH4NO3 on growth was better than that of KNO3. Seedlings nodulation was obviously inhibited by these nitrogenous compounds. Their inhibitory effects ranked NH4NO3 > (NH4)2SO4 > KNO3. The treatments of KNO3 and the lower concentration treatments of NH4NO3 and (NH4)2 SO4 didn't inhibit the nodulation of seedlings, but the higher concentration treatment of NH4NO3 and (NH4)2SO4 severely inhibited nodulation or even made a no formation of nodule. CONCLUSION: The results showed that ammonium nitrogen the higher inhibitory ability to the nodulation of seedlings of A. cantoniensis than nitrate nitrogen. Therefore, the application of ammonium nitrogen fertilizer should be controlled in culture of the herb, which is in favor of increasing the function of biological nitrogen fixation and the quality of the medicinal materials of A. cantoniensis.

Abrus↗