Calcium is involved in photomovement of cyanobacterium Synechocystis sp. PCC 6803

The unicellular cyanobacterium Synechocystis sp. PCC 6803 (Syn6803) exhibits photomovement through gliding motility. For a better understanding of photomovement in Syn6803, we examined the effects of Ca2+ on photoorientation and motility using a computer-assisted videomicroscope motion analysis system. When calcium ion was chelated from the basic motility medium by adding 0.5 mM ethylene glycol-bis-(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), the photoorientation was completely inhibited, whereas the gliding motility remained approximately 70% of the control. Photoorientation impaired by EGTA was nearly recovered within 30 min upon addition of 1 mM Ca2+. The recovery of photoorientation by Ca2+ was mimicked by either Mn2+ or Mg2+ but not by Ba2+ or Sr2+. Lanthanum ion at 10 microM completely inhibited both phototactic orientation and gliding motility of Syn6803. Furthermore, pimozide (voltage-gated L-type calcium channel inhibitor), orthovanadate (calcium efflux blocker) and A23187 (calcium ionophore) partially inhibited phototactic orientation and gliding motility. Interestingly, photoorientation was prevented with increasing concentrations of calmodulin antagonist such as trifluoperazine (TFP) and chlorpromazine, but gliding motility was inhibited in proportion to the concentration of TFP. The results we present strongly indicate that Ca2+ plays a significant role in regulating the photomovement of Syn6803.     

The Relationship Between New Ion Channels and Ectopic Discharges From a Region of Nerve Injury

Changes in ectopic discharges from axons in an injured nerve were examined while agents that interact with ion channels were applied to the site of the nerve injury. Tetraethylammonium (TEA) greatly facilitated spontaneous ectopic discharges or evoked ectopic firing in previously silent axons.Tetrodotoxin, an Na~+ channel blocker,completely blocked spontaneous discharges.Verapamil, La3~+, and Mn2~+, agents that interact with Ca2~+ channels,blocked spontaneous discharges and depressed the responses evoked by TEA, noradrenaline and high concentration of K~+.Increasing Ca2~+ levels facilitated ectopic discharges and this effect was blocked by La3~+ and Mn2~+. Normal axons (from uninjured nerves) were insensitive to all the effects seen in the axons from the injured nerve.These results suggest that following nerve injury the membrane of the regenerating sprout contains new ion channels, particularly Ca2~+ channels, anti that these channels are responsible for the generation of ectopic discharges.     

Cell-based fluorescence screen for K+ channels and transporters using an extracellular triazacryptand-based K+ sensor

K+ channels and K+-coupled membrane transporters are important targets for drug discovery. We previously developed a triazacryptand (TAC)-based K+ sensor, TAC-Red, and demonstrated its utility to image K+ waves in mouse brain in vivo (Padmawar et al. Nat. Methods. 2005, 2, 825-827). Here, we synthesized a green-fluorescing dextran conjugate of TAC-bodipy ("TAC-Limedex") for use as an extracellular K+ sensor and demonstrated its utility in measuring K+ transport across cell membranes. TAC-Limedex fluorescence increased by 50% with increasing [K+] from 0 to 2 mM and was insensitive to [Na+], [Cl-], or pH. K+ efflux from cells was quantified from increasing extracellular TAC-Limedex fluorescence following cell immersion in K+-free buffer. In HT-29 cells, K+ efflux was 2.0 +/- 0.1 micromol/cm2/s, increasing 8-fold following K+ channel activation by ATP; the increase in K+ efflux was inhibited by a K+ channel blocker or by preventing cytoplasmic calcium elevation. Electroneutral K+/Cl- cotransport was demonstrated in SiHa cells, in which K+ efflux was increased 3-fold by hypotonic challenge; the increase in K+ efflux was fully inhibited by a K+/Cl- transport blocker. K+ efflux measurements were adapted to a commercial fluorescence platereader for automated screening. The fluorescence-based K+ transport assay largely replaces assays requiring radioactive rubidium and is suitable for high-throughput identification of K+ transport modulators.     

Patch-clamp recording of human retinal photoreceptors and bipolar cells

Photoreceptors and retinal bipolar cells are considered as nonspiking neurons; however, we recently showed that human rod photoreceptors can generate sodium action potentials in response to membrane depolarization from membrane potentials of -60 or -70 mV (Kawai et al., Neuron 30 [2001] 451). We performed patch-clamp recording of human cone photoreceptors and retinal bipolar cells to examine whether functional voltage-gated sodium channels are expressed in these cells as well as rod photoreceptors. Under current-clamp conditions, the injection of depolarizing current steps into a cone photoreceptor-induced marked action potentials. These action potentials were blocked by 1 microM tetrodotoxin, a voltage-gated sodium channel blocker. Under voltage-clamp conditions, depolarizing voltage steps-induced a fast transient inward current in several bipolar cells (n = 4/78). This current was activated from -70 to + 20 mV (maximal at -10 mV) and inactivated within 5 ms. The 10-90% rise time of this current was shorter than another inward current (less than one-hundredth). These results indicate that human cones and bipolar cells express voltage-gated sodium channels as rod photoreceptors. Sodium channels may serve to amplify the release of a neurotransmitter and to accelerate the light-dark change in photosignals.     

Membrane potential of smooth muscle cells of human allantochorial placental vessels

The membrane potential of vessel endothelial and smooth muscle cells is central to their function of regulating blood flow. In the present study, the membrane potential (MP) of smooth muscle cells of human placental arteries and veins with or without endothelium is observed. MP is classically obtained using microelectrodes inserted into the smooth muscle cells, either through the endothelium or directly. MP was found to remain stable during 120–140 min and was independent of pH over a wide physiological range. Variation of external temperature induced depolarization at 20°C. Variations in external concentrations of Na⁺ and K⁺ did not influence MP values, while increases in Ca²⁺ and Mg²⁺ concentrations caused depolarization. The membranes of vascular smooth muscle cells were also depolarized by ouabain. These data suggest that endothelial cell exert a protective effect (release of constricting or relaxing factors) and that MP is regulated, in particular, by lipid-calcium interaction, opening of voltage-dependent Ca²⁺-channels and by ATPase.     

The role of anion and cation channels in volume regulatory responses in trout red blood cells

(1) An outwardly rectifying chloride channel (ORCC) of large conductance has been detected under isotonic conditions (320 mosM 1(-1)) in the plasma membrane of trout red blood cells (RBCs) using the excised inside-out configuration. The channel, with a permeability ratio P(Cl)/Pcation of 12, was inhibited by the Cl- channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) (50 microM), and 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) (100 microM) in the bathing solution. (2) In hypotonic conditions (215 mosM 1(-1)), 44% of cell-attached patches showed spontaneous single channel activity identified as nonselective cationic (NSC) channels. A second group, corresponding to 7% of cell-attached patches, showed spontaneous activity corresponding to a channel type presenting outward rectification and anionic selectivity. Finally, 49% of patches displayed a complex spontaneous signal corresponding to the superimposition of inward and outward currents probably due to activation of different channel types. (3) Giga-seals obtained without suction in intact cells under isotonic conditions possessed NSC channels that were quiescent but which could be activated either by mechanical deformation of cell membrane or by hypotonic cell swelling. (4) Hypotonically swollen RBCs exhibited regulatory volume decrease (RVD) over 3 h, which was linked to a fivefold to sixfold increase in unidirectional fluxes of K+, a net loss of intracellular K+ and net gain of extracellular Na+. RVD and the hypotonically activated, unidirectional K+ influx continued after replacement of Cl- by methylsulfonate (MeSF) albeit more slowly. (5) The NSC channel inhibitor, barium, and the Cl- channel inhibitor, NPPB, both inhibited the RVD response by approximately 50% in Cl- containing saline. When Cl- was replaced by MeSF, the inhibition was > 90% suggesting that NSC channels and ORCC play key roles in the chloride-independent component of RVD.     

The vasorelaxant mechanisms of a Rho kinase inhibitor DL0805 in rat thoracic aorta

Rho-kinase has been suggested as a potential therapeutic target in the treatment of cardiovascular diseases. The Rho-kinase signaling pathway is substantially involved in vascular contraction. The aim of the present study was to evaluate the vasorelaxant effects of Rho kinase inhibitor DL0805 in isolated rat aortic rings and to investigate its possible mechanism(s). It was found that DL0805 exerted vasorelaxation in a dose-dependent manner in NE or KCl-induced sustained contraction and partial loss of the vasorelaxation under endothelium-denuded rings. The DL0805-induced vasorelaxation was significantly reduced by the nitric oxide synthase inhibitor N(ω)-nitro-L-arginine methyl ester, the guanylate cyclase inhibitor methylene blue and the cyclooxygenase inhibitor indomethacin. The voltage-dependent K? channel blocker 4-aminopyridine remarkably attenuated DL0805-induced relaxations. However, the ATP-sensitive K? channel blocker glibenclamide and Ca2?-activated K? channel blocker tetraethylammonium did not affect the DL0805-induced relaxation. In the endothelium-denuded rings, DL0805 also reduced NE-induced transient contraction and inhibited contraction induced by increasing external calcium. These findings suggested that DL0805 is a novel vasorelaxant compound associated with inhibition of Rho/ROCK signaling pathway. The NO-cGMP pathway may be involved in the relaxation of DL0805 in endothelium-intact aorta. The vasorelaxant effect of DL0805 is partially mediated by the opening of the voltage-dependent K? channels.     

Inhibition of superoxide generation and of increase in intracellular Ca2+ concentration by zinc in rat neutrophils stimulated with zymosan

The effect of Zn2+ on the O2- generation and change in intracellular Ca2+ concentration ([Ca2+]i) of rat peritoneal neutrophils was studied. Zymosan (serum-treated zymosan (STZ))-induced O2- generation was inhibited by Zn2+ at concentrations as low as 10 microM. A large amount of the inhibition was observed in the absence of extracellular Ca2+ but the inhibition could not be restored by increasing the extracellular Ca2+ concentration, indicating that Zn2+ does not necessarily inhibit the O2- generation competitively with extracellular Ca2+. In the absence of extracellular Ca2+, Zn2+ inhibited STZ-induced transient increase in [Ca2+]i in the concentration range that evoked a marked inhibition in the O2- generation. On the other hand, Zn2+ did not inhibit significantly STZ-induced uptake of 45Ca2+ from extracellular medium by the cells. From these results, it is suggested that Zn2+ inhibits STZ-induced release of Ca2+ from intracellular storage sites, resulting in the suppression of the activation mechanism of neutrophils.     

Effects of Ca2+ and V5+ on glucose-6-phosphatase activity in rat liver microsomes: the Ca2+ effect is reversed by regucalcin

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on glucose-6-phosphatase in the microsomes of rat liver was investigated. Addition of Ca2+ up to 2.5 microM to the enzyme reaction mixture caused a significant increase of glucose-6-phosphatase activity in hepatic microsomes, while Ni2+, Zn2+, Cd2+, Cu2+, Mn2+ and Co2+ (20 microM) did not have an appreciable effect. Vanadate (V5+) markedly inhibited the enzyme activity; a significant inhibitory effect was seen at 10 microM V5+. The Ca2+-induced increase of glucose-6-phosphatase activity was reversed by the presence of regucalcin; the effect was complete at 1.0 microM of the protein. Regucalcium had no effect on the basal activity of the enzyme. Meanwhile, the inhibitory effect of V5+ (10-100 microM) on glucose-6-phosphatase was not appreciably blocked by the presence of regucalcin (up to 2.0 microM). The present data suggest that hepatic microsomal glucose-6-phosphatase is uniquely regulated by Ca2+ and V5+, of various metals, and that the Ca2+ effect is reversed by regucalcin. The present study supports the view that regucalcin plays an important role as a regulatory protein in liver cell function related to Ca2+.     

Artificial ion channel formed by cucurbit[n]uril derivatives with a carbonyl group fringed portal reminiscent of the selectivity filter of K+ channels

Novel artificial ion channels (1 and 2) based on CB[n] (n = 6 and 5, respectively) synthetic receptors with carbonyl-fringed portals (diameter 3.9 and 2.4 A, respectively) can transport proton and alkali metal ions across a lipid membrane with ion selectivity. Fluorometric experiments using large unilamellar vesicles showed that 1 mediates proton transport across the membranes, which can be blocked by a neurotransmitter, acetylcholine, reminiscent of the blocking of the K+ channels by polyamines. The alkali metal ion transport activity of 1 follows the order of Li+ > Cs+ approximately Rb+ > K+ > Na+, which is opposite to the binding affinity of CB[6] toward alkali metal ions. On the other hand, the transport activity of 2 follows the order of Li+ > Na+, which is also opposite to the binding affinity of 2 toward these metal ions, but virtually no transport was observed for K+, Rb+, and Cs+. It is presumably because the carbonyl-fringed portal size of 2 (diameter 2.4 A) is smaller than the diameters of these alkali metal ions. To determine the transport mechanism, voltage-clamp experiments on planar bilayer lipid membranes were carried out. The experiments showed that a single-channel current of 1 for Cs+ transport is approximately 5 pA, which corresponds to an ion flux of approximately 3 x 107 ions/s. These results are consistent with an ion channel mechanism. Not only the structural resemblance to the selectivity filter of K+ channels but also the remarkable ion selectivity makes this model system unique.     

Induction of intracellular Ca2+ and pH changes in Sf9 insect cells by rhodojaponin-III, a natural botanic insecticide isolated from Rhododendron molle

Many studies on intracellular calcium ([Ca2+](i)) and intracellular pH (pH(i)) have been carried out due to their importance in regulation of different cellular functions. However, most of the previous studies are focused on human or mammalian cells. The purpose of the present study was to characterize the effect of Rhodojaponin-III (R-III) on [Ca2+](i) and pH(i) and the proliferation of Sf9 cells. R-III strongly inhibited Sf9 cells proliferation with a time- and dose-dependent manner. Flow cytometry established that R-III interfered with Sf9 cells division and arrested them in G2/M. By using confocal scanning technique, effects of R-III on intracellular free calcium ([Ca2+](i)) and intracellular pH (pH(i)) in Sf9 cells were determined. R-III induced a significant dose-dependent (1, 10, 100, 200 μg/mL) increase in [Ca2+](i) and pH(i) of Sf9 cells in presence of Ca2+-containing solution (Hanks) and an irreversible decrease in the absence of extra cellular Ca2+. We also found that both extra cellular Ca2+ and intracellular Ca2+ stores contributed to the increase of [Ca2+](i), because completely treating Sf9 cells with CdCl(2) (5 mM), a Ca2+ channels blocker, R-III (100 μg/mL) induced a transient elevation of [Ca2+](i) in case of cells either in presence of Ca2+ containing or Ca2+ free solution. In these conditions, pH(i) showed similar changes with that of [Ca2+](i) on the whole. Accordingly, we supposed that there was a certain linkage for change of [Ca2+](i), cell cycle arrest, proliferation inhibition in Sf9 cells induced by R-III.     

Photodynamic Action of Methylene Blue on the Paramecium Membrane

An electrophysiological study of photodynamic action on the Paramecium membrane was carried out. In the presence of methylene blue (MB), light-spot stimulation of an anterior and a posterior part induced a depolarization and a hyperpolarization of the membrane, respectively. Under voltage-clamping, the anterior stimulation induced an inward current, while the posterior stimulation induced an outward current. The amplitudes of these currents were dependent on the membrane potential. When K⁺ channels were blocked with Cs⁺ and tetraethylammonium (TEA⁺), the posterior outward current was inhibited, while the anterior inward current was not inhibited. Intracellular application of the Ca²⁺ chelator, 1,2 -bis (2-aminophenoxy) ethane- N,N,N',N' -tetraacetic acid (BAPTA) also inhibited the posterior outward current, but the anterior inward current was unaffected. These results suggest that photodynamic action on the Paramecium membrane primarily opens the Ca²⁺ channels and the following influx of Ca²⁺ activates the Ca²⁺-dependent K⁺ channels localized mainly on the posterior part of the membrane.     

Identification of the Large-Conductance Ca2+-Regulated Potassium Channel in Mitochondria of Human Bronchial Epithelial Cells

Mitochondria play a key role in energy metabolism within the cell. Potassium channels such as ATP-sensitive, voltage-gated or large-conductance Ca²⁺-regulated channels have been described in the inner mitochondrial membrane. Several hypotheses have been proposed to describe the important roles of mitochondrial potassium channels in cell survival and death pathways. In the current study, we identified two populations of mitochondrial large-conductance Ca²⁺-regulated potassium (mitoBK_Ca) channels in human bronchial epithelial (HBE) cells. The biophysical properties of the channels were characterized using the patch-clamp technique. We observed the activity of the channel with a mean conductance close to 285 pS in symmetric 150/150 mM KCl solution. Channel activity was increased upon application of the potassium channel opener NS11021 in the micromolar concentration range. The channel activity was completely inhibited by 1 µM paxilline and 300 nM iberiotoxin, selective inhibitors of the BK_Ca channels. Based on calcium and iberiotoxin modulation, we suggest that the C-terminus of the protein is localized to the mitochondrial matrix. Additionally, using RT-PCR, we confirmed the presence of α pore-forming (Slo1) and auxiliary β3-β4 subunits of BK_Ca channel in HBE cells. Western blot analysis of cellular fractions confirmed the mitochondrial localization of α pore-forming and predominately β3 subunits. Additionally, the regulation of oxygen consumption and membrane potential of human bronchial epithelial mitochondria in the presence of the potassium channel opener NS11021 and inhibitor paxilline were also studied. In summary, for the first time, the electrophysiological and functional properties of the mitoBK_Ca channel in a bronchial epithelial cell line were described.     

Interaction of Cu+ with mitochondria.

The uptake of Cu+ by rat liver mitochondria is rapid and extensive. Respiration is stimulated by 10 microM Cu+ then inhibited and the inhibition could not be relieved with uncoupling agents. Collapse of the membrane potential is induced by 5-10 microM Cu+. These effects are partially inhibited by radical scavengers indicating the involvement of radical production in these events. Reduction of the GSH content and production of peroxidation products by higher amounts of Cu+ was also demonstrated. Swelling of non-respiring rat liver and heart mitochondria in sodium or lithium acetate was used to study effects of Cu+ on the Na+/H+ exchanger. Swelling is stimulated by 5-100 microM Cu+. In the presence of a radical scavenger the swelling is reduced. In sodium nitrate media diltiazem-sensitive stimulated swelling is observed. Amiloride was found to inhibit Cu(+)-induced efflux of Ca2+. At high concentrations of Cu+, a general increase in permeability was the dominant feature.     

Enhancement of zymosan-induced respiratory burst of rat neutrophils by lead in vitro

The effect of Pb2+ on serum-treated zymosan (STZ)-induced O2 consumption of rat peritoneal neutrophils was studied. Pb2+ was found to mimic effectively the enhancing action of Ca2+ on the O2 consumption depending on the concentration up to about 80 microM. However, at concentrations over 80 microM, Pb2+ inhibited the O2 consumption. The enhancing effect of Pb2+ on the O2 consumption was further examined using the intracellularly Ca2(+)-depleted neutrophils. Pb2+ also enhanced the O2 consumption of the Ca2(+)-depleted cells as effectively as Ca2+. The Pb2(+)-enhanced O2 consumption of the Ca2(+)-depleted cells was inhibited by N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7) based on its calmodulin antagonistic action. The effect of Pb2+ on the activity of activator-deficient 3',5'-cyclic nucleotide phosphodiesterase (PDE), a calmodulin-dependent enzyme, was examined. Pb2+ activated PDE as effectively as Ca2+ only in the presence of calmodulin. The Pb2(+)-activated PDE activity was also inhibited by W-7 only in the presence of calmodulin. These results indicated that Pb2+ could replace Ca2+ in the activation process(es) of the respiratory burst, suggesting a possible involvement of calmodulin in the enhancing mechanism of the O2 consumption by Pb2+.     

自组装杂化离子通道膜的构筑及阳离子传输机制

以3-异氰酸丙基三乙氧基硅烷和对甲氧基苯胺为原料合成了一种可以自组装形成有机-无机杂化材料的化合物--3-(脲基-4-甲氧基苯基)丙基三乙氧基硅烷. 采用FT-IR, ¹H NMR, DSC 和XRD 分析方法对该化合物的结构以及结晶性进行了表征. 将该化合物与聚乙烯醇(PVA)共混, 利用化合物的自组装性质构筑结构均一且致密无孔的离子通道杂化膜, 通过自制的膜运输实验装置测定膜对阳离子的传输性能并提出了相应的传输机制. SEM 照片显示, 自组装杂化膜致密无缺陷, 膜厚度为8 μm. 选择5 种阳离子进行运输实验测试, 结果表明, 自组装杂化离子通道膜对一价的碱金属离子Li⁺, Na⁺和K⁺有很好的传输功能, 这要归功于杂化材料中甲氧基苯基与碱金属阳离子形成的阳离子-π相互作用力. 碱金属阳离子在膜中的扩散过程可由溶解-扩散机制来解释, 结果显示, Li⁺, Na⁺和K⁺在杂化膜中传输的渗透率大小为: P_Na⁺ > P_K⁺ > P_Li⁺ , 说明本研究中的的自组装杂化离子通道膜对Na⁺有优先选择性. 杂化离子通道膜对二价的Ca²⁺和Mg²⁺没有传输作用, 此结果给一二价阳离子的分离带来很好的研究思路.     

5-Hydroxytryptamino-induced calcium sparks in cultured rat stomach fundus smooth muscle cells

With the imaging fluorescence probe of Ca2+ (fluo-3) and a laser scanning confocal micro-scope, the spontaneous localized calcium release event was first discovered in resting rat cardiac myocytes by Cheng[1] in 1993. A mathematical simulation is developed with computer in order to reveal the effect, which is immediately suggested that these events are likely to reflect the local-ized release of Ca2+ from a small cluster of ryanodine-sensitive Ca2+ release channels in sar-coplasmic reticulum …     

Active calcium treatment transport via coupling between the enzymatic and the ionophoric sites of Ca2+ + Mg2+-ATPase.

The 20K dalton fragment of Ca2+ + Mg2+-ATPase obtained from th tryptically digested sarcoplasmic reticulum has been further purified using Bio-Gel P-100. This removed low-molecular-weight UV-absorbing and positive Lowry-reacting contaminants. The ionophoric activity of the 20K fragment in both oxidized cholesterol and phosphatidylcholine:cholesterol membranes is unaltered by this further purification. The 20K selectivity sequence in phosphatidylcholine:cholesterol membrane is Ba2+ greater than Ca2+ greater than Sr2+ greater than Mn2+ Mg2+. Digestion of intact sarcoplasmic reticulum vesicles with trypsin, which results in the dissection of the hydrolytic site (30K) from the ionophoric site (20K), is shown to disrupt energy transduction between ATP hydrolysis and calcium transport. This further implicates the 20K dalton fragment as a calcium transport site. These data and previous evidence are discussed in terms of a proposed model for the ATPase molecular structure and the mechanisms of cation transport in sarcoplasmic reticulum.     

镧对心肌细胞钾通道的作用研究

用全细胞膜片钳记录方式研究了La^3^+对大鼠心室肌细胞钾通道的作用机理。对酶解分离的大鼠心室肌细胞施一跃迁电压可引出一非钙依赖性电压去激活的外向钾电流。将10μmol/LLa^3^+加入细胞外液后，非钙依赖性电压去激活的外向钾电流明显减小，这提示在大鼠心室肌细胞钾通道上存在La^3^+结合位点。     

Decationization and dealumination of clinoptilolite tuff and ammonium exchange on acid-modified tuff

The paper presents results of investigation of exchange of the clinoptilolite tuff cations with hydrogen ions from HCl solution of concentration 0.1 mmol cm(-3) and ammonium ions solutions of concentrations 0.0071 to 2.6 mmol cm(-3). Molal concentrations, x (mmol g(-1)) of cations exchanged in acid solution and in ammonium ions solutions were compared with molal concentrations of cations obtained by determination of the cation-exchange capacity of clinoptilolite tuff. The obtained results show that at ammonium ion concentrations lower than 0.1 mmol cm(-3), with regard to exchange capacity for particular ions, best exchanged are Na+ ions, followed by Mg2+ and Ca2+ ions, while exchange of K+ ions is the poorest (Na+ > Mg2+ > Ca2+ > K+). At ammonium concentrations from 0.2 to 1 mmol cm(-3) the order is Na+ > Ca2+ > Mg2+ > K+. At concentrations higher than 1 mmol cm(-3) the order is Na+ > Ca2+ > K+ > Mg2+. The results are a consequence of the uptake of hydrogen ions by zeolite samples in ammonium ions solutions at concentrations lower than 1 mmol cm(-3) and indicate the importance of Mg2+ (besides Na+ ions) for the exchange between clinoptilolite cations and H+ ions, in contrast to K+ ions, whose participation in the reaction with H+ ions is the lowest. During decationization of the clinoptilolite in acid solution, best exchanged are Na+, Mg2+, and Ca2+ ions, while exchange of K+ ions is the poorest. Due to poor exchange of K+ and H+ ions and good exchange of Na+, Mg2+, and Ca2+ ions, it is to be assumed that preservation of stability of the clinoptilolite structure is caused by K+ ions present in the channel C. Clinoptilolite is dissolved in the clinoptilolite A and B channels where Na+, Mg2+, and Ca2+ ions are present. On the acid-modified clinoptilolite samples, exchange of ammonium ions is poorer than on natural zeolite. The longer the contact time of the zeolite and acid solution, the worse ammonium ions exchange. It can be assumed that H+ ions exchanged with zeolite cations are consumed for solution of aluminum in the clinoptilolite structure; therefore the concentration of H+ ions as exchangeable cations decreases. In the ammonium ion solution at a concentration of 0.0065 mmol cm(-3), from the acid-modified zeolite samples, Al3+ ions are exchanged best, followed by Na+, Mg2+, Ca2+, and K+ ions. Further to the results, it is to be assumed that exchangeable Al3+ ions available from clinoptilolite dissolution are best exchanged with H+ ions in acid solution.