OBJECTIVETo study the salt stress tolerance of Hongxinju, Huangju and F1 seedlings from orthogonal and reciprocal cross under different salt treatments. Grope for transmissibility of salt tolerance between parents and F1 seedlings, and relativity between flavone, chlorogenic acid contents and salt tolerance.

METHODThe materials were put in 5 different concentrations of Hoagland nutrient solution (0, 40, 80, 120, 160 mmol x L(-1)) containing NaCl, keeping grads while raising the consistency of NaCl day by day. The injured leaf area per plant, proline, betaine, MDA, flavones and chlorogenic acid contents were measured and analyzed after treatment.

RESULTAs NaCl concentration was below 120 mmol x L(-1), the salt tolerance of Hongxinju was higher than that of Huangju, the salt tolerance of Hongxinju x Huangju higher than that of parents, the salt tolerance of Huangju x Hongxinju was at the level of parents. As NaCl concentration between 120 to 160 mmol x L(-1), the salt tolerance of Huangju was higher than that of Hongxinju, the salt tolerance of Huangju x Hongxinju higher than that of parents and the salt tolerance of Hongxinju x Huangju was at the level of parents.

CONCLUSIONSalt tolerance of F1 is more influenced by female parent, relativity showed between flavonoids, chlorogenic acid contents and salt tolerance.

Breeding ; China ; Chlorides ; metabolism ; Chrysanthemum ; genetics ; growth & development ; physiology ; Salt-Tolerance ; Seedlings ; genetics ; growth & development ; physiology

The gating mechanism of ClC-1 chloride channel was studied in this paper by heteroexpression of rat wild type ClC-1 gene in Xenopus oocytes and by two-electrode voltage clamping technique. The deactivation gating kinetic parameters were obtained by applying two exponential fitting of the deactivating currents at various extracellular chloride concentrations. It was found that decrease in extracellular chloride concentration increased the fractional amplitude of fast deactivating component, and depressed the fractional amplitude of slow deactivating component accompanied by a decrease in fast and slow deactivating time constants. These results demonstrate that the deactivation kinetic parameters of ClC-1 are largely dependent on the extracellular chloride concentration, which induces changes in channel gating.
Animals ; Chloride Channels ; drug effects ; physiology ; Chlorides ; pharmacology ; Electrophysiology ; Female ; In Vitro Techniques ; Ion Channel Gating ; drug effects ; physiology ; Oocytes ; physiology ; Rats ; Xenopus

gamma -aminobutyric acid (GABA) is an inhibitory neurotransmitter in adult mammalian central nervous system (CNS). During CNS development, the role of GABA is switched from an excitatory transmitter to an inhibitory transmitter, which is caused by an inhibition of calcium influx into postsynaptic neuron derived from release of GABA. The switch is influenced by the neuronal chloride concentration. When the neuronal chloride concentration is at a high level, GABA acts as an excitatory neurotransmitter. When neuronal chloride concentration decreases to some degree, GABA acts as an inhibitory neurotransmitter. The neuronal chloride concentration is increased by Na+-K+-Cl(-)-Cl(-) cotransporters 1 (NKCC1), and decreased by K+-Cl(-) cotransporter 2 (KCC2).
Animals ; Calcium Signaling ; physiology ; Cell Differentiation ; physiology ; Central Nervous System ; cytology ; embryology ; metabolism ; Chlorides ; metabolism ; Humans ; Neural Inhibition ; physiology ; Neurons ; cytology ; metabolism ; Synapses ; metabolism ; Synaptic Transmission ; physiology ; gamma-Aminobutyric Acid ; metabolism ; physiology

The effects of aluminum chloride (AlCl3) on the transient outward potassium and delayed rectifier K(+) current in hippocampal CA1 neurons of rats were studied by the whole-cell patch clamp technique. It was found that AlCl3 reduced the transient outward potassium current and delayed rectifier K(+) current in a dose-dependent manner. 1000 micromol/L AlCl3 resulted in change in voltage and slope of the half-activation and the half-inactivation of I(A) and I(K). These results imply that AlCl3 may damage potassium channel of the hippocampal CA1 neurons from rats and this may be related to the mechanism of the damage to the central nervous system by aluminum.
Aluminum Compounds ; toxicity ; Animals ; CA1 Region, Hippocampal ; cytology ; Cell Separation ; Chlorides ; toxicity ; Delayed Rectifier Potassium Channels ; physiology ; Female ; Male ; Neurons ; drug effects ; physiology ; Patch-Clamp Techniques ; Rats ; Rats, Wistar ; Shal Potassium Channels ; physiology

This study was designed to identify and characterize Na+ -activated K+ current (I(K(Na))) in guinea pig gastric myocytes under whole-cell patch clamp. After whole-cell configuration was established under 110 mM intracellular Na+ concentration ([Na+]i) at holding potential of -60 mV, a large inward current was produced by external 60 mM K+([K+] degree). This inward current was not affected by removal of external Ca2+. K+ channel blockers had little effects on the current (p>0.05). Only TEA (5 mM) inhibited steady-state current to 68+/-2.7% of the control (p<0.05). In the presence of K+ channel blocker cocktail (mixture of Ba2+, glibenclamide, 4-AP, apamin, quinidine and TEA), a large inward current was activated. However, the amplitude of the steadystate current produced under [K+]degree (140 mM) was significantly smaller when Na+ in pipette solution was replaced with K+ - and Li+ in the presence of K+ channel blocker cocktail than under 110 mM [Na+]i. In the presence of K+ channel blocker cocktail under low Cl- pipette solution, this current was still activated and seemed K+ -selective, since reversal potentials (E(rev)) of various concentrations of [K+]degree-induced current in current/voltage (I/V) relationship were nearly identical to expected values. R-56865 (10-20 microgram), a blocker of IK(Na), completely and reversibly inhibited this current. The characteristics of the current coincide with those of IK(Na) of other cells. Our results indicate the presence of IK(Na) in guinea pig gastric myocytes.
Tetraethylammonium Compounds/pharmacology ; Stomach/*physiology ; Sodium/metabolism/*pharmacology ; Potassium Channels/*physiology ; Potassium Channel Blockers/pharmacology ; Myocytes, Smooth Muscle/*physiology ; Membrane Potentials ; Male ; Guinea Pigs ; Female ; Chlorides/pharmacology ; Calcium/metabolism ; Animals

The immunofluorescence approach, the confocal microscopy and the patch-clamp technique were used to investigate the expression of ClC-3 (one of the candidates of volume-activated chloride channels) and its relationships with the volume-activated chloride current and the capacity of regulatory volume decrease (RVD) in the cell cycle of nasopharyngeal carcinoma cells (CNE-2Z cells). The results indicated that CNE-2Z cells expressed ClC-3. ClC-3 was located predominantly inside the cells but not in the membrane. Both the expression level and the distribution of ClC-3 were cell cycle dependent. ClC-3 expression was low in G1 but high in S phase. The cells in G2/M phase possessed an intermediate level of the expression. ClC-3 expression level was negatively correlated to the RVD capacity and amplitude of the volume-activated chloride current in the cell cycle. The results suggest that ClC-3 may be an important factor in the regulation of cell cycle progression, but that it is probably not the chloride channel associated with RVD in these cancer cells.
Adenosine Triphosphate ; pharmacology ; Cell Cycle ; physiology ; Chloride Channels ; metabolism ; physiology ; Chlorides ; metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Muscle Proteins ; metabolism ; physiology ; Nasopharyngeal Neoplasms ; genetics ; metabolism ; pathology ; Tumor Cells, Cultured

No abstract available.
Adenosine Triphosphate/pharmacology ; Anions/metabolism ; Bicarbonates/metabolism* ; Chlorides/metabolism* ; Cyclic AMP/pharmacology ; Cystic Fibrosis Transmembrane Conductance Regulator/physiology* ; Electric Conductivity ; Electrophysiology ; Gluconates/pharmacology ; Human ; Membrane Potentials/physiology ; Membrane Potentials/drug effects ; Potassium/pharmacology ; Sweat Glands/metabolism*

AIMTo study the effect of ZD7288 on synaptic transmission in the pathway from perforant pathway (PP) fibers to CA3 region in rat hippocampus.

METHODSThe extracellular recording technique in vivo was used to record the CA3 region field potentials. High-performance liquid chromatography (HPLC) with fluorescence detection was applied to measure the content of amino acids in hippocampal tissues. The effect of ZD7288 and CsCl on the amplitudes of population spike (PS) in CA3 region evoked by stimulation (0.5 Hz) of the perforant pathway (PP) fibers, and the content of amino acids in hippocampal tissue were observed.

RESULTSMicroinjection of ZD7288 (20, 100 and 200 nmol) and CsCl (1, 5 and 10 micromol) into CA3 region decreased the population spike (PS) amplitudes in a dose-dependent manner. The inhibitory effects appeared at 5 min after microinjection and lasted at least 90 min. In those rats treated with ZD7288 (100 nmol), the contents of glutamate, aspartate, glycine and GABA decreased significantly as compared to those of saline control (all P < 0.01, except P < 0.05 for that of glycine). A similar decrease in the contents of amino acids was observed when the rats were microinjected with CsCl (5 micromol). CONCLUSION; ZD7288 could obviously inhibit synaptic transmission in the pathway from PP fibers to CA3 region in rat hippocampus, and this action of ZD7288 may be associated with altered contents of amino acids.

Amino Acids ; metabolism ; Animals ; Cesium ; pharmacology ; Chlorides ; pharmacology ; Dose-Response Relationship, Drug ; Evoked Potentials ; Hippocampus ; metabolism ; physiology ; Male ; Microinjections ; Perforant Pathway ; physiology ; Pyrimidines ; administration & dosage ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Synaptic Transmission ; drug effects

OBJECTIVETo investigate the role of autophagy in MnCl2-induced apoptosis in human bronchial epithelial 16HBE cells.

METHODSCell proliferation was measured by MTT assay. Mitochondrial membrane potential (MMP) and apoptosis were measured by flow cytometry. Autophagic vacuoles were detected by fluorescence microscopy. Cellular levels of apoptosis and autophagy-related proteins were measured by western blotting.

RESULTS16HBE cell proliferation was inhibited by MnCl2 in a dose- and time-dependent manner. MnCl2-induced 16HBE cell growth inhibition was related to MMP depolarization prior to the induction of apoptosis. Our data revealed that MnCl2-induced apoptosis in 16HBE cells was mediated by decreased expression of Bcl-2 and increased levels of cleaved caspase-3. It was observed that when we exposed 16HBE cells to MnCl2 in a dose-dependent manner, the formation of autophagic vacuoles and the levels of LC-3B-II were elevated. RNA interference of LC3B in these MnCl2-exposed cells demonstrated that MMP loss and apoptosis were enhanced. Additionally, the pan-caspase inhibitor Z-VAD-FMK increased the cellular levels of Bcl-2 and decreased apoptosis, but did not affect the cellular levels of LC3B in MnCl2-treated 16HBE cells.

CONCLUSIONMnCl2 dose- and time-dependently inhibits 16HBE cell proliferation and induces MMP loss and apoptosis. Autophagy acts in a protective role against MnCl2-induced apoptosis in 16HBE cells.

Amino Acid Chloromethyl Ketones ; pharmacology ; Apoptosis ; drug effects ; Autophagy ; drug effects ; physiology ; Bronchi ; Cell Line ; Chlorides ; pharmacology ; Down-Regulation ; Epithelial Cells ; drug effects ; Gene Expression Regulation ; drug effects ; Humans ; Manganese Compounds ; pharmacology

OBJECTIVETo investigate the effects of inward rectifier potassium channel blockers (BaCl2, CsCl) on the functions of endothelial progenitor cells (EPCs).

METHODSDensity gradient centrifugation-isolated rat hone marrow mononuclear cells were cultured in vitro. EPCs were harvested and seeded on six culture dish when cells grew to 3-5 passages. Before testing the EPCs were synchronized with M199, which contain 2% fetal calf serum. In the end, EPCs were treated with different intervention. The experiment mainly included two parts: (1) BaCl2 (100 micromol/L) and free BaC2 of Tyrodes solution; (2) CsCl (1 mmol/L) and control. Cell pretreated with blockers above mentioned for 12 h, then the gene expression of stromal cell-derived factor-1 (SDF-1), epoprotenol (PGI2) were assessed, beyond that the ability of adhesion, migration were assayed with different tests. In addition, the medium was collected when EPCs were treated for 3 days. The levels of SDF-1 were measured by sandwich enzyme-linked immunosorbent assay (ELISA). Going even further, EPCs were treated with the signal pathway blockers in advance, after repeat the above steps, in order to analyze the change of SDF-1 and then discuss its mechanism.

RESULTSCompared with control group, BaCl2, CsCl could increase EPC adhesion and migration to same extent. Moreover, the gene expression of SDF-1, PGI2 was significantly up-regulated and the production of SDF-1 increased evidently. Furthermore, the mechanism of SDF-1 secretion increasing mainly was associated with eNOS signaling pathways.

CONCLUSIONBa2+ and Cs+ play important roles in increasing EPCs functions, such as adhesion, migration and secretion.

Animals ; Barium Compounds ; pharmacology ; Cells, Cultured ; Cesium ; pharmacology ; Chemokine CXCL12 ; metabolism ; Chlorides ; pharmacology ; Endothelial Cells ; cytology ; Enzyme-Linked Immunosorbent Assay ; Potassium Channels, Inwardly Rectifying ; antagonists & inhibitors ; physiology ; Rats ; Stem Cells ; cytology