Flavonoids have an ability to suppress various ion channels. We determined whether one of flavonoids, cyanidin-3-glucoside, affects adenosine 5'-triphosphate (ATP)-induced calcium signaling using digital imaging methods for intracellular free Ca2+ concentration ([Ca2+]i), reactive oxygen species (ROS) and mitochondrial membrane potential in PC12 cells. Treatment with ATP (100microM) for 90 sec induced [Ca2+]i increases in PC12 cells. Pretreatment with cyanidin-3-glucoside (1micro g/ml to 100microg/ml) for 30 min inhibited the ATP-induced [Ca2+]i increases in a concentration-dependent manner (IC50=15.3microg/ml). Pretreatment with cyanidin-3-glucoside (15microg/ml) for 30 min significantly inhibited the ATP-induced [Ca2+]i responses following removal of extracellular Ca2+ or depletion of intracellular [Ca2+]i stores. Cyanidin-3-glucoside also significantly inhibited the relatively specific P2X2 receptor agonist 2-MeSATP-induced [Ca2+]i responses. Cyanidin-3-glucoside significantly inhibited the thapsigargin or ATP-induced store-operated calcium entry. Cyanidin-3-glucoside significantly inhibited the ATP-induced [Ca2+]i responses in the presence of nimodipine and omega-conotoxin. Cyanidin-3-glucoside also significantly inhibited KCl (50 mM)-induced [Ca2+]i increases. Cyanidin-3-glucoside significantly inhibited ATP-induced mitochondrial depolarization. The intracellular Ca2+ chelator BAPTA-AM or the mitochondrial Ca2+ uniporter inhibitor RU360 blocked the ATP-induced mitochondrial depolarization in the presence of cyanidin-3-glucoside. Cyanidin-3-glucoside blocked ATP-induced formation of ROS. BAPTA-AM further decreased the formation of ROS in the presence of cyanidin-3-glucoside. All these results suggest that cyanidin-3-glucoside inhibits ATP-induced calcium signaling in PC12 cells by inhibiting multiple pathways which are the influx of extracellular Ca2+ through the nimodipine and omega-conotoxin-sensitive and -insensitive pathways and the release of Ca2+ from intracellular stores. In addition, cyanidin-3-glucoside inhibits ATP-induced formation of ROS by inhibiting Ca2+-induced mitochondrial depolarization.
Adenosine ; Adenosine Triphosphate ; Animals ; Calcium ; Calcium Signaling ; Flavonoids ; Ion Channels ; Ion Transport ; Membrane Potential, Mitochondrial ; Nimodipine ; omega-Conotoxins ; PC12 Cells* ; Reactive Oxygen Species ; Receptors, Purinergic P2X2 ; Thapsigargin

No abstract available.
Ion Transport* ; Translational Medical Research*

Ion channels and transporters represent two major types of pathways of transmembrane transport for ions. Distinct from ion channels which conduct passive ionic diffusion, ion transporters mediate active transport of ions. In the perspective of biochemistry, ion transporters are enzymes that catalyze the movement of ions across the plasma membrane. In the present review, we selected the Na(+)/HCO3(-) cotransporter (NBC) as an example to analyze the key biochemical and biophysical properties of ion transporters, including stoichiometry, turnover number and transport capacity. Moreover, we provided an analysis of the electrophysiological principles of NBC based on the laws of thermodynamics. Based on the thermodynamical analysis, we showed how the stoichiometry of an NBC determines the direction of its ion transport. Finally, we reviewed the methodology for experimental determination of the stoichiometry of NBC, as well as the physiological significance of the stoichiometry of NBCs in specific tissues.
Electrophysiological Phenomena ; Ion Transport ; Sodium-Bicarbonate Symporters

All urate transport occurs across the renal epithelial cells of the proximal tubule. Most of the filtered urate is reabsorbed in the S1 segment of the early proximal tubule. This is followed by tubular secretion in the S2 segment of the proximal tubule and approximately 50% of the filtered urate flows back into the tubular lumen. Most of the secreted urate undergoes postsecretory reabsorption that occurs predominantly in the last S3 segment of the proximal tubule. Recently, four proteins that transport urate have been identified at the molecular level. These proteins are an electrogenic urate uniporter, urate transporter/channel (UAT), two members of the organic anion transporter (OAT) family, OAT1 and OAT3, and a protein with some homology to OAT4, designated URAT1.
Epithelial Cells ; Humans ; Ion Transport ; Uric Acid*

OBJECTIVETo investigate the relationship between the changes of the L-type calcium current (I(Ca, L)) and the calcium-activated transient outward chloride current (I(Cl, Ca)), and the repolarization characteristic of action potential in phase 1 under isoprenaline (ISO) stimulation in atrium myocytes of rabbit.

METHODSAtrium myocytes were obtained by enzymatic dissociation from a section of atrial free wall. The membrane currents and action potential were recorded by the whole-cell patch-clamp technique.

RESULTSAfter recording I(Ca, L), atrium myocytes were perfused with ISO (1 micromol/L) immediately. Five minutes later, a transient outward current (I(to)) was significantly induced, and the peak of I(to) was gradually increased while I(Ca, L) gradually decreased with increasing in clamp voltage. The I(to) was resistant to 4-AP (3 mmol/L) but sensitive to DIDS (150 micromol/L, Cl(-) channel blocker). This current was blocked by CdCl(2) (200 micromol/L, Ca(2+) channel blocker). The elicited rate of I(to) was 91.67% (P < 0.05). (2) The shape of AP was like an inverse triangle with no plateau in Phase 2 after ISO (1 micromol/L) perfusion. Moreover, compared to the parameters of control group, APD(50) and APD(90) were significantly shortened from (65.4 +/- 4.2) ms and (95.8 +/- 3.8) ms to (12.8 +/- 3.8) ms and (27.0 +/- 4.7) ms, and reduced to 80.46% and 71.87%, respectively (P < 0.01, n = 12). 4-AP (3 mmol/L) had on obvious effect on the shape of AP, however, the plateau of AP in phase 2 was recovered by DIDS (150 micromol/L) perfusion, APD(50) and APD(90) were (41.1 +/- 4.5) ms and (79.6 +/- 3.4) ms respectively. Compared to the parameters of control group, there were no significant differences (P > 0.05, n = 12). These results indicated that ionic transport were changed by ISO perfusion in atrium myocytes and I(to) played an important role in the phase 1 repolarization of AP.

CONCLUSIONSBefore ISO administration, we could only observe I(Ca, L) in atrium myocytes of rabbit. After isoproterenol intervention, certain intracellular ionic consistency and membrane ionic channels were changed. Calcium activated chloride channel and I(to2) revealed obvious predominance which shorten APD significantly. Action potential showed a triangle with no plateau, suggesting an electrical remodeling in atrium myocytes. The remodeling of ionic channel is related possibly with the opening of Ca(2+)-activated Cl(-) current, which maybe the electrophysiological base of reentrant atrial tachycardia.

Animals ; Calcium ; metabolism ; Calcium Channels, L-Type ; metabolism ; Calcium Signaling ; Cells, Cultured ; Chloride Channels ; metabolism ; Heart Atria ; cytology ; metabolism ; Ion Transport ; Isoproterenol ; pharmacology ; Myocytes, Cardiac ; drug effects ; metabolism ; Patch-Clamp Techniques ; Rabbits

No abstract available.
Breast Neoplasms* ; Breast* ; Ion Transport* ; Sodium Iodide* ; Sodium*

No abstract available.
Breast Neoplasms* ; Breast* ; Ion Transport* ; Sodium Iodide* ; Sodium*

PURPOSE: To evaluate the differences of radiological outcomes of uniportal and biportal vertebroplasty in the point of bone cement distribution and leakage. MATERIALS AND METHODS: A retrospective study reviewing the period between May 2002 and January 2006 investigated 100 vertebrae which underwent vertebroplasty and followed for more than three months by uniportal approach (55 vertebrae, group 1) and biportal approach (45 vertebrae, group 2). The operative time, the amount of bone cement injected, anterior vertebral height restoration, kyphotic angle, bone cement distribution, and bone cement leakage were evaluated. RESULTS: The amount of injected bone cement of group 1 (3.9 cc) was statistically smaller than that of group 2 (5.1 cc) (p=0.016). There were no significant differences in the operative time, anterior vertebral height restoration, kyphotic angle in both groups. The rate of bone cement distribution over 8 zones was significantly higher in group 2 than in group 1 (p=0.014). However, the rate of bone cement distribution over 7 zones and the rate of bone cement distributed on whole anterior vertebral body were not significantly different in both groups. The cement leakage was not also significantly different in both groups. CONCLUSION: Although the amount of injected bone cement was smaller in uniportal vertebroplasty, the radiological results and cement leakage were similar to biportal vertebroplasty. These findings suggest that uniportal vertebroplasty can be the operative options in osteoporotic vertebral fracture.
Ion Transport* ; Operative Time ; Retrospective Studies ; Spine ; Vertebroplasty*

This study was undertaken to examine the effect of ethanol on Na+-dependent transport systems (glucose, phosphate, and dicarboxylate) in renal brush-border membrane vesicles (BBMV). Ethanol inhibited Na+-dependent uptakes of glucose, phosphate, and succinate in a dose-dependent manner, but not the uptakes of Na+-independent. The H+/TEA antiport was reduced by 8% ethanol. Kinetic analysis showed that ethanol caused a decrease in Vmax of three transport systems, leaving Km values unchanged. Ethanol decreased phlorizin binding, which was closely correlated with the decrease in Vmax of Na+-glucose uptake. These results indicate that ethanol inhibits Na+-dependent uptakes of glucose, phosphate, and dicaboxylate and that the reduction in Vmax of Na+-glucose uptake is caused by a decrease in the number of active carrier proteins in the membrane.
Carrier Proteins ; Ethanol* ; Glucose ; Ion Transport ; Membranes* ; Phlorhizin ; Succinic Acid

Iodide uptake across the membranes of thyroid follicular cells and cancer cells occurs through an active transport process mediated by the sodium-iodide symporter (NIS). The rat and human NIS-coding genes were cloned and identified in 1996. Evaluation of NIS gene and protein expression is critical for the management of thyroid cancer, and several approaches to increase NIS levels have been tried. Identification of the NIS gene has provided a means of expanding its role in radionuclide therapy and molecular target-specific theragnosis (therapy and diagnosis using the same molecular target). In this article, we describe the relationship between NIS expression and the thyroid carcinoma treatment using I-131 and alternative therapeutic approaches.
Animals ; Biological Transport, Active ; Clone Cells ; Diagnosis ; Humans ; Ion Transport ; Membranes ; Rats ; Thyroid Gland ; Thyroid Neoplasms*