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Chemical Compound Review

BARIUM ION     barium(+2) cation

Synonyms: barium(2+), Ba+2, Ba2+, Ba++, barium cation, ...
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Disease relevance of BARIUM

  • Here, we describe the effects of Zn(2+) on complex I to define whether complex I may contribute to mediating the pathological effects of zinc in states such as ischemia and to determine how Zn(2+) can be used to probe the mechanism of complex I. Zn(2+) inhibits complex I more strongly than Mg(2+), Ca(2+), Ba(2+), and Mn(2+) to Cu(2+) or Cd(2+) [1].
  • Tetanus toxin inhibited Ba(2+)- and Ca(2+)-dependent secretion to a similar extent [2].
  • Barium (Ba(2+)) sensitive K(ir) currents were >20-fold larger in mature astrocytes (4.06 +/- 1.1 nS/pF) than in glioma cells (0.169 +/- 0.033 nS/pF D54, 0.244 +/- 0.04 nS/pF STTG1), which had current densities closer to those of dividing, immature astrocytes (0.474 +/- 0.12 nS/pF) [3].
  • Application of Ba(2+) blocked membrane depolarization by respiratory acidosis, whereas significant depolarization in response to metabolic acidosis still remained after application of Cd(2+) and Ba(2+) [4].
  • Last, membrane blebs, which were numerous and spherical in Ca(2+)-containing solutions, were poorly defined and greatly reduced in number in the presence of Ba(2+) [5].

High impact information on BARIUM

  • BSC1 has slower kinetics of activation and inactivation than Na(+) channels, it is more selective for Ba(2+) than for Na(+), it is blocked by Cd(2+), and Na(+) currents through BSC1 are blocked by low concentrations of Ca(2+) [6].
  • X-ray crystallographic analyses of Q425 in the presence of Ca(2+), Ba(2+), or EDTA revealed an exposed metal-binding site, partially coordinated by five atoms contributed from four antibody complementarity-determining regions [7].
  • (iii) When Kir2.1 and Kir2.2 channels were coexpressed in Xenopus oocytes the IC(50) for Ba(2+) block of the inward rectifier current differed substantially from the value expected for independent expression of homomeric channels [8].
  • (ii) Expression of Kir2.x-Kir2.y concatemers in Xenopus oocytes produced inwardly rectifying, Ba(2+) sensitive currents [8].
  • We recorded single-channel currents across the Vicia guard cell plasma membrane using Ba(2+) as a charge-carrying ion [9].

Chemical compound and disease context of BARIUM


Biological context of BARIUM

  • Exchanging Ca(2+) for Ba(2+) abolished the effect of antisyntaxin 1 on both Ca(2+) channel activity and insulin exocytosis [11].
  • Mutagenesis of residues in H5 and M2 close to the selectivity filter also decreased Ba(2+) block of the channel [12].
  • In (+/+), (+/-), and (-/-) cardiomyocytes, an L-type Ba(2+) inward current (I(Ba)) was present that was stimulated by Bay K 8644 in all genotypes [13].
  • Transient transfection of COS cells with expression vectors encoding rTRP6A or rTRP6B increased Ca(2+) influx and gave rise to a novel Ba(2+) influx after activation of M(5) muscarinic acetylcholine receptors [14].
  • We found that internal Ba(2+) could still access its binding site when the channel was shut, which indicates that the ligand-sensitive gate lies above the Ba(2+)-block site, and thus within or above the selectivity filter [15].

Anatomical context of BARIUM

  • We measured Ca(2+) influx (as Mn(2+) quenching or Ba(2+) influx) and 2-deoxyglucose (2-DG) uptake in single muscle fibers isolated from limbs of adult mice; 2-DG uptake was also measured in isolated whole muscles [16].
  • The current associated with the efflux of H(+) is countered, in part, by the influx of K(+) via Ba(2+)- and Cs(+)-sensitive K(+) channels in the parasite plasma membrane [17].
  • The reduced rise in [Ca(2+)](i) was due to an inhibition of Na(+)/Ca(2+) exchange activity rather than increased Ca(2+) sequestration since the influx of Ba(2+), which is not sequestered by internal organelles, was also inhibited by a prior interval of Ca(2+) influx [18].
  • As in recordings from skeletal muscle, for heterologously expressed channels the peak inward Ba(2+) currents were small relative to Q(max) [19].
  • Notably, application of 0.3-1 mM Ba(2+) during capacitation prevented this hyperpolarization and decreased the subsequent exocytotic response to zona pellucida [20].

Associations of BARIUM with other chemical compounds

  • The co-immunoprecipitated synaptotagmin-sodium channel complexes were found to be Ca(2+)-dependent; this effect was mimicked by Ba(2+) and Sr(2+) but not Mg(2+) [21].
  • Using Fura-2-loaded platelets, we report that, in line with TRPC6 expression, 1-oleoyl-2-acetyl-sn-glycerol (OAG) stimulated the entry of Ca(++) and Ba(2+) independently of protein kinase C. Thrombin also induced the entry of Ca(++) and Ba(2+), but thapsigargin, which depletes the stores, induced the entry of only Ca(++) [22].
  • CCh-stimulated Ba(2+) entry, on the other hand, could be inhibited by suppression of any of the five endogenously expressed TRPC homologs, with the degree of inhibition being consistent with CCh stimulation of both store-operated and receptor-operated channels [23].
  • (2) Ba(2)(+) (100 microm) and ouabain (1 microm) each attenuated ACh-hyperpolarization by approximately 30% in smooth muscle cells (SMCs) but had only slight or no inhibition in endothelial cells (ECs) [24].
  • An in vitro preparation of the guinea-pig cornea was used to study the effects of the K(+) channel blockers 4-aminopyridine (4-AP), tetraethylammonium (TEA) and Ba(2+) on nerve terminal impulses (NTIs) recorded extracellularly from cold sensory receptors [25].

Gene context of BARIUM

  • The suppression of either TRPC3 or TRPC7, but not TRPC1, induced a high Ba(2+) leak flux that was inhibited by 2-APB and SKF96365, suggesting that the influx is via leaky store-operated channels [23].
  • Block of KCNQ2/3 channels by external Ba(2+) ions was voltage-independent, demonstrating unusual ionic occupation of the outer pore [26].
  • When Ba(2+) currents through L-type channels were studied, extracellular application of bFGF (10 ng/ml) led to a shift of the steady-state activation to more negative values [27].
  • Ba(2+) binding to this superficial site likely modifies the gating transitions states of KCNQ1 [28].
  • These responses were not observed in the presence of 3 mM Ba(2+), which blocks the GIRK channels [29].

Analytical, diagnostic and therapeutic context of BARIUM

  • Using the patch-clamp technique, we found that PKC activation by 4-alpha-phorbol 12-myristate 13-acetate (PMA) or rac-1-oleyl-2-acetylglycerol (OAG) caused a substantial reduction in Ba(2+) current through Ca(v)1.2 channels composed of alpha(1)1.2, beta(1b), and alpha(2)delta(1) subunits expressed in tsA-201 cells [30].
  • Mechanisms and residues responsible for slow activation and Ba(2+) block of the cardiac muscarinic K(+) channel, Kir3.1/Kir3.4, were investigated using site-directed mutagenesis [12].
  • Perfusion of Ba(2+) onto the cytoplasmic face did not alter P(o); moreover, in outside-out recordings, P(o) was decreased by replacing external Ca(2+) with Ba(2+) as a charge carrier, suggesting Ca(2+) influx through the channel may provide positive feedback [31].
  • To better understand possible discrepancies between and, we have undertaken both experimental studies using isothermal titration calorimetry to measure the binding energetics of Ba(2+) binding 18-crown-6 ether and 2'-CMP binding RNase A, along with a simulation of a system involving a molecule in conformational equilibrium coupled with binding [32].
  • Ba(2+) (30 microM) did not affect dilatation to ACh, but abolished 40% of dilatations to raised [K(+)](o) [33].


  1. The Inhibition of Mitochondrial Complex I (NADH:Ubiquinone Oxidoreductase) by Zn2+. Sharpley, M.S., Hirst, J. J. Biol. Chem. (2006) [Pubmed]
  2. Barium and calcium stimulate secretion from digitonin-permeabilized bovine adrenal chromaffin cells by similar pathways. TerBush, D.R., Holz, R.W. J. Neurochem. (1992) [Pubmed]
  3. Mislocalization of Kir channels in malignant glia. Olsen, M.L., Sontheimer, H. Glia (2004) [Pubmed]
  4. Mechanisms of CO2/H+ chemoreception by respiratory rhythm generator neurons in the medulla from newborn rats in vitro. Kawai, A., Onimaru, H., Homma, I. J. Physiol. (Lond.) (2006) [Pubmed]
  5. Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity. Wisnoskey, B.J., Estacion, M., Schilling, W.P. Am. J. Physiol., Cell Physiol. (2004) [Pubmed]
  6. A voltage-gated calcium-selective channel encoded by a sodium channel-like gene. Zhou, W., Chung, I., Liu, Z., Goldin, A.L., Dong, K. Neuron (2004) [Pubmed]
  7. Interfacial metal and antibody recognition. Zhou, T., Hamer, D.H., Hendrickson, W.A., Sattentau, Q.J., Kwong, P.D. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  8. Heteromerization of Kir2.x potassium channels contributes to the phenotype of Andersen's syndrome. Preisig-Müller, R., Schlichthörl, G., Goerge, T., Heinen, S., Brüggemann, A., Rajan, S., Derst, C., Veh, R.W., Daut, J. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
  9. Ca2+ channels at the plasma membrane of stomatal guard cells are activated by hyperpolarization and abscisic acid. Hamilton, D.W., Hills, A., Kohler, B., Blatt, M.R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  10. N-terminal chromogranin-derived peptides as dilators of bovine coronary resistance arteries. Brekke, J.F., Osol, G.J., Helle, K.B. Regul. Pept. (2002) [Pubmed]
  11. Syntaxin 1 interacts with the L(D) subtype of voltage-gated Ca(2+) channels in pancreatic beta cells. Yang, S.N., Larsson, O., Bränström, R., Bertorello, A.M., Leibiger, B., Leibiger, I.B., Moede, T., Köhler, M., Meister, B., Berggren, P.O. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  12. Residues and mechanisms for slow activation and Ba2+ block of the cardiac muscarinic K+ channel, Kir3.1/Kir3.4. Lancaster, M.K., Dibb, K.M., Quinn, C.C., Leach, R., Lee, J.K., Findlay, J.B., Boyett, M.R. J. Biol. Chem. (2000) [Pubmed]
  13. Functional embryonic cardiomyocytes after disruption of the L-type alpha1C (Cav1.2) calcium channel gene in the mouse. Seisenberger, C., Specht, V., Welling, A., Platzer, J., Pfeifer, A., Kühbandner, S., Striessnig, J., Klugbauer, N., Feil, R., Hofmann, F. J. Biol. Chem. (2000) [Pubmed]
  14. Muscarinic acetylcholine receptor regulation of TRP6 Ca2+ channel isoforms. Molecular structures and functional characterization. Zhang, L., Saffen, D. J. Biol. Chem. (2001) [Pubmed]
  15. The ligand-sensitive gate of a potassium channel lies close to the selectivity filter. Proks, P., Antcliff, J.F., Ashcroft, F.M. EMBO Rep. (2003) [Pubmed]
  16. The role of Ca2+ influx for insulin-mediated glucose uptake in skeletal muscle. Lanner, J.T., Katz, A., Tavi, P., Sandström, M.E., Zhang, S.J., Wretman, C., James, S., Fauconnier, J., Lännergren, J., Bruton, J.D., Westerblad, H. Diabetes (2006) [Pubmed]
  17. The membrane potential of the intraerythrocytic malaria parasite Plasmodium falciparum. Allen, R.J., Kirk, K. J. Biol. Chem. (2004) [Pubmed]
  18. Feedback inhibition of sodium/calcium exchange by mitochondrial calcium accumulation. Opuni, K., Reeves, J.P. J. Biol. Chem. (2000) [Pubmed]
  19. COOH-terminal truncated alpha(1S) subunits conduct current better than full-length dihydropyridine receptors. Morrill, J.A., Cannon, S.C. J. Gen. Physiol. (2000) [Pubmed]
  20. Inwardly rectifying K(+) channels in spermatogenic cells: functional expression and implication in sperm capacitation. Muñoz-Garay, C., De la Vega-Beltrán, J.L., Delgado, R., Labarca, P., Felix, R., Darszon, A. Dev. Biol. (2001) [Pubmed]
  21. Direct interaction between synaptotagmin and the intracellular loop I-II of neuronal voltage-sensitive sodium channels. Sampo, B., Tricaud, N., Leveque, C., Seagar, M., Couraud, F., Dargent, B. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  22. Expression and role of TRPC proteins in human platelets: evidence that TRPC6 forms the store-independent calcium entry channel. Hassock, S.R., Zhu, M.X., Trost, C., Flockerzi, V., Authi, K.S. Blood (2002) [Pubmed]
  23. Endogenous TRPC1, TRPC3, and TRPC7 proteins combine to form native store-operated channels in HEK-293 cells. Zagranichnaya, T.K., Wu, X., Villereal, M.L. J. Biol. Chem. (2005) [Pubmed]
  24. Electrical coupling and release of K+ from endothelial cells co-mediate ACh-induced smooth muscle hyperpolarization in guinea-pig inner ear artery. Jiang, Z.G., Nuttall, A.L., Zhao, H., Dai, C.F., Guan, B.C., Si, J.Q., Yang, Y.Q. J. Physiol. (Lond.) (2005) [Pubmed]
  25. Barium ions inhibit the dynamic response of guinea-pig corneal cold receptors to heating but not to cooling. Brock, J., Acosta, M.C., Al Abed, A., Pianova, S., Belmonte, C. J. Physiol. (Lond.) (2006) [Pubmed]
  26. Ionic permeation and conduction properties of neuronal KCNQ2/KCNQ3 potassium channels. Prole, D.L., Marrion, N.V. Biophys. J. (2004) [Pubmed]
  27. Fibroblast growth factor receptor 2 (FGFR2) in brain neurons and retinal pigment epithelial cells act via stimulation of neuroendocrine L-type channels (Ca(v)1.3). Rosenthal, R., Thieme, H., Strauss, O. FASEB J. (2001) [Pubmed]
  28. External barium affects the gating of KCNQ1 potassium channels and produces a pore block via two discrete sites. Gibor, G., Yakubovich, D., Peretz, A., Attali, B. J. Gen. Physiol. (2004) [Pubmed]
  29. Inhibition by various antipsychotic drugs of the G-protein-activated inwardly rectifying K(+) (GIRK) channels expressed in xenopus oocytes. Kobayashi, T., Ikeda, K., Kumanishi, T. Br. J. Pharmacol. (2000) [Pubmed]
  30. Inhibition of cardiac L-type calcium channels by protein kinase C phosphorylation of two sites in the N-terminal domain. McHugh, D., Sharp, E.M., Scheuer, T., Catterall, W.A. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  31. Ca2+-dependent regulation of a non-selective cation channel from Aplysia bag cell neurones. Lupinsky, D.A., Magoski, N.S. J. Physiol. (Lond.) (2006) [Pubmed]
  32. Van't Hoff and calorimetric enthalpies from isothermal titration calorimetry: are there significant discrepancies? Horn, J.R., Russell, D., Lewis, E.A., Murphy, K.P. Biochemistry (2001) [Pubmed]
  33. Potassium does not mimic EDHF in rat mesenteric arteries. Doughty, J.M., Boyle, J.P., Langton, P.D. Br. J. Pharmacol. (2000) [Pubmed]
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