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Chemical Compound Review

Omaha     lead(+2) cation

Synonyms: Lead-239, Lead ion, PB+2, Pb2+, Lead(2+), ...
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Disease relevance of LEAD


Psychiatry related information on LEAD

  • Exposure to heavy metal lead (Pb(2+)) has been reported to cause problems in cognitive functions of the brain, e.g. memory loss and difficulties in mental development [4].

High impact information on LEAD

  • We found that Pb(2+) induces vascular endothelial growth factor/vascular permeability factor (VEGF) in cultured astrocytes (J Biol Chem, 2000;275:27874-27882) [1].
  • Pb(2+) exposure increased phosphorylation of cerebellar Flk-1 VEGF receptors and the Flk-1 inhibitor CEP-3967 completely blocked cerebellar edema formation without affecting microhemorrhage formation or blood-brain barrier permeability [1].
  • No change in VEGF expression occurred in cerebral cortex that does not develop these histopathological complications of acute Pb(2+) intoxication [1].
  • We provide an introductory overview of the magnitude of the problem of Pb(2+) exposure to bring forth the reality that childhood Pb(2+) intoxication remains a major public health problem not only in the United States but worldwide [5].
  • During the last two decades, advances in behavioral, cellular and molecular neuroscience have provided the necessary experimental tools to begin deciphering the many and complex effects of Pb(2+) on neuronal processes and cell types that are essential for synaptic plasticity and learning and memory in the mammalian brain [5].

Chemical compound and disease context of LEAD

  • These sites include the highly inhibitory substitution of an enzymic cofactor Zn(2+) ion by Pb(2+) ions, which represents a major contribution towards understanding the molecular basis of lead poisoning [6].
  • When the off-gas from an aerobic culture of Klebsiella pneumoniae M426 grown in the absence of added heavy metals was passed through a solution of Hg(2+), Cd(2+), Pb(2+), or Cu(2+) a yellow-white (Hg), white (Cd, Pb), or blue (Cu) precipitate was formed [7].
  • Soil solution concentrations of free heavy metal ions (Cu(2+), Zn(2+), Cd(2+), Pb(2+)) were substantially lower than LOECs for toxicity towards vascular plants, whereas concentrations of Al(3+) were near to toxic levels at two locations [8].
  • Transgenic tobacco expressing the plasma-membrane-localized NtCBP4 exhibit improved tolerance to Ni(2+) and hypersensitivity to Pb(2+), which are associated with a decreased accumulation of Ni(2+) and an enhanced accumulation of Pb(2+) respectively [9].
  • These results suggest a molecular mechanism of Pb(2+) toxicity where low Pb(2+) levels can inappropriately perturb Ca(2+) regulated processes [10].

Biological context of LEAD

  • Our working hypothesis is that disruption of the ontogenetically defined pattern of NMDAR subunit expression and NMDAR-mediated calcium signaling in glutamatergic synapses is a principal mechanism for Pb(2+)-induced deficits in synaptic plasticity and in learning and memory documented in animal models of Pb(2+) neurotoxicity [5].
  • Lanthanide series metal ions, Pb(2+), and Zn(2+) were the most reactive ions in terms of catalyzing alkylation and fragmentation [11].
  • Several Ca(2+) channel phenotypes are quite sensitive to the inhibitory action of Pb(2+) [12].
  • Using membrane-impermeable and -permeable chelators it is demonstrated that intracellular Ca(2+) is not required for Pb(2+) -induced exocytosis [13].
  • Here we apply extended X-ray absorption fine structure (EXAFS) measurements to characterize the metal ion binding site, in frozen solution, of the unimolecular quadruplex formed by the thrombin binding aptamer, d(G(2)T(2)G(2)TGTG(2)T(2)G(2)) (TBA), in the presence of Pb(2+) ions [14].

Anatomical context of LEAD

  • To investigate the site of release of Pi from glucose-6-phosphate, we incubated microsomes with Pb(2+), which forms an insoluble complex with Pi, preventing its rapid exit from the microsomes [15].
  • OPC alone had antioxidant protective effects in the hippocampus but no removing capacity for lead in vivo despite showing higher affinity and stronger chelating ability for Pb(2+) than DMSA in vitro [16].
  • Ca(2+) -independent vesicular catecholamine release in PC12 cells by nanomolar concentrations of Pb(2+) [13].
  • We conclude that trophoblasts have the ability to clear Pb(2+) from the maternal circulation and deliver it to the fetus [17].
  • The Pb(2+) level in the lead-treated animals increased 2.5-6-fold in the blood (3.0-6.0 microg/dl) and 2.0-3.0-fold in the forebrain (78-103 ng/g wet weight), compared to control (saline) [18].

Associations of LEAD with other chemical compounds

  • The trivalent cations Gd(3+) and La(3+) and the divalent cations Cu(2+), Pb(2+), Cd(2+), Co(2+), and Ni(2+) (each at 100 microM) do not evoke currents themselves, but inhibit CaT1-mediated Ca(2+) transport [19].
  • Binding was described by simple second-order kinetics with a rate constant, k(on), of approximately 10(6)-10(7) M(-)(1) s(-)(1), at 4 degrees C. The activation energy of binding is similar for both Pb(2+) and Cd(2+); however, the entropy change is greater for Pb(2+) [20].
  • In addition, 1 can do ion-exchange with heavy-metal ions like Hg(2+), Pb(2+), and Ag(+) [21].
  • Addition of an Al(3+) or Pb(2+) ion to a solution of the ligand causes a blue-shifted absorption and enhanced fluorescence due to a declined resonance energy transfer (RET) upon excitation by one- and two-photon processes [22].
  • The effects of Pb(2+) on GABA release triggered by activation of alpha7* and alpha4beta2* nACRs were mimicked by the protein kinase C (PKC) activator phorbol-12-myristate-13-acetate (1 microM) and blocked by the indolocarbazole Go 7874 (50 nM) and the bisindolylmaleimide Ro-31-8425 (150 nM), which are selective PKC inhibitors [23].

Gene context of LEAD

  • Expression of zraP, a gene inversely oriented to hydH/G whose product seems to be involved in acquisition of tolerance to high Zn(2+) concentrations, is stimulated by high Zn(2+) and Pb(2+) concentrations and this stimulation requires both HydH and HydG [24].
  • These findings demonstrate that chronic exposure to environmentally relevant levels of Pb(2+) altered the subunit composition of NMDAR complexes with subsequent effects on calcium-sensitive signaling pathways involved in CREB phosphorylation [25].
  • There were no changes in the phosphorylation state of ERK and p38(MAPK) for 1-h incubation, whereas a significant increase of ERK1/2 and p38(MAPK) phosphorylation by Pb(2+) (5 microM) was observed for the 3-h incubation [18].
  • In order to investigate the effects of Pb(2+) on the gene expression of NR1 and NR2B subunits in neurons, primary cell cultures of rat cortical and hippocampal neurons were employed [4].
  • Hippocampal expression of N-methyl-D-aspartate receptor (NMDAR1) subunit splice variant mRNA is altered by developmental exposure to Pb(2+) [26].

Analytical, diagnostic and therapeutic context of LEAD


  1. Vascular endothelial growth factor mediates vasogenic edema in acute lead encephalopathy. Hossain, M.A., Russell, J.C., Miknyoczki, S., Ruggeri, B., Lal, B., Laterra, J. Ann. Neurol. (2004) [Pubmed]
  2. Ionomycin, a carboxylic acid ionophore, transports Pb(2+) with high selectivity. Erdahl, W.L., Chapman, C.J., Taylor, R.W., Pfeiffer, D.R. J. Biol. Chem. (2000) [Pubmed]
  3. Conserved Aspartic Acid 714 in Transmembrane Segment 8 of the ZntA Subgroup of P(1B)-Type ATPases Is a Metal-Binding Residue. Dutta, S.J., Liu, J., Hou, Z., Mitra, B. Biochemistry (2006) [Pubmed]
  4. Different trends in modulation of NMDAR1 and NMDAR2B gene expression in cultured cortical and hippocampal neurons after lead exposure. Lau, W.K., Yeung, C.W., Lui, P.W., Cheung, L.H., Poon, N.T., Yung, K.K. Brain Res. (2002) [Pubmed]
  5. Lead neurotoxicity: from exposure to molecular effects. Toscano, C.D., Guilarte, T.R. Brain Res. Brain Res. Rev. (2005) [Pubmed]
  6. MAD analyses of yeast 5-aminolaevulinate dehydratase: their use in structure determination and in defining the metal-binding sites. Erskine, P.T., Duke, E.M., Tickle, I.J., Senior, N.M., Warren, M.J., Cooper, J.B. Acta Crystallogr. D Biol. Crystallogr. (2000) [Pubmed]
  7. A new approach to the remediation of heavy metal liquid wastes via off-gases produced by Klebsiella pneumoniae M426. Essa, A.M., Creamer, N.J., Brown, N.L., Macaskie, L.E. Biotechnol. Bioeng. (2006) [Pubmed]
  8. Potentially toxic metals in ombrotrophic peat along a 400 km English-Scottish transect. Smith, E.J., Hughes, S., Lawlor, A.J., Lofts, S., Simon, B.M., Stevens, P.A., Stidson, R.T., Tipping, E., Vincent, C.D. Environ. Pollut. (2005) [Pubmed]
  9. Cyclic-nucleotide- and Ca2+/calmodulin-regulated channels in plants: targets for manipulating heavy-metal tolerance, and possible physiological roles. Arazi, T., Kaplan, B., Sunkar, R., Fromm, H. Biochem. Soc. Trans. (2000) [Pubmed]
  10. The effect of Pb(2+) on the structure and hydroxyapatite binding properties of osteocalcin. Dowd, T.L., Rosen, J.F., Mints, L., Gundberg, C.M. Biochim. Biophys. Acta (2001) [Pubmed]
  11. Metal ion-catalyzed nucleic Acid alkylation and fragmentation. Browne, K.A. J. Am. Chem. Soc. (2002) [Pubmed]
  12. Characteristics of block by Pb2+ of function of human neuronal L-, N-, and R-type Ca2+ channels transiently expressed in human embryonic kidney 293 cells. Peng, S., Hajela, R.K., Atchison, W.D. Mol. Pharmacol. (2002) [Pubmed]
  13. Ca(2+) -independent vesicular catecholamine release in PC12 cells by nanomolar concentrations of Pb(2+). Westerink, R.H., Vijverberg, H.P. J. Neurochem. (2002) [Pubmed]
  14. Pb EXAFS studies on DNA quadruplexes: identification of metal ion binding site. Smirnov, I.V., Kotch, F.W., Pickering, I.J., Davis, J.T., Shafer, R.H. Biochemistry (2002) [Pubmed]
  15. Novel arguments in favor of the substrate-transport model of glucose-6-phosphatase. Gerin, I., Noël, G., Van Schaftingen, E. Diabetes (2001) [Pubmed]
  16. The effects of meso-2,3-dimercaptosuccinic acid and oligomeric procyanidins on acute lead neurotoxicity in rat hippocampus. Zhang, J., Wang, X.F., Lu, Z.B., Liu, N.Q., Zhao, B.L. Free Radic. Biol. Med. (2004) [Pubmed]
  17. Lead enters Rcho-1 trophoblastic cells by calcium transport mechanisms and complexes with cytosolic calcium-binding proteins. Evans, T.J., James-Kracke, M.R., Kleiboeker, S.B., Casteel, S.W. Toxicol. Appl. Pharmacol. (2003) [Pubmed]
  18. Lead stimulates ERK1/2 and p38MAPK phosphorylation in the hippocampus of immature rats. Cordova, F.M., Rodrigues, A.L., Giacomelli, M.B., Oliveira, C.S., Posser, T., Dunkley, P.R., Leal, R.B. Brain Res. (2004) [Pubmed]
  19. Molecular cloning and characterization of a channel-like transporter mediating intestinal calcium absorption. Peng, J.B., Chen, X.Z., Berger, U.V., Vassilev, P.M., Tsukaguchi, H., Brown, E.M., Hediger, M.A. J. Biol. Chem. (1999) [Pubmed]
  20. Kinetic analysis of metal binding to the amino-terminal domain of ZntA by monitoring metal-thiolate charge-transfer complexes. Dutta, S.J., Liu, J., Mitra, B. Biochemistry (2005) [Pubmed]
  21. Heavy-Metal-Ion Capture, Ion-Exchange, and Exceptional Acid Stability of the Open-Framework Chalcogenide (NH(4))(4)In(12)Se(20). Manos, M.J., Malliakas, C.D., Kanatzidis, M.G. Chemistry (Weinheim an der Bergstrasse, Germany) (2007) [Pubmed]
  22. Metal Ion Sensing Novel Calix[4]crown Fluoroionophore with a Two-Photon Absorption Property. Kim, J.S., Kim, H.J., Kim, H.M., Kim, S.H., Lee, J.W., Kim, S.K., Cho, B.R. J. Org. Chem. (2006) [Pubmed]
  23. Pb2+ via protein kinase C inhibits nicotinic cholinergic modulation of synaptic transmission in the hippocampus. Braga, M.F., Pereira, E.F., Mike, A., Albuquerque, E.X. J. Pharmacol. Exp. Ther. (2004) [Pubmed]
  24. The hydH/G Genes from Escherichia coli code for a zinc and lead responsive two-component regulatory system. Leonhartsberger, S., Huber, A., Lottspeich, F., Böck, A. J. Mol. Biol. (2001) [Pubmed]
  25. Developmental Pb2+ exposure alters NMDAR subtypes and reduces CREB phosphorylation in the rat brain. Toscano, C.D., Hashemzadeh-Gargari, H., McGlothan, J.L., Guilarte, T.R. Brain Res. Dev. Brain Res. (2002) [Pubmed]
  26. Hippocampal expression of N-methyl-D-aspartate receptor (NMDAR1) subunit splice variant mRNA is altered by developmental exposure to Pb(2+). Guilarte, T.R., McGlothan, J.L., Nihei, M.K. Brain Res. Mol. Brain Res. (2000) [Pubmed]
  27. A modular microfluidic architecture for integrated biochemical analysis. Shaikh, K.A., Ryu, K.S., Goluch, E.D., Nam, J.M., Liu, J., Thaxton, C.S., Chiesl, T.N., Barron, A.E., Lu, Y., Mirkin, C.A., Liu, C. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  28. Simple detection of trace Pb2+ by enrichment on cerium phosphate membrane filter coupled with color signaling. Suzuki, T.M., Llosa Tanco, M.A., Pacheco Tanaka, D.A., Hayashi, H., Takahashi, Y. The Analyst. (2005) [Pubmed]
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