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Chemical Compound Review

AC1L2HRB     trimethyltin

Synonyms: LS-153874, BRN 3903051, 5089-96-3, Trimethyltin ion, Trimethyltin(1+), ...
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Disease relevance of Trimethylstannane

  • Pathogenesis of trimethyltin neuronal toxicity. Ultrastructural and cytochemical observations [1].
  • Experiments where the slice has been used to study the neurotoxin trimethyltin are discussed, along with its use as a model for investigating the neurodegenerative problems associated with hypoxia, ischemia, and epilepsy [2].
  • To study the role of cytokines in the early stages of brain injury, we examined alterations in the 17-day-old mouse hippocampus during trimethyltin-induced neurodegeneration characterized by neuronal necrosis, microglia activation in the dentate, and astrocyte reactivity throughout the hippocampus [3].
  • Administration of trimethyltin (TMT) to the rat results in loss of hippocampal neurons and an ensuing gliosis without BBB compromise [4].
  • The cerebellum shows limited if any damage after TMT; however, in combination with the i.c.v. injection, elevations were seen in GFAP and in EB-22, a murine acute-phase response gene homologous to the alpha (1)-antichymotrypsin gene [5].

Psychiatry related information on Trimethylstannane

  • We describe detailed clinical observations, serial neuropsychological test results, electroencephalographic findings, and exposure data in this patient, confirming the limbic system effects of trimethyltin and relating them to the known histopathologic pattern of this condition [6].
  • After a period of recovery from the typical signs of trimethyltin toxicity, each rat was tested at 72-hr intervals for its locomotor activity in an open field apparatus, the floor of which was divided into square grids [7].
  • 6. These results show that, in contrast to the previously reported amnesia models, the impairments induced after exposure to CO or intoxication with trimethyltin could be alleviated not only by sigma1 receptor agonists but also by sigma2 agonists [8].
  • Trimethyltin (TMT) impairs auditory thresholds within minutes of systemic administration [9].
  • Two time intervals were investigated: 5 days after trimethyltin treatment, when CA3 damage becomes manifest and is associated with increased aggression, seizure susceptibility, and memory deficit, and 16 days after trimethyltin, when neuronal damage is almost maximal and seizure susceptibility is declining [10].

High impact information on Trimethylstannane

  • The interactions of four chemicals (lead, ethanol, polychlorinated biphenyls, and trimethyltin) with different cell signaling systems, particularly the phospholipid hydrolysis/protein kinase C pathway, are discussed [11].
  • Acute administration of TMT caused large dose- and time-dependent decreases in synapsin I and p38 in hippocampus; the same proteins were largely unaffected in a nonlimbic structure, the frontal cortex [12].
  • Immunohistochemistry of GFAP revealed widespread astrocytic reactivity as a consequence of exposure to TMT, a response that resulted in part from the proliferation of astrocytes [12].
  • TMT caused large dose- and time-dependent increases in GFAP that were not confined to hippocampus [12].
  • Brain weights and histology were used to verify the cytopathological effects of TMT [12].

Chemical compound and disease context of Trimethylstannane


Biological context of Trimethylstannane


Anatomical context of Trimethylstannane


Associations of Trimethylstannane with other chemical compounds


Gene context of Trimethylstannane


Analytical, diagnostic and therapeutic context of Trimethylstannane


  1. Pathogenesis of trimethyltin neuronal toxicity. Ultrastructural and cytochemical observations. Bouldin, T.W., Goines, N.D., Bagnell, R.C., Krigman, M.R. Am. J. Pathol. (1981) [Pubmed]
  2. The hippocampal tissue slice in animal models of CNS disorders. Armstrong, D.L. Neuroscience and biobehavioral reviews. (1991) [Pubmed]
  3. Cellular localization and temporal elevation of tumor necrosis factor-alpha, interleukin-1 alpha, and transforming growth factor-beta 1 mRNA in hippocampal injury response induced by trimethyltin. Bruccoleri, A., Brown, H., Harry, G.J. J. Neurochem. (1998) [Pubmed]
  4. Chemically induced neuronal damage and gliosis: enhanced expression of the proinflammatory chemokine, monocyte chemoattractant protein (MCP)-1, without a corresponding increase in proinflammatory cytokines(1). Little, A.R., Benkovic, S.A., Miller, D.B., O'Callaghan, J.P. Neuroscience (2002) [Pubmed]
  5. Differential modulation of hippocampal chemical-induced injury response by ebselen, pentoxifylline, and TNFalpha-, IL-1alpha-, and IL-6-neutralizing antibodies. Jean Harry, G., Bruccoleri, A., Lefebvre d'Hellencourt, C. J. Neurosci. Res. (2003) [Pubmed]
  6. Trimethyltin encephalopathy. Feldman, R.G., White, R.F., Eriator, I.I. Arch. Neurol. (1993) [Pubmed]
  7. Antagonism by d-amphetamine of trimethyltin-induced hyperactivity evidence toward an animal model of hyperkinetic behavior. Swartzwelder, H.S., Holahan, W., Myers, R.D. Neuropharmacology (1983) [Pubmed]
  8. The attenuation of learning impairments induced after exposure to CO or trimethyltin in mice by sigma (sigma) receptor ligands involves both sigma1 and sigma2 sites. Maurice, T., Phan, V.L., Noda, Y., Yamada, K., Privat, A., Nabeshima, T. Br. J. Pharmacol. (1999) [Pubmed]
  9. Trimethyltin disrupts loudness recruitment and auditory threshold sensitivity in guinea pigs. Liu, Y., Fechter, L.D. Neurotoxicology and teratology. (1995) [Pubmed]
  10. Trimethyltin intoxication induces marked changes in neuropeptide expression in the rat hippocampus. Tsunashima, K., Sadamatsu, M., Takahashi, Y., Kato, N., Sperk, G. Synapse (1998) [Pubmed]
  11. Signal transduction in environmental neurotoxicity. Costa, L.G. Annu. Rev. Pharmacol. Toxicol. (1998) [Pubmed]
  12. Quantitative changes in the synaptic vesicle proteins synapsin I and p38 and the astrocyte-specific protein glial fibrillary acidic protein are associated with chemical-induced injury to the rat central nervous system. Brock, T.O., O'Callaghan, J.P. J. Neurosci. (1987) [Pubmed]
  13. Protein kinase C epsilon regulates tumor necrosis factor-alpha-induced stannin gene expression. Reese, B.E., Davidson, C., Billingsley, M.L., Yun, J. J. Pharmacol. Exp. Ther. (2005) [Pubmed]
  14. The protein stannin binds 14-3-3zeta and modulates mitogen-activated protein kinase signaling. Davidson, C.E., Reese, B.E., Billingsley, M.L., Yun, J.K. Brain Res. Mol. Brain Res. (2005) [Pubmed]
  15. Peripheral and central nervous system lesions caused by triethyl- and trimethyltin salts in rats. O'Shaughnessy, D.J., Losos, G.J. Toxicologic pathology. (1986) [Pubmed]
  16. Beneficial effects of FK506 for experimental temporal lobe epilepsy. Nishimura, T., Imai, H., Minabe, Y., Sawa, A., Kato, N. Neurosci. Res. (2006) [Pubmed]
  17. Potential efficacy and toxicity of GM1 ganglioside against trimethyltin-induced brain lesions in rats: comparison with protracted food restriction. Bollweg, G., Balaban, C., Cox, H.J., Berra, B., Sparber, S.B. Neurotoxicology (1995) [Pubmed]
  18. The behavioral and neuropathologic sequelae of intoxication by trimethyltin compounds in the rat. Brown, A.W., Aldridge, W.N., Street, B.W., Verschoyle, R.D. Am. J. Pathol. (1979) [Pubmed]
  19. Structure, dynamics, and membrane topology of stannin: a mediator of neuronal cell apoptosis induced by trimethyltin chloride. Buck-Koehntop, B.A., Mascioni, A., Buffy, J.J., Veglia, G. J. Mol. Biol. (2005) [Pubmed]
  20. Molecular profiles of mRNA levels in laser capture microdissected murine hippocampal regions differentially responsive to TMT-induced cell death. Lefebvre d'Hellencourt, C., Harry, G.J. J. Neurochem. (2005) [Pubmed]
  21. Trimethyltin-induced neuronal damage in the rat brain: comparative studies using silver degeneration stains, immunocytochemistry and immunoassay for neuronotypic and gliotypic proteins. Balaban, C.D., O'Callaghan, J.P., Billingsley, M.L. Neuroscience (1988) [Pubmed]
  22. Serotonin transport in isolated platelet granules. Coupling to the electrochemical proton gradient. Carty, S.E., Johnson, R.G., Scarpa, A. J. Biol. Chem. (1981) [Pubmed]
  23. Systemic administration of atipamezole, a selective antagonist of alpha-2 adrenoceptors, facilitates behavioural activity but does not influence short-term or long-term memory in trimethyltin-intoxicated and control rats. Niittykoski, M., Lappalainen, R., Jolkkonen, J., Haapalinna, A., Riekkinen, P., Sirviö, J. Neuroscience and biobehavioral reviews. (1998) [Pubmed]
  24. Molecular neurotoxicology of trimethyltin: identification of stannin, a novel protein expressed in trimethyltin-sensitive cells. Toggas, S.M., Krady, J.K., Billingsley, M.L. Mol. Pharmacol. (1992) [Pubmed]
  25. Stannin, a protein that localizes to the mitochondria and sensitizes NIH-3T3 cells to trimethyltin and dimethyltin toxicity. Davidson, C.E., Reese, B.E., Billingsley, M.L., Yun, J.K. Mol. Pharmacol. (2004) [Pubmed]
  26. Cellular and molecular effects of trimethyltin and triethyltin: relevance to organotin neurotoxicity. Aschner, M., Aschner, J.L. Neuroscience and biobehavioral reviews. (1992) [Pubmed]
  27. Interactions of alkyltin salts with biological dithiols: dealkylation and induction of a regular beta-turn structure in peptides. Buck, B.A., Mascioni, A., Cramer, C.J., Veglia, G. J. Am. Chem. Soc. (2004) [Pubmed]
  28. Effects of organotins on rat brain astrocytes in culture. Richter-Landsberg, C., Besser, A. J. Neurochem. (1994) [Pubmed]
  29. Trimethyltin syndrome as a hippocampal degeneration model: temporal changes and neurochemical features of seizure susceptibility and learning impairment. Ishida, N., Akaike, M., Tsutsumi, S., Kanai, H., Masui, A., Sadamatsu, M., Kuroda, Y., Watanabe, Y., McEwen, B.S., Kato, N. Neuroscience (1997) [Pubmed]
  30. Type II glucocorticoid receptors are involved in neuronal death and astrocyte activation induced by trimethyltin in the rat hippocampus. Imai, H., Nishimura, T., Sadamatsu, M., Liu, Y., Kabuto, M., Kato, N. Exp. Neurol. (2001) [Pubmed]
  31. Ascorbate attenuates trimethyltin-induced oxidative burden and neuronal degeneration in the rat hippocampus by maintaining glutathione homeostasis. Shin, E.J., Suh, S.K., Lim, Y.K., Jhoo, W.K., Hjelle, O.P., Ottersen, O.P., Shin, C.Y., Ko, K.H., Kim, W.K., Kim, D.S., Chun, W., Ali, S., Kim, H.C. Neuroscience (2005) [Pubmed]
  32. Erythropoietin protects primary hippocampal neurons increasing the expression of brain-derived neurotrophic factor. Viviani, B., Bartesaghi, S., Corsini, E., Villa, P., Ghezzi, P., Garau, A., Galli, C.L., Marinovich, M. J. Neurochem. (2005) [Pubmed]
  33. In vivo activation of c-Jun N-terminal kinase signaling cascade prior to granule cell death induced by trimethyltin in the dentate gyrus of mice. Ogita, K., Nitta, Y., Watanabe, M., Nakatani, Y., Nishiyama, N., Sugiyama, C., Yoneda, Y. Neuropharmacology (2004) [Pubmed]
  34. S100b counteracts effects of the neurotoxicant trimethyltin on astrocytes and microglia. Reali, C., Scintu, F., Pillai, R., Donato, R., Michetti, F., Sogos, V. J. Neurosci. Res. (2005) [Pubmed]
  35. Age-dependent cytokine responses: trimethyltin hippocampal injury in wild-type, APOE knockout, and APOE4 mice. Harry, G.J., Lefebvre d'Hellencourt, C., Bruccoleri, A., Schmechel, D. Brain Behav. Immun. (2000) [Pubmed]
  36. Trimethyltin retinopathy. Relationship of subcellular response to neuronal subspecialization. Bouldin, T.W., Goines, N.D., Krigman, M.R. J. Neuropathol. Exp. Neurol. (1984) [Pubmed]
  37. Grafts containing fetal hippocampal tissue reduce activity and improve passive avoidance in hippocampectomized or trimethyltin-exposed rats. Woodruff, M.L., Baisden, R.H., Whittington, D.L., Shelton, N.L., Wray, S. Exp. Neurol. (1988) [Pubmed]
  38. Neurotoxicant-induced elevation of adrenomedullin expression in hippocampus and glia cultures. Jahnke, G.D., Brunssen, S., Maier, W.E., Harry, G.J. J. Neurosci. Res. (2001) [Pubmed]
  39. Altered expression of amyloid protein precursor mRNA in the rat hippocampus following trimethyltin intoxication: an in situ hybridization study. O'Connell, A.W., Strada, O., Earley, B., Leonard, B.E. Neurochem. Int. (1997) [Pubmed]
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