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Chemical Compound Review

Hexaethylditin     triethyltin

Synonyms: AG-I-01562, NSC-341995, CTK3I7892, NSC341995, [(C2H5)3Sn]2, ...
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Disease relevance of triethyltin

  • Trimethyltin, unlike triethyltin, does not produce white matter edema in rats but does cause bilateral and symmetrical neuronal alterations involving the hippocampus (largely sparing the Sommer sector), pyriform cortex, amygdaloid nucleus, and neocortex [1].
  • For clarification of the beneficial effects of the extract of Ginkgo biloba (EGB) on triethyltin (TET) toxicity in rats, the phosphodiesterase (PDE) activities of the cerebral tissue were measured under in vitro and ex vivo conditions [2].
  • The possible involvement of cerebral cAMP-phosphodiesterase (PDE) in the intoxication and brain edema formation after exposure to triethyltin (TET) has been studied in vitro and in vivo in the rat [3].
  • In group 1 (survival group) triethyltin was administered i.p. once in a dose of 2.5 mg/kg body weight and in group 2 (terminal group) the animals received triethyltin in a dose of 9 mg/kg of body weight [4].
  • Four days after triethyltin poisoning, the brains of control rats receiving maintenance hydration had a mean percentage of water of 79.56%; dehydration (5% of body weight) and overhydration groups were not statistically different at 79.95% and 79.86%, respectively [5].
 

Psychiatry related information on triethyltin

 

High impact information on triethyltin

 

Chemical compound and disease context of triethyltin

 

Biological context of triethyltin

  • The purified yeast oligomycin-sensitive ATPase complex contains approximately six binding sites for triethyltin/mol of enzyme complex [18].
  • It is concluded that decrease of matrix substrate content is probably not the major cause of the greater sensitivity of oxidative phosphorylation to triethyltin in a KCl medium observed previously [19].
  • It is concluded that energy from either the oxidation of substrate or the hydrolysis of ATP is associated with the generation of sufficient OH- to enable the triethyltin-mediated Cl-/OH- exchange to occur under the metabolic conditions relevant to this action of triethyltin [20].
  • If substrate oxidation is blocked by respiratory-chain inhibitors the Cl- uptake mediated by triethyltin is inhibited except in the media containing ATP, when the characteristics of Cl- uptake similar to that found in the medium containing ATP alone are observed [20].
  • Cerebral oxygen consumption was augmented by about 18% 12 h after triethyltin injection in group 1 [4].
 

Anatomical context of triethyltin

 

Associations of triethyltin with other chemical compounds

 

Gene context of triethyltin

  • Inactivation of yeast hexokinase B by triethyltin bromide [25].
  • Effects of an extract of Ginkgo biloba on the 3',5'-cyclic AMP phosphodiesterase activity of the brain of normal and triethyltin-intoxicated rats [2].
  • This study examined the early response of pro-inflammatory and regulatory cytokines in the mouse brain following triethyltin (TET)-induced myelin injury characterized by edematous vacuolation [27].
  • During spontaneous recovery, astroglial cells in the edematous white matter of TET-intoxicated animals showed short and swollen processes containing few organelles, low levels of NADH- and NADPH-tetrazolium reductase activities and glial fibrillary acidic protein (GFAP)-immunofluorescence for about 2 weeks [28].
  • Effects of continual intravenous posttreatment with D-CPP-ene, a potent competitive N-methyl-D-aspartate receptor antagonist, on rat brain edema induced by injection of triethyltin into the cerebral hemisphere [29].
 

Analytical, diagnostic and therapeutic context of triethyltin

References

  1. 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]
  2. Effects of an extract of Ginkgo biloba on the 3',5'-cyclic AMP phosphodiesterase activity of the brain of normal and triethyltin-intoxicated rats. Macovschi, O., Prigent, A.F., Nemoz, G., Pacheco, H. J. Neurochem. (1987) [Pubmed]
  3. Decreased adenosine cyclic 3',5'-monophosphate phosphodiesterase activity in rat brain following triethyltin intoxication. Macovschi, O., Prigent, A.F., Nemoz, G., Pageaux, J.F., Pacheco, H. Biochem. Pharmacol. (1984) [Pubmed]
  4. Acute poisoning with triethyltin in the rat. Changes in cerebral blood flow, cerebral oxygen consumption, arterial and cerebral venous blood gases. Pluta, R., Ostrowska, B. Exp. Neurol. (1987) [Pubmed]
  5. Effect of hydration on experimentally induced cerebral edema. Morse, M.L., Milstein, J.M., Haas, J.E., Taylor, E. Crit. Care Med. (1985) [Pubmed]
  6. Triethyltin decreases maximal electroshock seizure severity in adult rats. Fox, D.A., Doctor, S.V. Toxicol. Appl. Pharmacol. (1983) [Pubmed]
  7. Diurnal patterns in homecage behavior of rats after acute exposure to triethyltin. Bushnell, P.J., Evans, H.L. Toxicol. Appl. Pharmacol. (1986) [Pubmed]
  8. Neonatal exposure to triethyltin disrupts olfactory discrimination learning in preweanling rats. Stanton, M.E. Neurotoxicology and teratology. (1991) [Pubmed]
  9. A system for assessing toxicity of chemicals by continuous monitoring of homecage behaviors. Evans, H.L., Bushnell, P.J., Taylor, J.D., Monico, A., Teal, J.J., Pontecorvo, M.J. Fundamental and applied toxicology : official journal of the Society of Toxicology. (1986) [Pubmed]
  10. The effects of triethyltin bromide on red cell and brain cyclic AMP-dependent protein kinases. Siebenlist, K.R., Taketa, F. J. Biol. Chem. (1983) [Pubmed]
  11. Cellular and molecular effects of trimethyltin and triethyltin: relevance to organotin neurotoxicity. Aschner, M., Aschner, J.L. Neuroscience and biobehavioral reviews. (1992) [Pubmed]
  12. Triethyltin-induced stress responses and apoptotic cell death in cultured oligodendrocytes. Stahnke, T., Richter-Landsberg, C. Glia (2004) [Pubmed]
  13. Measurement of edema in the nervous system. Use of Percoll density gradients for determination of specific gravity in cerebral cortex and white matter under normal conditions and in experimental cytotoxic brain edema. Tengvar, C., Forssén, M., Hultström, D., Olsson, Y., Pertoft, H., Pettersson, A. Acta Neuropathol. (1982) [Pubmed]
  14. Sodium selenite-induced hypothermia in mice: indirect evidence for a neural effect. Watanabe, C., Suzuki, T. Toxicol. Appl. Pharmacol. (1986) [Pubmed]
  15. Inhibitory effect of triethyltin on taurine transport by glioma cells. Martin, D.L., Waniewski, R.A., Wolpaw, E.W. Toxicol. Appl. Pharmacol. (1983) [Pubmed]
  16. Tri-n-butyltin-induced change in cellular level of glutathione in rat thymocytes: a flow cytometric study. Okada, Y., Oyama, Y., Chikahisa, L., Satoh, M., Kanemaru, K., Sakai, H., Noda, K. Toxicol. Lett. (2000) [Pubmed]
  17. Vascular permeability in acute triethyltin-induced brain edema studied with FITC-dextrans, sodium fluorescein and horseradish peroxidase as tracers. Hultström, D., Forssén, M., Pettersson, A., Tengvar, C., Jarild, M., Olsson, Y. Acta neurologica Scandinavica. (1984) [Pubmed]
  18. Studies of energy-linked reactions. Localization of the site of action of trialkyltin in yeast mitochondria. Cain, K., Griffiths, D.E. Biochem. J. (1977) [Pubmed]
  19. The decrease of mitochondrial substrate uptake caused by trialkyltin and trialkyl-lead compounds in chloride media and its relevance to inhibition of oxidative phosphorylation. Skilleter, D.N. Biochem. J. (1975) [Pubmed]
  20. The influence of adenine nucleotides and oxidizable substrates on triethyltin-mediated chloride uptake by rat liver mitochondria in potassium chloride media. Skilleter, D.N. Biochem. J. (1976) [Pubmed]
  21. The binding of triethyltin to rat brain myelin. Lock, E.A., Aldridge, W.N. J. Neurochem. (1975) [Pubmed]
  22. Effects of organotins on rat brain astrocytes in culture. Richter-Landsberg, C., Besser, A. J. Neurochem. (1994) [Pubmed]
  23. Studies on the nature of the high-affinity trialkyltin binding site of rat liver mitochondria. Dawson, A.P., Farrow, B.G., Selwyn, M.J. Biochem. J. (1982) [Pubmed]
  24. Oxidative phosphorylation. Halide-dependent and halide-independent effects of triorganotin and trioganolead compounds on mitochondrial functions. Aldridge, W.N., Street, B.W., Skilleter, D.N. Biochem. J. (1977) [Pubmed]
  25. Inactivation of yeast hexokinase B by triethyltin bromide. Siebenlist, K.R., Taketa, F. Biochemistry (1983) [Pubmed]
  26. Mitochondrial adenosine triphosphatase of the fission yeast, Schizosaccharomyces pombe 972h-. Changes in activity and inhibitor-sensitivity in response to catabolite repression. Lloyd, D., Edwards, S.W. Biochem. J. (1976) [Pubmed]
  27. Increase in brain stem cytokine mRNA levels as an early response to chemical-induced myelin edema. Mehta, P.S., Bruccoleri, A., Brown, H.W., Harry, G.J. J. Neuroimmunol. (1998) [Pubmed]
  28. Stimulation of astrocytes affects cytotoxic brain edema. Sancesario, G., Kreutzberg, G.W. Acta Neuropathol. (1986) [Pubmed]
  29. Effects of continual intravenous posttreatment with D-CPP-ene, a potent competitive N-methyl-D-aspartate receptor antagonist, on rat brain edema induced by injection of triethyltin into the cerebral hemisphere. Demura, N., Kuroda, J., Tanaka, K., Seno, N., Kanazawa, I. Neurosci. Lett. (1995) [Pubmed]
  30. Inactivation of yeast hexokinase B by triethyltin bromide and reactivation by dithiothreitol and glucose. Siebenlist, K.R., Taketa, F. Biochemistry (1983) [Pubmed]
  31. Increase in cerebral fluid in rats after treatment with triethyltin. Lujinsky, W., Aldridge, W.N. Biochem. Pharmacol. (1975) [Pubmed]
  32. Investigation of the interaction of triethyltin with rat liver mitochondria using binding studies and Mössbauer spectroscopy. Farrow, B.G., Dawson, A.P. Eur. J. Biochem. (1978) [Pubmed]
  33. A study of the effects of vigabatrin on the central nervous system and retina of Sprague Dawley and Lister-Hooded rats. Butler, W.H., Ford, G.P., Newberne, J.W. Toxicologic pathology. (1987) [Pubmed]
  34. Flow cytometric comparison of the effects of trialkyltins on the murine erythroleukemic cell. Zucker, R.M., Elstein, K.H., Easterling, R.E., Massaro, E.J. Toxicology (1989) [Pubmed]
 
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