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Chemical Compound Review

TOCP     1-bis(2- methylphenoxy)phosphoryloxy- 2...

Synonyms: TOTP, Phosflex 179C, NSC-438, SureCN35762, NSC438, ...
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Disease relevance of TRICRESYL PHOSPHATE

  • Effects of neuropathic and non-neuropathic isomers of tricresyl phosphate and their microsomal activation on the production of axon-like processes by differentiating mouse N2a neuroblastoma cells [1].
  • The adduct pattern after in vivo treatment with tri-o-tolyl phosphate was identical with that found in bacteria and hepatoma cells treated with 2-phenoxy-4H-1,3,2-benzo-dioxaphosphorin 2-oxide, the major adduct being N3-(o-hydroxybenzyl)deoxycytidine 3' monophosphate and the minor N3-(o-hydroxybenzyl)deoxyuridine 3' monophosphate [2].
  • The toxicity of T-2 toxin in mice was enhanced by pre-treatment with tri-o-cresyl phosphate (TOCP), a specific carboxylesterase inhibitor [3].
  • This condition is characterized by ataxia that progresses to paralysis concurrent with a central-peripheral distal axonopathy after a delay period of 1-2 weeks following exposure to an organophosphorus compound causing delayed neurotoxicity, such as tri-o-cresyl phosphate (TOCP) [4].
  • We have investigated the genotoxicity of this saligenin phosphate and the structure of adducts formed by incubation of 2-phenoxy-4H-1,3,2-benzodioxaphosphorin 2-oxide with nucleosides and DNA. o-Tolyl phosphate was mutagenic in the Ames test (695 revertants/mumol, Salmonella typhimurium TA 100) only with metabolic activation [5].

High impact information on TRICRESYL PHOSPHATE


Chemical compound and disease context of TRICRESYL PHOSPHATE


Biological context of TRICRESYL PHOSPHATE


Anatomical context of TRICRESYL PHOSPHATE


Associations of TRICRESYL PHOSPHATE with other chemical compounds




Analytical, diagnostic and therapeutic context of TRICRESYL PHOSPHATE


  1. Effects of neuropathic and non-neuropathic isomers of tricresyl phosphate and their microsomal activation on the production of axon-like processes by differentiating mouse N2a neuroblastoma cells. Fowler, M.J., Flaskos, J., McLean, W.G., Hargreaves, A.J. J. Neurochem. (2001) [Pubmed]
  2. DNA adduct formation in Salmonella typhimurium, cultured liver cells and in Fischer 344 rats treated with o-tolyl phosphates and their metabolites. Mentzschel, A., Vamvakas, S., Dekant, W., Henschler, D. Carcinogenesis (1993) [Pubmed]
  3. Metabolism of T-2 toxin by rat liver carboxylesterase. Johnsen, H., Odden, E., Lie, O., Johnsen, B.A., Fonnum, F. Biochem. Pharmacol. (1986) [Pubmed]
  4. Biochemical changes in sciatic nerve of hens treated with tri-o-cresyl phosphate: increased phosphorylation of cytoskeletal proteins. Lapadula, E.S., Lapadula, D.M., Abou-Donia, M.B. Neurochem. Int. (1992) [Pubmed]
  5. Genotoxicity of neurotoxic triaryl phosphates: identification of DNA adducts of the ultimate metabolites, saligenin phosphates. Mentzschel, A., Schmuck, G., Dekant, W., Henschler, D. Chem. Res. Toxicol. (1993) [Pubmed]
  6. Calcium and calmodulin-enhanced in vitro phosphorylation of hen brain cold-stable microtubules and spinal cord neurofilament triplet proteins after a single oral dose of tri-o-cresyl phosphate. Suwita, E., Lapadula, D.M., Abou-Donia, M.B. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  7. Evaluation of the hazards of industrial exposure to tricresyl phosphate: a review and interpretation of the literature. Craig, P.H., Barth, M.L. Journal of toxicology and environmental health. Part B, Critical reviews. (1999) [Pubmed]
  8. Aberrant activation of CDK5 is involved in the pathogenesis of OPIDN. Wang, Y.P., Mou, D.L., Song, J.F., Rao, Z.R., Li, D., Ju, G. J. Neurochem. (2006) [Pubmed]
  9. Paraoxon hydrolysis vs. covalent binding in the elimination of paraoxon in the rabbit. Butler, E.G., Eckerson, H.W., La Du, B.N. Drug Metab. Dispos. (1985) [Pubmed]
  10. Peripheral nerve damage in chicks following treatment with organophosphorus compounds in ovo. Sheets, L., Norton, S. Toxicol. Appl. Pharmacol. (1985) [Pubmed]
  11. Tricresyl phosphate inhibits the formation of axon-like processes and disrupts neurofilaments in cultured mouse N2a and rat PC12 cells. Flaskos, J., McLean, W.G., Fowler, M.J., Hargreaves, A.J. Neurosci. Lett. (1998) [Pubmed]
  12. The toxicity of organophosphate compounds towards cultured PC12 cells. Flaskos, J., McLean, W.G., Hargreaves, A.J. Toxicol. Lett. (1994) [Pubmed]
  13. Relationship of tri-O-cresyl phosphate-induced delayed neurotoxicity to enhancement of in vitro phosphorylation of hen brain and spinal cord proteins. Patton, S.E., Lapadula, D.M., Abou-Donia, M.B. J. Pharmacol. Exp. Ther. (1986) [Pubmed]
  14. Morphologic alterations in leg muscles of chicks treated with triorthocresyl phosphate in ovo. Sheets, L., Norton, S. Toxicol. Appl. Pharmacol. (1985) [Pubmed]
  15. The interaction of Sertoli and Leydig cells in the testicular toxicity of tri-o-cresyl phosphate. Chapin, R.E., Phelps, J.L., Somkuti, S.G., Heindel, J.J., Burka, L.T. Toxicol. Appl. Pharmacol. (1990) [Pubmed]
  16. Pathogenesis of cholesteryl lipidosis of adrenocortical and ovarian interstitial cells in F344 rats caused by tricresyl phosphate and butylated triphenyl phosphate. Latendresse, J.R., Azhar, S., Brooks, C.L., Capen, C.C. Toxicol. Appl. Pharmacol. (1993) [Pubmed]
  17. Brain acetylcholinesterase, acid phosphatase, and 2',3'-cyclic nucleotide-3'-phosphohydrolase and plasma butyrylcholinesterase activities in hens treated with a single dermal neurotoxic dose of S,S,S-tri-n-butyl phosphorotrithioate. Abou-Donia, M.B., Abdo, K.M., Timmons, P.R., Proctor, J.E. Toxicol. Appl. Pharmacol. (1986) [Pubmed]
  18. Chronic treatment with cholinesterase inhibitors increases alpha 2-adrenoceptors in rat brain. Hollingsworth, P.J. Eur. J. Pharmacol. (1988) [Pubmed]
  19. Comparative metabolism and disposition of ethyl carbamate (urethane) in male Fischer 344 rats and male B6C3F1 mice. Nomeir, A.A., Ioannou, Y.M., Sanders, J.M., Matthews, H.B. Toxicol. Appl. Pharmacol. (1989) [Pubmed]
  20. Metabolic pathways of 1-butyl [3-13C]acrylate. Identification of urinary metabolites in rat using nuclear magnetic resonance and mass spectroscopy. Linhart, I., Hrabal, R., Smejkal, J., Mitera, J. Chem. Res. Toxicol. (1994) [Pubmed]
  21. The effects of tri-o-cresyl phosphate and metabolites on rat Sertoli cell function in primary culture. Chapin, R.E., Phelps, J.L., Burka, L.T., Abou-Donia, M.B., Heindel, J.J. Toxicol. Appl. Pharmacol. (1991) [Pubmed]
  22. Calcium and calmodulin stimulated in vitro phosphorylation of rooster brain tubulin and MAP-2 following a single oral dose of tri-o-cresyl phosphate. Suwita, E., Lapadula, D.M., Abou-Donia, M.B. Brain Res. (1986) [Pubmed]
  23. Effect of oral administration of tri-o-cresyl phosphate on in vitro phosphorylation of membrane and cytosolic proteins from chicken brain. Patton, S.E., O'Callaghan, J.P., Miller, D.B., Abou-Donia, M.B. J. Neurochem. (1983) [Pubmed]
  24. Triphenyl phosphate allergy from spectacle frames. Carlsen, L., Andersen, K.E., Egsgaard, H. Contact Derm. (1986) [Pubmed]
  25. Effect of beta-naphthoflavone on o-tolyl saligenin phosphate-induced delayed neuropathy in two lines of chickens. Bursian, S.J., Lehning, E.J., Correll, L., Ehrich, M. Journal of toxicology and environmental health. (1989) [Pubmed]
  26. Preparation of refractive index matching polymer film alternative to oil for use in a portable surface-plasmon resonance phenomenon-based chemical sensor method. Masadome, T., Asano, Y., Imato, T., Ohkubo, S., Tobita, T., Tabei, H., Iwasaki, Y., Niwa, O., Fushinuki, Y. Analytical and bioanalytical chemistry. (2002) [Pubmed]
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