The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

Capsidol     (E)-N-[(4-hydroxy-3-methoxy- phenyl)methyl]...

Synonyms: Capzasin, Capsaicin, Zostrix, Axsain, CAPSAICINE, ...
 
 
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.
 

Disease relevance of Capsaicin

 

Psychiatry related information on Capsaicin

  • These data show that A beta is neurotoxic in vivo and suggest that apoptosis may be responsible for the accompanying neuronal loss, the principal underlying cellular feature of Alzheimer's disease [8].
  • Although Purkinje cells are relatively resistant to loss, the observed disturbance of AMPA receptors may contribute to the neurotoxic process in other vulnerable brain regions and clinically to the development of dementia [9].
  • The cause of Huntington's disease is expansion of polyglutamine (polyQ) domain in huntingtin, which makes this protein both neurotoxic and aggregation prone [10].
  • Within brain tissues, the endogenous neurotoxic reservoir can slowly release free BMAA, thereby causing incipient and recurrent neurological damage over years or even decades, which may explain the observed long latency period for neurological disease onset among the Chamorro people [11].
  • Neurotoxic BLA lesions did not alter either motor activity or shock reactivity [12].
 

High impact information on Capsaicin

 

Chemical compound and disease context of Capsaicin

 

Biological context of Capsaicin

  • To test whether the hypothesis that the Alzheimer's A beta peptide is neurotoxic, we introduced a transgene into mice to direct expression of this peptide to neurons [8].
  • Low cell densities cause neurotoxic signs and fish death, followed by rapid algal encystment and dormancy unless live fish are added [23].
  • Study of the relationship between the chemical structure of organophosphorus esters and their neurotoxic potencies suggests that two hydrophobic areas may be present in the vicinity of the active site of the neurotoxicity protein [24].
  • Recent studies have shown that delayed neurotoxic organophosphorus compounds interact with Ca2+/calmodulin kinase II (CaM kinase II), an enzyme responsible for the endogenous phosphorylation of cytoskeletal proteins, i.e. microtubules, neurofilaments, and MAP-2 [25].
  • Increases in the extracellular concentration of excitatory amino acids to neurotoxic levels take place only as membrane potential falls rapidly towards 0mV, coincident with massive changes in ion gradients [26].
 

Anatomical context of Capsaicin

 

Associations of Capsaicin with other chemical compounds

  • Suppression of reversed uptake by the low pH occurring in ischaemia will slow the Ca(2+)-independent release of glutamate with can raise [glu]o to a neurotoxic level, and will thus protect the brain during a transient loss of blood supply [32].
  • This feature of NMDA receptors could be relevant to neurotoxic activation of NMDA receptors during ischaemia, as well as to seizure generation, as extracellular proton changes occur during both of these pathological situations [33].
  • After 20 milligrams of p-chloroamphetamine per kilogram there was also evidence of neurotoxic effects on cells within the substantia nigra [34].
  • 2,5-Hexanedione, the principal neurotoxic metabolite of the industrial solvents n-hexane and methyl n-butyl ketone causes axonal degeneration in the mammillary body and visual nuclei of cats [35].
  • There are accumulating data indicating that under specific circumstances, dopamine, which occurs in high concentrations in the basal ganglia, might be neurotoxic [36].
 

Gene context of Capsaicin

  • In humans, presenilins that are associated with Alzheimer's disease stimulate overproduction of the neurotoxic 42-amino-acid beta-amyloid derivative (Abeta42) of the amyloid-precursor protein APP [37].
  • The central questions in common AD focus on whether cerebral and cerebrovascular Abeta accumulation is (a) a final neurotoxic pathway, common to all forms of AD; (b) a toxic by-product of an independent primary metabolic lesion that, by itself, is also neurotoxic; or (c) an inert by-product of an independent primary neurotoxic reaction [38].
  • Mutations in the presenilin-1 (PS1) gene are associated with Alzheimer's disease and cause increased secretion of the neurotoxic amyloid-beta peptide (Abeta) [39].
  • Neurotoxic insults deregulate Cdk5 activity, which leads to neuronal apoptosis and may contribute to neurodegeneration [40].
  • EDN, ECP-1, and ECP-2 had neurotoxic activity, causing the Gordon phenomenon at doses down to 0.15 micrograms when injected into the cisterna magna; the proteins were comparable in their activities [41].
  • Prior exposure of cells to N-acetyl-L -cysteine blocked not only the ROS production but also the nuclear translocation of Nrf2 and its ARE binding, as well as HO-1 induction by capsaicin [42].
  • Diarylpropionitrile (ERbeta agonist) also inhibited capsaicin-induced TRPV1 currents, whereas propylpyrazole triol (ERalpha agonist) and 17alpha-estradiol (inactive analog) were inactive, and 17beta-estradiol conjugated to BSA (membrane-impermeable agonist) caused a small increase [43].
 

Analytical, diagnostic and therapeutic context of Capsaicin

References

  1. Postoperative chemotherapy and delayed radiation in children less than three years of age with malignant brain tumors. Duffner, P.K., Horowitz, M.E., Krischer, J.P., Friedman, H.S., Burger, P.C., Cohen, M.E., Sanford, R.A., Mulhern, R.K., James, H.E., Freeman, C.R. N. Engl. J. Med. (1993) [Pubmed]
  2. Central nervous system damage produced by expression of the HIV-1 coat protein gp120 in transgenic mice. Toggas, S.M., Masliah, E., Rockenstein, E.M., Rall, G.F., Abraham, C.R., Mucke, L. Nature (1994) [Pubmed]
  3. Nitric oxide: a neural messenger. Jaffrey, S.R., Snyder, S.H. Annu. Rev. Cell Dev. Biol. (1995) [Pubmed]
  4. 1-methyl-4-phenylpyridine is neurotoxic to the nigrostriatal dopamine pathway. Bradbury, A.J., Costall, B., Domeney, A.M., Jenner, P., Kelly, M.E., Marsden, C.D., Naylor, R.J. Nature (1986) [Pubmed]
  5. Acceptors for botulinum neurotoxin reside on motor nerve terminals and mediate its internalization. Dolly, J.O., Black, J., Williams, R.S., Melling, J. Nature (1984) [Pubmed]
  6. Intraprostatic capsaicin injection as a novel model for nonbacterial prostatitis and effects of botulinum toxin A. Chuang, Y.C., Yoshimura, N., Wu, M., Huang, C.C., Chiang, P.H., Tyagi, P., Chancellor, M.B. Eur. Urol. (2007) [Pubmed]
  7. Capsaicin is a novel blocker of constitutive and interleukin-6-inducible STAT3 activation. Bhutani, M., Pathak, A.K., Nair, A.S., Kunnumakkara, A.B., Guha, S., Sethi, G., Aggarwal, B.B. Clin. Cancer Res. (2007) [Pubmed]
  8. The Alzheimer's A beta peptide induces neurodegeneration and apoptotic cell death in transgenic mice. LaFerla, F.M., Tinkle, B.T., Bieberich, C.J., Haudenschild, C.C., Jay, G. Nat. Genet. (1995) [Pubmed]
  9. Decreased expression of AMPA receptor messenger RNA and protein in AIDS: a model for HIV-associated neurotoxicity. Everall, I.P., Hudson, L., al-Sarraj, S., Honavar, M., Lantos, P., Kerwin, R. Nat. Med. (1995) [Pubmed]
  10. Huntington toxicity in yeast model depends on polyglutamine aggregation mediated by a prion-like protein Rnq1. Meriin, A.B., Zhang, X., He, X., Newnam, G.P., Chernoff, Y.O., Sherman, M.Y. J. Cell Biol. (2002) [Pubmed]
  11. A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam. Murch, S.J., Cox, P.A., Banack, S.A. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  12. Overtraining does not mitigate contextual fear conditioning deficits produced by neurotoxic lesions of the basolateral amygdala. Maren, S. J. Neurosci. (1998) [Pubmed]
  13. Aluminum neurotoxicity in preterm infants receiving intravenous-feeding solutions. Bishop, N.J., Morley, R., Day, J.P., Lucas, A. N. Engl. J. Med. (1997) [Pubmed]
  14. Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study. Watt, G., Theakston, R.D., Hayes, C.G., Yambao, M.L., Sangalang, R., Ranoa, C.P., Alquizalas, E., Warrell, D.A. N. Engl. J. Med. (1986) [Pubmed]
  15. Targeting angiogenesis with a conjugate of HPMA copolymer and TNP-470. Satchi-Fainaro, R., Puder, M., Davies, J.W., Tran, H.T., Sampson, D.A., Greene, A.K., Corfas, G., Folkman, J. Nat. Med. (2004) [Pubmed]
  16. Lipoprotein receptor-mediated induction of matrix metalloproteinase by tissue plasminogen activator. Wang, X., Lee, S.R., Arai, K., Lee, S.R., Tsuji, K., Rebeck, G.W., Lo, E.H. Nat. Med. (2003) [Pubmed]
  17. Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders. Caughey, B., Lansbury, P.T. Annu. Rev. Neurosci. (2003) [Pubmed]
  18. Electrogenic glutamate uptake in glial cells is activated by intracellular potassium. Barbour, B., Brew, H., Attwell, D. Nature (1988) [Pubmed]
  19. Quinolinic acid: an endogenous metabolite that produces axon-sparing lesions in rat brain. Schwarcz, R., Whetsell, W.O., Mangano, R.M. Science (1983) [Pubmed]
  20. Cisplatin combined with carboplatin: a new way of intensification of platinum dose in the treatment of advanced ovarian cancer. Belgian Study Group for Ovarian Carcinoma. Piccart, M.J., Nogaret, J.M., Marcelis, L., Longrée, H., Ries, F., Kains, J.P., Gobert, P., Domange, A.M., Sculier, J.P., Gompel, C. J. Natl. Cancer Inst. (1990) [Pubmed]
  21. Effect of exposure of miners to aluminium powder. Rifat, S.L., Eastwood, M.R., McLachlan, D.R., Corey, P.N. Lancet (1990) [Pubmed]
  22. Primary brain tumours in adults. Behin, A., Hoang-Xuan, K., Carpentier, A.F., Delattre, J.Y. Lancet (2003) [Pubmed]
  23. New 'phantom' dinoflagellate is the causative agent of major estuarine fish kills. Burkholder, J.M., Noga, E.J., Hobbs, C.H., Glasgow, H.B., Smith, S.A. Nature (1992) [Pubmed]
  24. Organophosphorus ester-induced delayed neurotoxicity. Abou-Donia, M.B. Annu. Rev. Pharmacol. Toxicol. (1981) [Pubmed]
  25. Mechanisms of organophosphorus ester-induced delayed neurotoxicity: type I and type II. Abou-Donia, M.B., Lapadula, D.M. Annu. Rev. Pharmacol. Toxicol. (1990) [Pubmed]
  26. The early events of oxygen and glucose deprivation: setting the scene for neuronal death? Martin, R.L., Lloyd, H.G., Cowan, A.I. Trends Neurosci. (1994) [Pubmed]
  27. Conservation of hippocampal memory function in rats and humans. Bunsey, M., Eichenbaum, H. Nature (1996) [Pubmed]
  28. The glial cell glutamate uptake carrier countertransports pH-changing anions. Bouvier, M., Szatkowski, M., Amato, A., Attwell, D. Nature (1992) [Pubmed]
  29. Intraneuronal generation of a pyridinium metabolite may cause drug-induced parkinsonism. Markey, S.P., Johannessen, J.N., Chiueh, C.C., Burns, R.S., Herkenham, M.A. Nature (1984) [Pubmed]
  30. Secretion of neurotoxins by mononuclear phagocytes infected with HIV-1. Giulian, D., Vaca, K., Noonan, C.A. Science (1990) [Pubmed]
  31. The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"). Green, A.R., Mechan, A.O., Elliott, J.M., O'Shea, E., Colado, M.I. Pharmacol. Rev. (2003) [Pubmed]
  32. Modulation of non-vesicular glutamate release by pH. Billups, B., Attwell, D. Nature (1996) [Pubmed]
  33. Proton inhibition of N-methyl-D-aspartate receptors in cerebellar neurons. Traynelis, S.F., Cull-Candy, S.G. Nature (1990) [Pubmed]
  34. P-Chloramphetamine: Selective neurotoxic action in brain. Harvey, J.A., McMaster, S.E., Yunger, L.M. Science (1975) [Pubmed]
  35. Environmental hydrocarbons produce degeneration in cat hypothalamus and optic tract. Schaumburg, H.H., Spencer, P.S. Science (1978) [Pubmed]
  36. Neuronal cell death in Huntington's disease: a potential role for dopamine. Jakel, R.J., Maragos, W.F. Trends Neurosci. (2000) [Pubmed]
  37. Neurogenic phenotypes and altered Notch processing in Drosophila Presenilin mutants. Ye, Y., Lukinova, N., Fortini, M.E. Nature (1999) [Pubmed]
  38. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease. Gandy, S. J. Clin. Invest. (2005) [Pubmed]
  39. Presenilin-1 differentially facilitates endoproteolysis of the beta-amyloid precursor protein and Notch. Capell, A., Steiner, H., Romig, H., Keck, S., Baader, M., Grim, M.G., Baumeister, R., Haass, C. Nat. Cell Biol. (2000) [Pubmed]
  40. Cdk5-mediated inhibition of the protective effects of transcription factor MEF2 in neurotoxicity-induced apoptosis. Gong, X., Tang, X., Wiedmann, M., Wang, X., Peng, J., Zheng, D., Blair, L.A., Marshall, J., Mao, Z. Neuron (2003) [Pubmed]
  41. Biochemical and functional similarities between human eosinophil-derived neurotoxin and eosinophil cationic protein: homology with ribonuclease. Gleich, G.J., Loegering, D.A., Bell, M.P., Checkel, J.L., Ackerman, S.J., McKean, D.J. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  42. Capsaicin induces heme oxygenase-1 expression in HepG2 cells via activation of PI3K-Nrf2 signaling: NAD(P)H:quinone oxidoreductase as a potential target. Joung, E.J., Li, M.H., Lee, H.G., Somparn, N., Jung, Y.S., Na, H.K., Kim, S.H., Cha, Y.N., Surh, Y.J. Antioxid. Redox Signal. (2007) [Pubmed]
  43. 17beta-estradiol activates estrogen receptor beta-signalling and inhibits transient receptor potential vanilloid receptor 1 activation by capsaicin in adult rat nociceptor neurons. Xu, S., Cheng, Y., Keast, J.R., Osborne, P.B. Endocrinology (2008) [Pubmed]
  44. Self-reported exposure to neurotoxic chemical combinations in the Gulf War. A cross-sectional epidemiologic study. Haley, R.W., Kurt, T.L. JAMA (1997) [Pubmed]
  45. Prospects for clinically tolerated NMDA antagonists: open-channel blockers and alternative redox states of nitric oxide. Lipton, S.A. Trends Neurosci. (1993) [Pubmed]
  46. Cytoskeletal architecture and immunocytochemical localization of microtubule-associated proteins in regions of axons associated with rapid axonal transport: the beta,beta'-iminodipropionitrile-intoxicated axon as a model system. Hirokawa, N., Bloom, G.S., Vallee, R.B. J. Cell Biol. (1985) [Pubmed]
  47. Pharmacology of glutamate receptor antagonists in the kindling model of epilepsy. Löscher, W. Prog. Neurobiol. (1998) [Pubmed]
 
WikiGenes - Universities