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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Chemical Compound Review

CID121986     aluminum(+3) cation; 3-hydroxy-2-methyl...

Synonyms:
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Disease relevance of MALTOL

 

Psychiatry related information on MALTOL

 

High impact information on MALTOL

  • In the present investigation, we have examined the effect of chronic lithium treatment on hippocampus, as monitored by changes at the subcellular level of apoptosis-regulatory proteins which have been induced by the neurotoxin, aluminum maltolate [4].
  • Aluminum-maltolate induces apoptosis and necrosis in neuro-2a cells: potential role for p53 signaling [5].
  • Aluminum maltolate (Al-malt) causes neurodegeneration following in vivo exposure, and apoptosis plays a prominent role [5].
  • In animals treated intracisternally with the neurotoxin aluminum-maltolate, although pro-caspase-3 levels are higher in the cytosolic fractions, p17, the active caspase-3, is localized mainly in the endoplasmic reticulum [6].
  • Investigations in our laboratory have focused on neuronal injury resulting from the intracisternal administration of aluminum maltolate to New Zealand white rabbits, an animal system relevant to a study of human disease in that it reflects many of the histological and biochemical changes associated with Alzheimer's disease [7].
 

Biological context of MALTOL

 

Anatomical context of MALTOL

 

Associations of MALTOL with other chemical compounds

  • In this report, optimized conditions for tissue digestion and permeabilization using Proteinase K and Triton X and a quantification method for apoptosis detection are described using brain sections from aluminum maltolate-treated aged and young rabbits as compared to untreated matched controls [14].
 

Gene context of MALTOL

References

  1. Aluminum maltolate-induced toxicity in NT2 cells occurs through apoptosis and includes cytochrome c release. Griffioen, K.J., Ghribi, O., Fox, N., Savory, J., DeWitt, D.A. Neurotoxicology (2004) [Pubmed]
  2. Quantitative image analysis of temporal changes in tau and neurofilament proteins during the course of acute experimental neurofibrillary degeneration; non-phosphorylated epitopes precede phosphorylation. Savory, J., Huang, Y., Herman, M.M., Wills, M.R. Brain Res. (1996) [Pubmed]
  3. Memory deficit in mice administered aluminum-maltolate complex. Kaneko, N., Takada, J., Yasui, H., Sakurai, H. Biometals (2006) [Pubmed]
  4. Lithium inhibits aluminum-induced apoptosis in rabbit hippocampus, by preventing cytochrome c translocation, Bcl-2 decrease, Bax elevation and caspase-3 activation. Ghribi, O., Herman, M.M., Spaulding, N.K., Savory, J. J. Neurochem. (2002) [Pubmed]
  5. Aluminum-maltolate induces apoptosis and necrosis in neuro-2a cells: potential role for p53 signaling. Johnson, V.J., Kim, S.H., Sharma, R.P. Toxicol. Sci. (2005) [Pubmed]
  6. The endoplasmic reticulum is the main site for caspase-3 activation following aluminum-induced neurotoxicity in rabbit hippocampus. Ghribi, O., Herman, M.M., Savory, J. Neurosci. Lett. (2002) [Pubmed]
  7. Co-involvement of mitochondria and endoplasmic reticulum in regulation of apoptosis: changes in cytochrome c, Bcl-2 and Bax in the hippocampus of aluminum-treated rabbits. Ghribi, O., DeWitt, D.A., Forbes, M.S., Herman, M.M., Savory, J. Brain Res. (2001) [Pubmed]
  8. Orally administrated aluminum-maltolate complex enhances oxidative stress in the organs of mice. Kaneko, N., Yasui, H., Takada, J., Suzuki, K., Sakurai, H. J. Inorg. Biochem. (2004) [Pubmed]
  9. Quantitative studies on aluminum deposition and its effects on neurofilament protein expression and phosphorylation, following the intraventricular administration of aluminum maltolate to adult rabbits. Savory, J., Herman, M.M., Hundley, J.C., Seward, R.L., Griggs, C.M., Katsetos, C.D., Wills, M.R. Neurotoxicology (1993) [Pubmed]
  10. The absence of extracellular calcium potentiates the killing of cultured hepatocytes by aluminum maltolate. Snyder, J.W., Serroni, A., Savory, J., Farber, J.L. Arch. Biochem. Biophys. (1995) [Pubmed]
  11. Tau immunoreactivity associated with aluminum maltolate-induced neurofibrillary degeneration in rabbits. Savory, J., Huang, Y., Herman, M.M., Reyes, M.R., Wills, M.R. Brain Res. (1995) [Pubmed]
  12. Aluminum-induced alteration of surface anionic sites in cultured brain microvascular endothelial cells. Vorbrodt, A.W., Trowbridge, R.S. Acta Neuropathol. (1993) [Pubmed]
  13. Peri-nuclear clustering of mitochondria is triggered during aluminum maltolate induced apoptosis. Dewitt, D.A., Hurd, J.A., Fox, N., Townsend, B.E., Griffioen, K.J., Ghribi, O., Savory, J. J. Alzheimers Dis. (2006) [Pubmed]
  14. Modifications to the in situ TUNEL method for detection of apoptosis in paraffin-embedded tissue sections. Rao, J.K., Letada, P., Haverstick, D.M., Herman, M.M., Savory, J. Ann. Clin. Lab. Sci. (1998) [Pubmed]
  15. Brain-derived neurotrophic factor protects cultured rat hippocampal neurons from aluminum maltolate neurotoxicity. Kawahara, M., Kato-Negishi, M., Hosoda, R., Imamura, L., Tsuda, M., Kuroda, Y. J. Inorg. Biochem. (2003) [Pubmed]
 
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