β-Amyloid-induced cell toxicity: Enhancement of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide-dependent cell death

Journal of Neurochemistry

Volumn 67, Issue 1, 1996, Pages 272-276

  Hertel, C ^a   Hauser, N ^a   Schubenel, R ^a   Seilheimer, B ^a   Kemp, J A ^a  

^a F HOFFMANN LA ROCHE LTD   (Switzerland)

Author keywords

3 (4,5 Dimethylthiazol 2 yl) 2,5 diphenyltetrazolium bromide reduction; Alzheimer's disease; Cell toxicity; Glia cells; Neuronal cells; Oxidoreductase; Amyloid

Indexed keywords

3 (4,5 DIMETHYL 2 THIAZOLYL) 2,5 DIPHENYLTETRAZOLIUM BROMIDE; AMYLOID BETA PROTEIN;

ALZHEIMER DISEASE; ANIMAL CELL; ARTICLE; CELL DEATH; CONTROLLED STUDY; GLIA CELL; NERVE CELL NECROSIS; NEUROTOXICITY; NONHUMAN; PHEOCHROMOCYTOMA CELL; PRIORITY JOURNAL; RAT;

AMYLOID BETA-PROTEIN; ANIMALS; CELL DEATH; KINETICS; NEUROTOXINS; PC12 CELLS; RATS; SENSITIVITY AND SPECIFICITY; TETRAZOLIUM SALTS; THIAZOLES;

ANIMALIA;

EID: 0029902540     PISSN: 00223042     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1471-4159.1996.67010272.x     Document Type: Article

References (15)

1. Barltrop J. A. and Owen T. C. (1991) 5-(3-Carboxymethoxyphenyl)-2-(4,5-dimethylthiazolyl)-3-(4-sulfophenyl) tetrazolium, inner salt (MTS) and related analogues of 3-(4,5-dimethylthiazolyl)-2,5-diphenyltetrazolium bromide (MTT) reducing to purple water-soluble formazans as cell-viability indicators. Bioorg. Med. Chem. Lett. 1, 611-614.
2. Behl C., Davis J., Cole G. M., and Schubert D. (1992) Vitamin E protects nerve cells from amyloid beta protein toxicity. Biochem. Biophys. Res. Commun. 186, 944-950.
3. Behl C., Davis J. B., Lesley R., and Schubert D. (1994) Hydrogen peroxide mediates amyloid β protein toxicity. Cell 77, 817-826.
4. Bottenstein J. E. and Sato G. H. (1979) Growth of a rat neuroblastoma cell line in serum-free supplemented medium. Proc. Natl. Acad. Sci. USA 76, 514-517.
5. Busciglio J., Lorenzo A., and Yankner B. A. (1992) Methodological variables in the assessment of beta amyloid neurotoxicity. Neurobiol. Aging 13, 609-612.
6. Döbeli H., Draeger N., Huber G., Jakob P., Schmidt D., Seilheimer B., Stüber D., Wipf B., and Zulauf M. (1995) A biotechnical method provides access to aggregation competent monomeric Alzheimer's 1-42 residue amyloid peptide. Biotechnology 13, 988-993.
7. Kaneko I., Yamada N., Sakuraba Y., Kamenosono M., and Tutumi S. (1995) Suppression of mitochondrial succinate dehydrogenase, a primary target of β-amyloid, and its derivative racemized at Ser residue. J. Neurochem. 65, 2585-2593.
8. Loo D. T., Copani A., Pike C. J., Whitemore E. R., Walencewicz A. J., and Cotman C. W. (1993) Apoptosis is induced by β-amyloid in cultured central nervous system neurons. Proc. Natl. Acad. Sci. USA 90, 7951-7955.
9. Mullan M. and Crawford F. (1993) Genetic and molecular advances in Alzheimer's disease. Trends Neurosci. 16, 398-402.
10. Seelig J., Lehrmann R., and Terzi E. (1995) Domain formation induced by lipid-ion and lipid-peptide interactions. Mol. Membr. Biol. 12, 51-57.
11. Shearman M. S., Ragan C. I., and Iversen L. L. (1994) Inhibition of PC12 cell redox activity is a specific, early indicator of the mechanism of β-amyloid-mediated cell death. Proc. Natl. Acad. Sci. USA 91, 1470-1474.
12. Shearman M. S., Hawtin S. R., and Tailor V. J. (1995) The intracellular component of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction is specifically inhibited by β-amyloid peptides. J. Neurochem. 65, 218-227.
13. Slater T. F., Sawyer B., and Sträubli U. (1963) Studies on succinate-tetrazolium reductase systems. III. Points of coupling of four different tetrazolium salts. Biochim. Biophys. Acta 77, 383-393.
14. Terzi E., Hölzemann G., and Seelig J. (1994) Alzheimer β-amyloid peptide 25-35: electrostatic interactions with phospholipid membranes. Biochemistry 33, 7434-7441.
15. Terzi E., Hölzemann G., and Seelig J. (1995) Self-association of β-amyloid peptide (1-40) in solution and binding to lipid membranes. J. Mol. Biol. 252, 633-642.