Cytotoxic amyloid peptides inhibit cellular 3-(4,5-dimethylthiazol-2- yl)-2,5-diphenyltetrazolium bromide (MTT) reduction by enhancing MTT formazan exocytosis

Journal of Neurochemistry

Volumn 69, Issue 6, 1997, Pages 2285-2293

  Liu, Yuanbin ^a   Schubert, David ^a  

^a SALK INSTITUTE FOR BIOLOGICAL STUDIES   (United States)

Author keywords

3 (4,5 Dimethylthiazol 2 yl) 2,5 diphenyltetrazolium bromide; Alzheimer's disease; Amyloid peptides; Cytotoxicity; Exocytosis

Indexed keywords

3 (4,5 DIMETHYL 2 THIAZOLYL) 2,5 DIPHENYLTETRAZOLIUM BROMIDE; AMYLIN; AMYLOID; CALCITONIN; FORMAZAN; TRANSFERRIN;

ALZHEIMER DISEASE; ARTICLE; CELL VIABILITY; CYTOTOXICITY; ENDOCYTOSIS; EXOCYTOSIS; IMMUNOBLOTTING; MICROSCOPY; NEUROTOXICITY; PATHOGENESIS; PEPTIDE SYNTHESIS; PRIORITY JOURNAL; SIGNAL TRANSDUCTION;

EID: 0030695856     PISSN: 00223042     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1471-4159.1997.69062285.x     Document Type: Article

References (24)

1. Behl C., Davis J. B., Cole G. M., and Schubert D. (1992) Vitamin E protects nerve cells from amyloid β protein toxicity. Biochem. Biophys. Res. Commun. 186, 944-952.
2. Behl C., Davis J. B., Lesley R., and Schubert D. (1994) Hydrogen peroxide mediates amyloid β protein toxicity. Cell 77, 817-827.
3. 3H]norepinephrine from a clonal line of pheochromocytoma cells (PC12) by nicotinic cholinergic stimulation. Brain Res. 137, 521-528.
4. Greene L. A. and Tischler A. S. (1976) Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor. Proc. Natl. Acad. Sci. USA 73, 2424-2428.
5. Hertel C., Hauser N., Schubenel R., Seilheimer B., and Kemp J. A. (1996) β-Amyloid-induced cell toxicity: enhancement of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide-dependent cell death. J. Neurochem. 67, 272-276.
6. 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.
7. Klausner R. D., van Renswoude J., Kempf C., Rao K., Bateman J. L., and Robbins A. R. (1984) Failure to release iron from transferrin in a Chinese hamster ovary cell mutant pleiotropically defective in endocytosis. J. Cell Biol. 98, 1098-1101.
8. Knauer M. F., Soreghan B., Burdick D., Kosmoski J., and Glabe C. G. (1992) Intracellular accumulation and resistance to degradation of the Alzheimer's amyloid A4/β protein. Proc. Natl. Acad. Sci. USA 89, 7437-7441.
9. Liu Y. and Schubert D. (1997) Beta amyloid toxicity does not require RAGE protein. Biochem. Biophys. Res. Commun. (in press).
10. Liu Y., Peterson D. A., Kimura H., and Schubert D. (1997) The mechanism of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction. J. Neurochem. 69, 581-593.
11. Lorenzo A. and Yankner B. A. (1994) β-Amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc. Natl. Acad. Sci. USA 91, 12243-12247.
12. Lorenzo A., Razzaboni B., Weir G. C., and Yankner B. A. (1994) Pancreatic islet cell toxicity of amylin associated with type-2 diabetes mellitus. Nature 368, 756-760.
13. Mosmann T. (1983) Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity. J. Immunol. Methods 65, 55-63.
14. Pike C. J., Cummings B. J., and Cotman C. W. (1991) In vitro aging of β-amyloid protein causes peptide aggregation and neurotoxicity. Brain Res. 563, 311-314.
15. Pollack S. J., Sadler I. I. J., Hawtin S. R., Tailor V. J., and Shearman M. S. (1995a) Sulfated glycosaminoglycans and dyes attenuate the neurotoxic effects of β-amyloid in rat PC12 cells. Neurosci. Lett. 184, 113-116.
16. Pollack S. J., Sadler I. I. J., Hawtin S. R., Tailor V. J., and Shearman M. S. (1995b) Sulfonated dyes attenuate the toxic effects of β-amyloid in a structure-specific fashion. Neurosci. Lett. 197, 211-214.
17. Schubert D., Heinemann S., Carlisle W., Tarika H., Kimes B., Steinbach J. H., Culp W., and Brandt B. L. (1974) Clonal cell lines from the rat central nervous system. Nature 249, 224-227.
18. Schubert D., Behl C., Lesley R., Brack A., Dargusch R., Sagara Y., and Kimura H. (1995) Amyloid peptides are toxic via a common oxidative mechanism. Proc. Natl. Acad. Sci. USA 92, 1989-1993.
19. Shearman M. S., Ragan C. I., and Iversen L. L. (1994) Inhibition of PC-12 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.
20. Shearman M. S., Hawtin S. R., and Tailor V. J. (1995) The intracellular component of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction is specifically inhibited by β-amyloid peptides. J. Neurochem. 65, 218-227.
21. West M. A., Bretscher M. S., and Watts C. (1989) Distinct endocytic pathways in epidermal growth factor-stimulated human carcinoma A431 cells. J. Cell Biol. 109, 2731-2739.
22. Yan S. U., Chen X., Fu J., Chen M., Zhu H., Roher A., Slattery T., Zhao L., Nagashima M., Morser J., Migheli A., Nawroth P., Stern D., and Schmidt A.M. (1996) RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease. Nature 382, 685-691.
23. Yankner B. A. (1996) Mechanism of neuronal degeneration in Alzheimer's disease. Neuron 16, 921-932.
24. Yankner B. A., Duffy L. K., and Kirschner D. A. (1990) Neurotrophic and neurotoxic effects of amyloid β protein: reversal by tachykinin neuropeptides. Science 250, 279-282.