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Title |
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aluminium blunts the proliferative response, and increases apoptosis of cultured human cells: putative relationship to alzheimer’s disease
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Authors |
Paolo Prolo 1-4 *, Francesco Chiappelli1-4, Enzo Grasso5, Maria Gabriella Rosso5, Negoita Neagos4, Andrea Dovio6, Maria Luisa Sartori6, Paola Perotti6, Fausto Fantò7, Massimo Civita8, Adriano Fiorucci8
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Affiliation |
1Laboratory of Psychoneuroimmunology, Division of Oral Biology & Medicine, UCLA School of Dentistry; 2 Dental Research Institute, UCLA Center for the Health Sciences; 3 Brain Research Institute, UCLA Center for the Health Sciences; 4 Psychoneuroimmunology Group, Inc., Los Angeles, California; 5 A.S.O. S.Croce & Carle, Neurology, Cuneo, Italy; 6 Department of Clinical and Biological Sciences, Internal Medicine, University of Turin, Italy; 7 Department of Clinical and Biological Sciences, Geriatrics, University of Turin, Italy; 8 Politecnico, Turin, Italy
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| Phone |
+310 794-7134 |
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| Fax |
+310 794-7109; * Corresponding author |
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Article Type |
Current Trends
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Date |
received June 06,
2007; accepted June 13, 2007; published online July 04, 2007 |
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Abstract |
Aluminium (Al) has been investigated as a neurotoxic substance. Al ranks among the potential environmental risk factors for Alzheimer’s disease (AD). Epidemiological studies tested the relationship between Al in drinking water and AD, showing a significant correlation between elevated levels of monomeric Al in water and AD, although data to date remain inconclusive with respect to total Al. The aim of this study was to test whether or not Al exacerbates cellular toxicity mediated by the Amyloid-β (Aβ) peptide. We evaluated the role of Al in modulating programmed cell death (apoptosis) in human cell cultures. We used the osteosarcoma cell line monolayer (SaOs-2) to demonstrate that treatment of SaOs-2 cultures with the Aβ peptide mid-fragment (25-35) at 10-9M, followed by co-incubation with physiological concentrations of AlCl3, which release monomeric Al in solution, led to marked expression of caspase 3, but not caspase 9, key markers of the apoptotic process. The same experimental conditions were shown to blunt significantly the proliferative response of normal human peripheral blood mononuclear cells (PBMC) to phytohemagglutinin (PHA) stimulation. Our observations support the hypothesis that Al significantly impairs certain cellular immune responses, and confirm that Al-mediated cell toxicity may play an important role in AD.
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Keywords
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human peripheral blood mononuclear cells; phytohemagglutinin (PHA); apoptosis; caspase; osteosarcoma cultures
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Citation |
Prolo et al., Bioinformation 2(1): 24-27 (2007) |
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Edited by |
P. Kangueane
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ISSN |
0973-2063
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Publisher |
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License |
This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.
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