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Prolo P, Chiappelli F, Grasso E, et al. Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease. Bioinformation. 2007;2(1):24-7doi: 10.6026/97320630002024.
Prolo, P., Chiappelli, F., Grasso, E., Rosso, M. G., Neagos, N., Dovio, A., Sartori, M. L., Perotti, P., Fantò, F., Civita, M., Fiorucci, A., Villanueva, P., & Angeli, A. (2007). Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease. Bioinformation, 2(1), 24-7. https://doi.org/10.6026/97320630002024
Prolo, Paolo, et al. "Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease." Bioinformation vol. 2,1 (2007): 24-7. doi: https://doi.org/10.6026/97320630002024
Prolo P, Chiappelli F, Grasso E, Rosso MG, Neagos N, Dovio A, Sartori ML, Perotti P, Fantò F, Civita M, Fiorucci A, Villanueva P, Angeli A. Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease. Bioinformation. 2007 Jun 04;2(1):24-7. doi: 10.6026/97320630002024. PMID: 18084647; PMCID: PMC2139997.
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Bioinformation. 2007 Jun 04;2(1):24-7. doi: 10.6026/97320630002024.

Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease.

Bioinformation

Paolo Prolo, Francesco Chiappelli, Enzo Grasso, Maria Gabriella Rosso, Negoita Neagos, Andrea Dovio, Maria Luisa Sartori, Paola Perotti, Fausto Fantò, Massimo Civita, Adriano Fiorucci, Pablo Villanueva, Alberto Angeli

Affiliations

  1. Laboratory of Psychoneuroimmunology, Division of Oral Biology and Medicine, UCLA School of Dentistry, CA, USA. [email protected]

PMID: 18084647 PMCID: PMC2139997 DOI: 10.6026/97320630002024

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 beta (Abeta) 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 Abeta peptide mid-fragment (25 to 35) at nano M, followed by co-incubation with physiological concentrations of aluminium chloride, 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.

Keywords: apoptosis; caspase; human peripheral blood mononuclear cells; osteosarcoma cultures; phytohemagglutinin (PHA)

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