Aluminum increases levels of β-amyloid and ubiquitin in neuroblastoma but not in glioma cells

Several epidemiological studies suggest the involvement of aluminum (AI) in the pathogenesis of Alzheimer's disease (AD). There is an increase in the levels of A beta and ubiquitin in the pathological lesions of AD. Therefore, we have investigated whether aluminum (Al) treatment alters the levels of A beta and ubiquitin in murine neuroblastoma (NBP2) and rat glioma (C-6) cell cultures. At a low concentration (10 mu M), aluminum sulfate stimulated the level of immunoreactive A beta and ubiquitin in NBP2 cells without changing the levels of the amyloid precursor protein (APP). However, at higher concentrations (100 and 500 mu M), aluminum failed to elicit any significant effect on beta-amyloid, whereas ubiquitin levels continued to increase. No changes in the A beta and ubiquitin content were found in the C-6 glioma cells following treatment with Al at any of the concentrations tested. Exposure of cells to aluminum salts did not alter the rate of proliferation in either of the two cell lines. These date suggest that one of the mechanisms by which Al may play a role in AD is by promoting the formation of A beta and ubiquitin in neurons.