Differential Toxicity of Aluminum Salts in Human Cell Lines of Neural Origin: Implications for Neurodegeneration

Pro-inflammatory effects of aluminum in human glioblastoma cells

“…We have all of which mirror changes seen in the AD brain [36]. In previously shown that the amount of positively charged the present study, a 6-day exposure of human glioblastoma Al-species capable of interacting with the Al-specific dye, cells to Al caused a significant increase in the levels of Morin, decreased as the solution aged [8]. This may be due TNF-a.…”

“…At this time, the well as in clarifying fats and oils, antiperspirants, and same treated cells were re-seeded at a ratio of 1:5, exposed agricultural pesticides. This dose was selected based on to the salts prepared previously, and allowed to grow for previous results in our laboratory [7,8]. Lipopolysaccharide the other time-points.…”

“…Although some aggregated aluminum complexes, Cells were lysed by several freeze-thaw cycles and the formed when Al sulfate was brought to neutral pH, was resulting cell extract was stored at 270 8C. The amount of removed, we have previously demonstrated that the filtered protein in 1 ml of the cell extract was determined by the solution still contains Al species capable of selectively BioRad protein assay [5] and 20 mg of each sample, 32 binding to the Al-specific Morin dye [8]. The solutions, incubated with P-labeled oligonucleotides containing the along with the media, were then incubated with the treated NF-kB consensus sequence, was loaded onto the gel.…”

Aluminum and copper interact in the promotion of oxidative but not inflammatory events: Implications for Alzheimer's disease

“…In the present study it was found that Al causes the same effect on Cure lated ROS production in cell culture. Colloidal Al may bind these metals and thus modulate their ability to promote metal-based oxidative events [8]. This may give further impetus to the concept of the production of ROS by colloidal compounds that complex pro-oxidant metals and thus allow them to participate in Fenton reactions for a longer period [55).…”

Gene expression in primary cultured astrocytes affected by aluminum: alteration of chaperons involved in protein folding

“…Nevertheless, several recent findings have implicated astrocytes as the principal target of the toxic action of aluminum [19][20][21][22] and that aluminum can cause astrocyte death via apoptosis [23][24][25]. However, these reports only showed morphological evidence of apoptosis, and the molecular mechanisms by which aluminum causes astrocyte death are yet to be unraveled.…”