Comparative study of aluminum (Al) speciation on apoptosis-promoting process in PC12 cells: Correlations between morphological characteristics and mitochondrial kinetic disorder.

Aluminum contamination in environment is very serious and the central nervous system is the main target of aluminum toxicity. The neurotoxic of aluminum is closely related to its speciation. PC12 cells were taken as the cell model to compare the morphological characteristics and mitochondrial kinetic disorder of two speciation of aluminum compounds (AlCl and aluminum-maltolate (Al(mal))). When the concentration of AlCl was 3 mM, the intracellular aluminum ion content was 3.87 times that of the 0.5 mM Al(mal) treatment group. At the 3 mM AlCl treatment group, intracellular ion homeostasis was disrupted. Abnormally elevated Ca levels inhibited protein kinase B (AKT) phosphorylation, resulting in impaired cell morphology. At the 0.5 mM Al(mal) treatment group, abnormally high levels of Ca caused mitochondrial kinetic disorder, which led to impaired cellular energy metabolism. Al(mal) had shown more cytotoxic in PC12 than AlCl at the same concentration. AlCl tended to inhibit the phosphorylation of AKT and damages cell morphology. Al(mal) mainly affected mitochondrial kinetic disorder, which led to impaired cellular energy metabolism. These findings provided experimental evidence for in-depth research on aluminum-induced neurotoxicity.