The massive industrial use of aluminum, the most abundant metal in the Earth's crust, has implied its introduction into the biosphere, contrary to previous natural conditions in which complex geochemical cycles prevented its solubilization. Consequently, humans are nowadays highly exposed to this metal, a fact linked to various diseases, starting from early evidence of dialysis encephalopathy or osteodystrophy in patients with renal failure under dialysis treatment to more recent evidence linking aluminum to several neurodegenerative disorders. However, the molecular bases for these toxic effects are still not well understood, partially due to the inherent difficulties of interpreting experimental data. In this sense, theoretical calculations have become fundamental to get insight into the bioinorganic chemistry of aluminum and its potentially harmful effects. The pro-oxidant ability of aluminum is one of its most known toxic effects, a factor frequently underestimated due to its nonredox nature. That is, the oxidation state +3 of aluminum in a biological system is maintained unaltered in different biochemical environments, as demonstrated recently. However, this does not imply that aluminum can not alter important redox cycles in vitro and in vivo. The early hypothesis of the possibility of forming an aluminum-superoxide complex, which would augment the lifetime of this radical species, has been proven computationally. The thermodynamic stabilization of a metalsuperoxide complex is not by itself explanatory of the mechanism behind the pro-oxidant ability of aluminum. However, Fukuzumi et al. have reported a linear relationship between the strength of a metal-superoxide interaction and its oxidant activity of a metal. Despite these circumstantial pieces of evidence that point to aluminum as a promoter of oxidative stress, the topic is still highly controversial due to the lack of direct measures of the effect of aluminum in the redox potentials of radical species.