However, ROS increases markedly uncontrolled in an aged brain or under different circumstances due to mitochondrial dysfunction. In this context, the presence and accumulation of exometals can induce or enhance oxidative stress in the cell. The co-localization of aluminum and neurofibrillary tangles in familial Alzheimer's disease and aluminum and iron in nuclei of nerve cells in the brains of patients with Alzheimer's disease have been recently unambiguously established. The presence of aluminum, in addition to the wellknown implication of oxidative stress in neurodegeneration, suggests that this metal can promote oxidative damage to DNA or inhibit the repair of oxidatively damaged DNA. In previous work, we demonstrated how aluminum could thermodynamically stabilize a superoxide anion, promoting Fenton reaction and the generation of radical species. In the present work, we underline the effect aluminum could have in promoting a radical scavenging reaction. Both phenomena are of different nature, in that in the former, there is a promotion of oxidative activity, whereas, in the latter, there is a protective effect. However, both cases have in common the ability of aluminum to alter the thermodynamics of key redox processes in biological systems. Indeed, long-term exposure to AlCl 3 even at a low dose promotes oxidative stress, although high aluminum concentrations tend to decrease oxidative stress in zebrafish. In any case, aluminum is affecting the concentration of radical species. This behavior is due to the physicochemical properties of Al +3 , a strong Lewis acid with a substantial stabilization ability of negatively charged ions. This property allows aluminum to alter the thermodynamics of biological essential redox processes in different and subtle ways.