Toxic effects of aluminum nanoparticles: a review

The objective of this state-of-the-art review is to summarize contemporary data on the potential toxic effects of aluminum nanoparticles (AlNPs) and discuss the underlying molecular mechanisms. In vivo studies using laboratory rodents demonstrate that lungs, liver, brain, and the immune system are the primary targets for AlNPs toxicity. Specifically, inhalation exposure to AlNPs induces lung damage by promoting inflammatory infiltration, airway remodeling, septal thickening, and bronchial hyperresponsiveness. AlNPs-induced liver damage is characterized by hepatocyte degeneration and necrosis, liver sinusoid congestion, inflammation, and fibrosis. AlNPs induces neurotoxicity resulting in neurodegeneration, neuroinflammation, altered neurotransmitter metabolism, and subsequent adverse neurobehavioral outcome. In turn, immunotoxicity of AlNPs is characterized by promotion of systemic inflammation along with impaired phagocytosis. In addition to the toxicity exerted by Al₂O₃NPs itself, the observed toxic effects of AlNPs may be attributed to Al³⁺ release from the particles with the subsequent induction of oxidative stress, inflammation, mitochondrial dysfunction, genotoxicity, cell cycle dysregulation, and cell death due to apoptosis, necrosis, and ferroptosis. It is also evident that both the size and the form of AlNPs significantly affect its cytotoxicity. However, further studies are required to explore the mechanisms of toxic effects of AlNPs, as well as its potential adverse effects on human health.