Potential Toxic Effects of Aluminum Nanoparticles: An overview

Abstract

Alumina (aluminum oxide) nanoparticles (AlNPs) have been categorized among the most important nano-metals, with wide applications in many fields as in food, agriculture, industry, engineering, pharmacy, medicine and others. The extensive use of AlNPs results in a massive release of them into the environment resulting in potential adverse impacts on animals and human health. Toxicokinetic studies demonstrated the rapid absorption and the systemic distribution of AlNPs to different organs. AlNPs mainly induced their toxic damage by induction of oxidative stress and mitochondrial dysfunction. Cellular accumulation of AlNPs resulted in interaction with cell components and binding with proteins and genetic materials (DNA and RNA) with producing other different chemical compounds resulting in cellular oxidative damage. Also, AlNPs induced cell death by disrupting the integrity of the mitochondrial membrane, depleting the mitochondrial thiols, activating apoptotic caspases (9 and 3) and generating more ROS. Previous in vivo and in vitro studies revealed hepato-, nephro-, myocardial, reproductive and neuro-toxic effects of AlNPs. Moreover, AlNPs exert inflammatory, apoptotic and geno-toxic effects. The aim here is to spot on previous studies demonstrating the toxic effects of AlNPs.

Quercetin Abates Aluminum Trioxide Nanoparticles and Lead Acetate Induced Altered Sperm Quality, Testicular Oxidative Damage, and Sexual Hormones Disruption in Male Rats

“…Nevertheless, Al 2 O 3 NPs have been reported to cause the release of reactive oxygen species (ROS), DNA mutations, and pro-inflammatory cytokines, which cause significant damage to the kidneys, brain, liver, and immune system [ 14 ]. Recently, in vitro and in vivo studies have revealed that Al 2 O 3 NPs have hepatotoxicity, nephrotoxicity, myocardial toxicity, reproductive toxicity, and neurotoxicity effects [ 15 ].…”

Ameliorative effects of quercetin against hepatic toxicity of oral sub-chronic co-exposure to aluminum oxide nanoparticles and lead-acetate in male rats

“…Cellular accumulation of Al 2 O 3 NPs resulted in interaction with cell components and binding with proteins and nucleic acids producing cellular oxidative damage. Also, cell death was caused by Al 2 O 3 NPs due to their ability to compromise mitochondrial membranes, deplete mitochondrial thiols, activate apoptotic caspases (9 and 3), and increase ROS production (Alshatwi et al 2013 ; Elkhadrawy et al 2021 ). Additionally, Liu et al ( 2020 ) stated that Al 2 O 3 NPs toxicity induced apoptosis; subsequently, the expression of BCL-2, cyclin D1, Mdm2, and phospho-Rb was decreased and that of p53, Bax, p21, and Rb was increased.…”

The Cultivation Modality and Barrier Maturity Modulate the Toxicity of Industrial Zinc Oxide and Titanium Dioxide Nanoparticles on Nasal, Buccal, Bronchial, and Alveolar Mucosa Cell-Derived Barrier Models

“…Al NPs can act neurodegenerative, [ 35 ] while its oxide compound intracellularly up taken as Al 2 O 3 [ 36 ] can interfere with intracellular proteins, genomic deoxyribonucleic acid (DNA), and messenger ribonucleic acids (mRNAs) [ 37 ]. In general, the accumulation of NPs in organs over time can additionally give rise to a systemic, inflammatory response and interfere with the immune system as shown in animal model studies on Au, Ag as well as Al NPs [ 38 , 39 , 40 ].…”