Industrial and consumer products containing meta-based nanomaterials are becoming more widespread. One particle used for its wide range of beneficial properties is aluminum nanoparticles (AlNPs).   The potential toxicity of AlNPs are not fully understood. Toxicological assessments are warranted due to the detrimental interactions of aluminum ions within cellular mitochondria (i.e. changes in respiration rate and ATP production). In addition, other nanoparticles have recently been studied to assess propensity to trigger mitophagy, a process of mitochondrial specific degradation. Because of their size and ability to generate reactive oxygen species, we asked if AlNPs could elicit a measurable dysregulation of mitochondrial health and induce mitophagy. To answer this question, three different types of human lung cells (i.e. cancerous, asthmatic, and normal primary) were characterized before and after exposure to AlNPs (1 ppm in aqueous suspension).  Microscopy was used to determine AlNP uptake (darkfield hyperspectral imaging), mitochondrial morphology (transmission electron microscopy), and evidence of mitophagy (fluorescence microscopy). Our data shows that mitochondrial dysregulation, as measured by a significant change in mitochondria size, shape, and number of autophagosomes, as well as evidence of mitophagy, as measured by intracellular mitochondria endocytosis, was induced after exposure to AlNPs and was most pronounced in the normal primary cells.  This method demonstrates how microscopy methods can be used to determine changes in cellular/mitochondrial structure and function.  These findings will help guide future research using mitochondrial health as a biomarker to assess environmental health indices.

Utilizing microscopy techniques to monitor differential induction of mitophagy after exposure to engineered nanomaterials

ACS Fall 2020 Virtual Meeting

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