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Zinc oxide nanoparticles (ZnO NP) are commonly used engineered NPs with extensive usage in consumer products, thus leading to direct exposure to humans. The direct route of exposure is through inhalation. Once inhaled, these particles accumulate in the lungs, increasing the chances of respiratory tract illness through cellular organelle damage. Zinc oxide nanoparticle-treated lung cells are reported to display cytotoxicity, increase DNA damage, and induce oxidative stress. The current study focused on the effects of ZnO NPs on mitochondrial dynamics (fission and fusion) in human lung epithelial cells (A549). The lung cells were exposed to ZnO NPs at 50 and 100 μg/ml concentrations, and their mitochondrial dynamics were assessed to understand the effects of the NPs. Treatment with ZnO NPs reduced the activity of mitochondrial complex I and complex III and altered mitochondrial structural and functional characteristics in a concentration-dependent manner. Zinc oxide nanoparticles exposure showed an increase in small and round-shaped mitochondria. The expression of various fission proteins (Drp1 and Fis1) and fusion proteins (Mfn1, Mfn2, and OPA1) was altered upon exposure to ZnO NPs. Our studies showed dysfunction of the mitochondria induced by ZnO NPs. In fibroblast mitochondrial dynamics, fission symbolizes threshold damage. In this paper, we have shown that the mitochondrial fission phenotype increased upon exposure to ZnO NPs. The paper emphasizes that these particles enter mitochondria, triggering a stress response that results in the removal of mitochondria via fission. It provides relevant data for safety guidelines to ensure the safer use of these particles. [ABSTRACT FROM AUTHOR]

Aluminum oxide (Al2O3) nanoparticles (NPs) have a wide number of applications which cause intentional and unintentional exposure to humans, making it important to understand the nano-bio interaction. In this study, we made an attempt to evaluate the toxic effects of Al2O3 NPs chronic exposure on Drosophila melanogaster. Flies were exposed to Al2O3 NPs at concentration 0.1 and 1 mM via ingestion throughout their lifespan and progeny flies were screened for behavioral and phenotypic abnormalities. Behavioral abnormalities in flies were recorded through larval crawling, climbing in flies and two taste testing. Chronic exposure of Al2O3 NPs resulted in the loss of appendages in flies resulting in five legs flies, four legs flies and absence of haltere. Exposure to Al2O3 NPs caused renal failure in flies as observed by swollen abdomen. Our observations clearly showed that these NPs could cause detrimental health ailments which relate to human birth deformities and kidney failure. Damage at the cellular level was studied through proteomic profiling. Three hundred and seven unique proteins were expressed on exposure to Al2O3 NPs and 51 proteins were differentially expressed. Enrichment analysis of differentially expressed proteins showed significant alteration in striated muscle cell differentiation, digestive tract morphogenesis, phototransduction, regulation of chromatin organization and DNA duplex unwinding. [ABSTRACT FROM AUTHOR]

ZnO nanoparticles (ZnO NPs) are widely used engineered nanomaterials. Due to induced genotoxicity, increased oxidative stress, and teratogenicity, these NPs have been reported to be toxic. In the present study, we emphasise the role of vital proteins in regulating ZnO NP-induced abnormal phenotypes, particularly the deformed thorax and single wing in the Drosophila melanogaster progeny fed on 0.1–10 mM ZnO NPs. To understand how protein expression regulates this particular phenotype on ZnO NPs exposure, toxicoproteomics profile of control and abnormal phenotype flies was generated using LC/MS/MS. Gene ontology enrichment studies of proteomics data were carried out using CLUEGO and STRAP software. The bioinformatics tool STRING was used to generate a protein–protein interaction map of key proteins of enrichment analysis. Following ZnO NP exposure, the differential expression of key proteins of the Wnt pathway was prominent. Altered expression of various proteins of the Wnt pathway (CaMKII), cytoskeleton (Actin), and calponin resulted in developmental defects in drosophila progeny. In addition, immunohistology studies showed a significant deviation in the expression of wingless protein of ZnO NPs treated larvae in comparison to control. According to these findings, the interaction of the wnt pathway and cytoskeletal proteins with ZnO NPs caused developmental abnormalities in the subsequent generation of drosophila, highlighting the transgenerational toxic effects of these nanoparticles. [Display omitted] • ZnO NPs alters wnt signaling pathway in Drosophila melanogaster. • Interaction of ZnO NPs with cytoskeleton proteins caused developmental deformities. • Transgenerational toxicity profile of flies shows lethal effects of ZnO NPs. [ABSTRACT FROM AUTHOR]