Abstract
Metal oxide nanoparticles and carbon nanoparticles, as common nanoparticles (NPs), can cause autophagy in certain cells, which will lead to biohealth risk issues. This study determined the difference in autophagy induced by zinc oxide nanoparticles (ZnO NPs) and single-walled carbon nanotubes (SWCNTs) in respiratory epithelial cells. ICP-OES results showed that NPs uptake as well as the intercellular contents of particles affected cytotoxicity in a dose-dependent manner. ZnO NPs-30 nm had a distinct green dot structure representing autophagy, the SWCNTs exposure group had a few green light spots at a concentration of 10 μg/L. The ROS content of the ZnO NP-30 nm exposure group had the greatest increase at a concentration of 1000 μg/L, which was 2.5 times higher than that of the control, the SWCNTs exposure group showed a 2.2-fold increase. A slight downregulation of p-mTOR was detected, and the ZnO NPs-30 nm treatment group had the significant downregulation rate. The gene and protein expression levels of Beclin-1 and LC3B were upregulated as the exposure concentration increased. The protein expression of Beclin-1 and LC3B in the 1000 μg/L ZnO NPs-30 nm exposure group were 5.21 times and 4.12 times that of the control, respectively. The mRNA expression of Beclin-1 and LC3B in the 1000 μg/L ZnO NPs-30 nm exposure group were 5.04 times and 3.61 times that of the control, respectively. At any concentration, the effect of ZnO NPs-30 nm was greater than that of the SWCNTs. Interaction and crosstalk analysis showed that exposure to ZnO NPs-30 nm caused autophagy through the aggregation of undegraded autophagosomes, whereas SWCNTs exposure induced diminished intercellular oxidative stress to inhibit autophagy. Therefore, this study demonstrated that the effects of autophagy induced by ZnO NPs-30 nm and SWCNTs were different. The health risks of ZnO-30 nm NPs are higher than those of SWCNTs.
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