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Toxic effects of nanoplastics on a model of dog aortic cells
Giuseppina Basini1, Martina Tambassi2, Simona Bussolati1
1Dipartimento di Scienze Medico-Veterinarie, Università degli Studi di Parma, Via del Taglio 10, Parma 43126, Italy.
Abstract:
Nanoplastic fragments (NP) are a growing concern and using dog aortic endothelial cells (CnAEOC) and fluorescence microscopy, we observed an interaction between NP and cells, demonstrating a localization at the cytoplasmic level. Furthermore, the data collected show a disruption of both cell proliferation and metabolic activity. The results also show the induction of oxidative stress. In detail, NP caused an increase in the levels of ROS production and an inhibition of enzymatic defence systems. On the contrary, there was no alteration of the non-enzymatic defence mechanism. The analysis conducted to evaluate a possible induction of autophagy, a survival mechanism implemented by cells, following exposure to NP reported the absence of autophagy involvement in the model analysed. Finally, investigations were conducted regarding the involvement of NP in gene expression processes. Both RNA-seq and RT-PCR did not highlight differentially expressed genes in treated cells.
Insights
Nanoplastic fragments (NP) interact with dog aortic endothelial cells, disrupting cell proliferation and metabolic activity. NP also induce oxidative stress by increasing ROS production and inhibiting enzymatic defenses, but do not affect gene expression or autophagy.
Area of Science:
- Environmental Science
- Cell Biology
- Toxicology
Background:
- Nanoplastic fragments (NP) pose a growing environmental and health concern.
- Understanding the cellular effects of NP is crucial for risk assessment.
Purpose of the Study:
- To investigate the interaction of NP with dog aortic endothelial cells (CnAEOC).
- To assess the impact of NP on cell proliferation, metabolic activity, oxidative stress, autophagy, and gene expression.
Main Methods:
- Fluorescence microscopy to observe NP-cell interaction.
- Assays for cell proliferation, metabolic activity, reactive oxygen species (ROS) production, and enzymatic/non-enzymatic antioxidant defenses.
- Analysis of autophagy markers and gene expression profiling (RNA-seq, RT-PCR).
Main Results:
- NP localized within the cytoplasm of CnAEOC.
- Significant disruption of cell proliferation and metabolic activity observed.
- NP induced oxidative stress, evidenced by increased ROS production and inhibited enzymatic defenses, while non-enzymatic defenses remained unaffected.
- No induction of autophagy or differential gene expression was detected in NP-treated cells.
Conclusions:
- Nanoplastics induce cytotoxicity and oxidative stress in aortic endothelial cells.
- Cellular defense mechanisms like enzymatic antioxidants are compromised by NP exposure.
- NP do not appear to trigger autophagy or alter gene expression in this cellular model.
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