4.7 Article

Toxicity assessment of core-shell and superabsorbent polymers in cell-based systems

Journal

ENVIRONMENTAL RESEARCH
Volume 228, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2023.115772

Keywords

Polymers; Core-shell; SAPs; Oxidative stress; Toxicity; Non -monotonic dose-responses; Hormesis

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Toxicological investigations have shown that the examined polymers have an impact on cell viability and cellular redox state, but do not cause acute toxic effects. The study also revealed cell-specific effects on redox homeostasis and lipid peroxidation.
The identification of health risks arising from occupational exposure to submicron/nanoscale materials is of particular interest and toxicological investigations designed to assess their hazardous properties can provide valuable insights. The core-shell polymers poly (methyl methacrylate)@poly (methacrylic acid-co-ethylene glycol dimethacrylate) [PMMA@P (MAA-co-EGDMA)] and poly (n-butyl methacrylate-co-ethylene glycol dimethacrylate)@poly (methyl methacrylate) [P (nBMA-co-EGDMA)@PMMA] could be utilized for the debonding of coatings and for the encapsulation and targeted delivery of various compounds. The hybrid superabsorbent core-shell polymers poly (methacrylic acid-co-ethylene glycol dimethacrylate)@silicon dioxide [P (MAA-co-EGDMA)@SiO2] could be utilized as internal curing agents in cementitious materials. Therefore, the characterization of their toxicological profile is essential to ensure their safety throughout manufacturing and the life cycle of the final products. Based on the above, the purpose of the present study was to assess the acute toxic effects of the above mentioned polymers on cell viability and on cellular redox state in EA. hy926 human endothelial cells and in RAW264.7 mouse macrophages. According to our results, the examined polymers did not cause any acute toxic effects on cell viability after any administration. However, the thorough evaluation of a panel of redox biomarkers revealed that they affected cellular redox state in a cell-specific manner. As regards EA. hy926 cells, the polymers disrupted redox homeostasis and promoted protein carbonylation. Concerning RAW264.7 cells, P (nBMA-co-EGDMA)@PMMA caused disturbances in redox equilibrium and special emphasis was placed on the triphasic dose-response effect detected in lipid peroxidation. Finally, P (MAA-co-EGDMA) @SiO2 activated cellular adaptive mechanisms in order to prevent from oxidative damage.

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