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Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5... Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Toxicology Wiley

Integrative proteomics and metabolomics analysis of non‐observable acute effect level PM2.5 induced accumulative effects in AC16 cells

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References (61)

Publisher
Wiley
Copyright
© 2023 John Wiley & Sons, Ltd.
ISSN
0260-437X
eISSN
1099-1263
DOI
10.1002/jat.4500
Publisher site
See Article on Publisher Site

Abstract

Chronic exposure to very low ambient PM2.5 has been linked to cardiovascular risks in epidemiological observation, which also brought doubts on its safety threshold. In this study, we approached this question by chronic exposure of AC16 to the non‐observable acute effect level (NOAEL) PM2.5 5 μg/mL and its positive reference 50 μg/mL, respectively. The doses were respectively defined on the cell viabilities >95% (p = 0.354) and >90% (p = 0.004) when treated acutely (24 h). To mimic the long‐term exposure, AC16 was cultured from the 1st to 30th generations and treated with PM2.5 24 h in every three generations. The integration of proteomic and metabolomic analysis was applied, and 212 proteins and 172 metabolites were significantly altered during the experiments. The NOAEL PM2.5 induced both dose‐ and time‐dependent disruption, which showed the dynamic cellular proteomic response and oxidation accumulation, the main metabolomics changes were ribonucleotide, amino acid, and lipid metabolism that have involved in stressed gene expression, and starving for energy metabolism and lipid oxidation. In summary, these pathways interacted with the monotonically increasing oxidative stress and led to the accumulated damage in AC16 and implied that the safe threshold of PM2.5 may be non‐existent when a long‐term exposure occurred.

Journal

Journal of Applied ToxicologyWiley

Published: Nov 1, 2023

Keywords: AC16; chronic exposure; integrative proteomic and metabolomic analysis; non‐observable acute effect level (NOAEL); PM 2.5

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