4.6 Article

Biotransformation of rare earth oxide nanoparticles eliciting microbiota imbalance

期刊

PARTICLE AND FIBRE TOXICOLOGY
卷 18, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12989-021-00410-5

关键词

Rare earth oxide; Nanotoxicity; Biotransformation; Microbiota imbalance; Pulmonary inflammation

资金

  1. Key Projects for International Science and Technology Cooperation Program, Ministry of Science and Technology of China [2018YFE0120400]
  2. National Natural Science Foundation of China [21806116, 21976126, U1967217]
  3. Key Projects of Social Development of Jiangsu Province [BE2018653]
  4. China Postdoctoral Science Foundation [2019 M652069, 2019 T120506]

向作者/读者索取更多资源

This study revealed the distinct toxic mechanisms of La2O3 as a representative REO in G(-) and G(+) bacteria, indicating that La2O3-induced membrane damages of G(-) cells accumulated into pulmonary microbiota imbalance exhibiting synergistic pulmonary toxicity.
Background Disruption of microbiota balance may result in severe diseases in animals and phytotoxicity in plants. While substantial concerns have been raised on engineered nanomaterial (ENM) induced hazard effects (e.g., lung inflammation), exploration of the impacts of ENMs on microbiota balance holds great implications. Results This study found that rare earth oxide nanoparticles (REOs) among 19 ENMs showed severe toxicity in Gram-negative (G(-)) bacteria, but negligible effects in Gram-positive (G(+)) bacteria. This distinct cytotoxicity was disclosed to associate with the different molecular initiating events of REOs in G(-) and G(+) strains. La2O3 as a representative REOs was demonstrated to transform into LaPO4 on G(-) cell membranes and induce 8.3% dephosphorylation of phospholipids. Molecular dynamics simulations revealed the dephosphorylation induced more than 2-fold increments of phospholipid diffusion constant and an unordered configuration in membranes, eliciting the increments of membrane fluidity and permeability. Notably, the ratios of G(-)/G(+) reduced from 1.56 to 1.10 in bronchoalveolar lavage fluid from the mice with La2O3 exposure. Finally, we demonstrated that both IL-6 and neutrophil cells showed strong correlations with G(-)/G(+) ratios, evidenced by their correlation coefficients with 0.83 and 0.92, respectively. Conclusions This study deciphered the distinct toxic mechanisms of La2O3 as a representative REO in G(-) and G(+) bacteria and disclosed that La2O3-induced membrane damages of G(-) cells cumulated into pulmonary microbiota imbalance exhibiting synergistic pulmonary toxicity. Overall, these findings offered new insights to understand the hazard effects induced by REOs.

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