4.6 Article

UV-B radiation enhances the toxicity of TiO2 nanoparticles to the marine microalga Chlorella pyrenoidosa by disrupting the protection function of extracellular polymeric substances

Journal

ENVIRONMENTAL SCIENCE-NANO
Volume 9, Issue 5, Pages 1591-1604

Publisher

ROYAL SOC CHEMISTRY
DOI: 10.1039/d1en01198g

Keywords

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Funding

  1. National Natural Science Foundation of China [41706130, 41976143]
  2. Key Technology Research and Development Program of Shandong province [2020CXGC010703]
  3. NSFC-Shandong Joint Fund for Marine Ecology and Environmental Sciences [U1806213]
  4. Central Public-interest Scientific Institution Basal Research Fund, CAFS [2020TD12]

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This study investigated the bioavailability and toxicity of TiO2 nanoparticles (NPs) to marine microalgae under ultraviolet-B radiation (UVBR). The results showed that UVBR enhanced the growth inhibition caused by TiO2 NPs. Additionally, UVBR and TiO2 NPs exhibited significant antagonistic interaction on the extracellular polymeric substances (EPS) secreted by the microalgae, allowing more NPs to enter the algal cells. Internalized TiO2 NPs triggered the production of intracellular reactive oxygen species, leading to lipid peroxidation and serious cellular damage in the microalgae. Overall, weakened EPS protection was identified as the key mechanism for the enhanced toxicity of TiO2 NPs under UVBR conditions.
Enhanced UV-B radiation (UVBR) has been a global environmental problem for decades due to stratospheric ozone depletion. Simultaneously, the potential environmental risks of TiO2 nanoparticles (NPs) have increasingly attracted attention. In the natural environment, marine microalgae could be simultaneously exposed to enhanced UVBR and TiO2 NPs. Owing to their photocatalytic properties, the toxicity of TiO2 NPs to marine microalgae might be exacerbated by UVBR. However, the combined effects and toxicity mechanisms of TiO2 NPs and UVBR on marine microalgae remain poorly understood. In this study, we investigated the bioavailability and toxicity of TiO2 NPs to the marine microalga Chlorella pyrenoidosa under UVBR. The results demonstrated that growth inhibition derived from TiO2 NPs was further enhanced by UVBR. Although UVBR accelerated the sedimentation of TiO2 NPs, the remaining suspended particles had smaller hydrodynamic diameters and caused stronger growth inhibition, indicating elevated effects of TiO2 NPs on algal cells after UVBR exposure because of the size-effect. Importantly, TiO2 NPs and UVBR showed a significant antagonistic interaction on the extracellular polymeric substances (EPS) secreted by C. pyrenoidosa with increasing concentration/dose, thus allowing more TiO2 NPs to enter the algal cells. The production of intracellular reactive oxygen species was triggered by internalized TiO2 NPs under UVBR exposure, resulting in lipid peroxidation and serious cellular damage in C. pyrenoidosa. Photosynthesis of C. pyrenoidosa was inhibited after exposure to TiO2 NPs combined with UVBR due to a combination of oxidative damage and NP shading. Overall, weakened EPS protection of algal cells, which contributed to the increased internalization of TiO2 NPs, was identified as the key mechanism for the enhanced toxicity of TiO2 NPs under UVBR conditions. This work provides new insights into the marine environmental risks associated with TiO2 NPs under increasing UVBR conditions.

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