Neurotoxicity study of lead-based perovskite nanoparticles

Lead-based halide perovskite nanoparticles (Pb-PNPs) are promising alternatives for the next-generation of optoelectronic materials, while their nonnegligible biological behavior after exposure are still an enigma. Here, we clarify the translocation, biotransformation, and biodistribution related neurotoxicity of re-presentative CsPbBr3 PNPs in C57BL/6J mice after intranasal administration through a combination of the feat of advanced synchrotron radiation (SR) and traditional analytical techniques. SR-based microscopic X-ray fluorescence scanning, inductively coupled plasma mass spectrometry and behavioral data demonstrate that CsPbBr3 PNPs can be transported and accumulated in the hippocampus, easily triggering Ca overload, causing severe damage of hippocampus-dependent learning, memory, and cognition behavior. Meanwhile, SR-based X-ray absorption near-edge spectroscopy analysis also reveals that CsPbBr3 PNPs can transform into soluble and insoluble lead compounds in different physiological environments. The toxicity of CsPbBr3 PNPs is higher than that of soluble Pb(Ac)2 due to the sustained release of Pb ions. The CsPbBr3 PNPs cause nerve cell apoptosis through triggering intracellular Ca2+ overload, upregulating reactive oxygen species production, while disordering the mitochondrial membrane potential. Our work provides significant in-sights into the neurological effects and mechanism of Pb-PNPs.(c) 2023 Elsevier Ltd. All rights reserved.

Automated summary

We investigated the translocation, biotransformation, and biodistribution of CsPbBr3 PNPs in C57BL/6J mice and found that they can accumulate in the hippocampus, leading to Ca overload and severe damage to learning, memory, and cognition behavior. CsPbBr3 PNPs also undergo transformations into soluble and insoluble lead compounds in different physiological environments. The toxicity of CsPbBr3 PNPs is higher than that of soluble Pb(Ac)2 due to sustained release of Pb ions. The neurotoxic effects of Pb-PNPs were attributed to intracellular Ca2+ overload, reactive oxygen species production, and disruption of mitochondrial membrane potential.