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 representative CsPbBr 3 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 CsPbBr 3 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 CsPbBr 3 PNPs can transform into soluble and insoluble lead compounds in different physiological environments. The toxicity of CsPbBr 3 PNPs is higher than that of soluble Pb(Ac) 2 due to the sustained release of Pb ions. The CsPbBr 3 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 insights into the neurological effects and mechanism of Pb-PNPs. [Display omitted] • The neurotoxicity of lead-based perovskite nanoparticles was studied in vivo and in vitro for the first time. • The biodistribution and biotransformation of CsPbBr 3 PNPs were studied by advanced synchrotron radiation techniques. • CsPbBr 3 PNPs can induce Ca overload in brain and damage hippocampal-dependent learning and memory behavior. • CsPbBr 3 PNPs can induce intracellular Ca²⁺ overload and release reactive oxygen species, leading to neurotoxicity. [ABSTRACT FROM AUTHOR]