黑磷量子点（BPQD）最近已成为从药物输送系统到癌症治疗方式等生物医学应用中极具前景的竞争者。然而，潜在的毒性及其对人类健康的影响需要彻底调查。在本研究中，我们利用多组学整合方法来探索 BPQD 诱导肾损伤的复杂机制。首先，组织学检查显示雄性小鼠在亚急性暴露于1mg/kg BPQDs 28天后出现严重的肾损伤。随后，对暴露于 BPQD 的肾组织进行转录组学和代谢组学分析，鉴定出与铁死亡相关的差异表达基因和代谢物，铁死亡是受调节细胞死亡的一个新兴方面。我们的研究结果强调了多组学综合方法在预测和阐明纳米材料潜在毒理学结果方面的实用性。此外，我们的研究提供了对 BPQD 引起的肾损伤驱动机制的全面了解，强调了将铁死亡作为与 BPQD 相关的潜在毒性机制的重要性。版权所有 © 2024。由 Elsevier B.V. 出版。

Black phosphorus quantum dots (BPQDs) have recently emerged as a highly promising contender in biomedical applications ranging from drug delivery systems to cancer therapy modalities. Nevertheless, the potential toxicity and its effects on human health need to be thoroughly investigated. In this study, we utilized multi-omics integrated approaches to explore the complex mechanisms of BPQDs-induced kidney injury. First, histological examination showed severe kidney injury in male mice after subacute exposure to 1 mg/kg BPQDs for 28 days. Subsequently, transcriptomic and metabolomic analyses of kidney tissues exposed to BPQDs identified differentially expressed genes and metabolites associated with ferroptosis, an emerging facet of regulated cell death. Our findings highlight the utility of the multi-omics integrated approach in predicting and elucidating potential toxicological outcomes of nanomaterials. Furthermore, our study provides a comprehensive understanding of the mechanisms driving BPQDs-induced kidney injury, underscoring the importance of recognizing ferroptosis as a potential toxic mechanism associated with BPQDs.Copyright © 2024. Published by Elsevier B.V.