自噬
串扰
细胞毒性
细胞质
PI3K/AKT/mTOR通路
程序性细胞死亡
平衡
细胞生物学
化学
信号转导
生物
细胞凋亡
生物化学
物理
体外
光学
作者
Xiaofei Zhou,Weitao Jin,Rui Zhang,Ming Xuan,Jianbo Jia,Hongyu Zhou
标识
DOI:10.1016/j.jes.2022.12.029
摘要
Increasing risks of incidental and occupational exposures to two-dimensional transition metal dichalcogenides (2D TMDCs) due to their broad application in various areas raised their public health concerns. While the composition-dependent cytotoxicity of 2D TMDCs has been well-recognized, how the outer chalcogenide atoms and inner transition metal atoms differentially contribute to their perturbation on cell homeostasis at non-lethal doses remains to be identified. In the present work, we compared the autophagy induction and related mechanisms in response to WS2, NbS2, WSe2 and NbSe2 nanosheets exposures in MH-S murine alveolar macrophages. All these 2D TMDCs had comparable physicochemical properties, overall cytotoxicity and capability in triggering autophagy in MH-S cells, but showed outer chalcogen-dependent subcellular localization and activation of autophagy pathways. Specifically, WS2 and NbS2 nanosheets adhered on the cell surface and internalized in the lysosomes, and triggered mTOR-dependent activation of autophagy. Meanwhile, WSe2 and NbSe2 nanosheets had extensive distribution in cytoplasm of MH-S cells and induced autophagy in an mTOR-independent manner. Furthermore, the 2D TMDCs-induced perturbation on autophagy aggravated the cytotoxicity of respirable benzo[a]pyrene. These findings provide a deeper insight into the potential health risk of environmental 2D TMDCs from the perspective of homeostasis perturbation.
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