title: Spectroscopic and Microscopic Studies on the Mechanism of Mitochondrial Toxicity Induced by CdTe QDs Modified with Different Ligands.
abstract: Quantum dots (QDs) are increasingly applied in sensing, drug delivery, biomedical imaging, electronics industries, etc. Consequently, it is urgently required to examine their potential threat to humans and the environment. In the present work, the toxicity of CdTe QDs with nearly identical maximum emission wavelength but modified with two different ligands (MPA and BSA) to mitochondria was investigated using flow cytometry, spectroscopic, and microscopic methods. The results showed that QDs induced mitochondrial permeability transition (MPT), which resulted in mitochondrial swelling, collapse of the membrane potential, inner membrane permeability to H(+) and K(+), the increase of membrane fluidity, depression of respiration, alterations of ultrastructure, and the release of cytochrome c. Furthermore, the protective effects of CsA and EDTA confirmed QDs might be able to induce MPT via a Ca(2+)-dependent domain. However, the difference between the influence of CdTe QDs and that of Cd(2+) on mitochondrial membrane fluidity indicated the release of Cd(2+) was not the sole reason that QDs induced mitochondrial dysfunction, which might be related to the nanoscale effect of QDs. Compared with MPA-CdTe QDs, BSA-CdTe QDs had a greater effect on the mitochondrial swelling, membrane fluidity, and permeabilization to H(+) and K(+) by mitochondrial inner membrane, which was caused the fact that BSA was more lipophilic than MPA. This study provides an important basis for understanding the mechanism of the toxicity of CdTe QDs to mitochondria, and valuable information for safe use of QDs in the future.
authors.affiliation: State Key Laboratory of Virology & Key Laboratory of Analytical Chemistry for Biology and Medicine (Ministry of Education), College of Chemistry and Molecule Sciences, Wuhan University, Wuhan, 430072, People's Republic of China.
authors.forename: Lu
authors.initials: L
authors.lastname: Lai
authors.forename: Jian-Cheng
authors.initials: JC
authors.lastname: Jin
authors.forename: Zi-Qiang
authors.initials: ZQ
authors.lastname: Xu
authors.forename: Yu-Shu
authors.initials: YS
authors.lastname: Ge
authors.forename: Feng-Lei
authors.initials: FL
authors.lastname: Jiang
authors.forename: Yi
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000818:Animals; D019187:Cadmium Compounds / Q000737:chemistry*; D008930:Mitochondria, Liver / Q000378:metabolism* / Q000648:ultrastructure; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism / Q000648:ultrastructure; D051336:Mitochondrial Membranes / Q000378:metabolism* / Q000648:ultrastructure; D000083162:Mitochondrial Permeability Transition Pore; D010648:Phenylacetates / Q000737:chemistry; D045663:Quantum Dots / Q000737:chemistry*; D051381:Rats; D017208:Rats, Wistar; D012710:Serum Albumin, Bovine / Q000737:chemistry; D013691:Tellurium / Q000737:chemistry*
chemical_list: D019187:Cadmium Compounds; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D010648:Phenylacetates; D012710:Serum Albumin, Bovine; C512803:alpha-methoxy-alpha-phenylacetic acid; D013691:Tellurium; C028337:cadmium telluride