Spectroscopic and Microscopic Studies on the Mechanism of Mitochondrial Toxicity Induced by CdTe QDs Modified with Different Ligands.

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.