CdTe quantum dot inhibits cell survival and induces mitochondrial dysfunction in primary human umbilical vein endothelial cells / 中国药理学与毒理学杂志

ABSTRACT

OBJECTIVE To elucidate the toxicological properties of CdTe quantum dots (CdTe QD) by investigating their effect on mitophagy in human umbilical vein endothelial cells (HUVECs).METHODS The purity of primarily cultured HUVECs was detected by immunofluorescence.Then,HUVECs were incubated with CdTe QD 0.1-100 mg· L-1 for 24 h.After treatment,the cell viability of HUVECs was detected with MT-T assay.The mitochondrial morphology was observed under a laser scanning confocal microscope after labeling with Mitotracker.The treated HUVECs were also labeled with JC-1 probe,and the mitochondrial membrane potential (MMP) was then examined by flow cytometry.The expression of mitophagy-related proteins including microtubule-associated protein 1 light chain 3 Ⅰ /Ⅱ (LC3 Ⅰ /Ⅱ),moesin-like BCL2-induced protein1(Beclin1),phosphatase and tensin (PTEN) homologinduced putative kinase 1(PINK1) and dynamin-related protein Ⅰ (DRP1) was determined by Westem blotting.RESULTS More than 95％ of the cultured cells expressed vascular endothelial cadherin and herein were vascular endothelial cells.The MTT result showed that the cell survival of HUVECs was significantly decreased after incubation with CdTe QD (0.1-100 mg,L-1) for 24 h (P＜0.05,P＜0.01).CdTe QD also induced extensive fragmentation of the mitochondrial network.The results of JC-1 assay showed that CdTe QD (0.1-100 mg· L-1) caused the disruption of MMP.The percentage of HUVECs with higher MMP was reduced from (91.8±0.6)％ in cell control group to (90.2±1.1)％,(84.4±0.9)％ (P＜0.05) and (78.1 ±1.3)％ (P＜0.01),respectively.The Western blotting data suggested that CdTe QD 10 mg·L-1 significantly increased the expression of autophagy-related protein beclin 1 and the ratio of LC3 Ⅱ/LC3 Ⅰ (P＜0.05,P＜0.01),CdTe QD 1 mg· L-1 also raised the level of mitophagy-related proteins like PINK1 and DRP1.CONCULSION CdTe QD can induce mitochondrial dysfunction as well as mitophagy in HUVECs.