ZIF-8 nanoparticles (NPs) has been demonstrated with good potential in drug delivery, which causes an increasing attention on relevant toxicity study. In this work, MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide), glutathione (GSH), reactive oxygen species (ROS), stain analysis and gene detection assays were performed on ZIF-8 (50, 90 and 200 nm) incubated HepG2 cells. Moreover, time-resolved inductively coupled plasma mass spectrometry (TRA-ICP-MS) was applied for single cell analysis; the variation in cellular zinc amount and the proportion of zinc up-taken cells was investigated as a function of NPs size, incubation concentration/time and elimination. Smaller size of ZIF-8 NPs would lead to higher zinc accumulation and toxicity. The function of ZIF-8 on cells is assumed to be mainly related to zinc intracellular accumulation. The possible action path is presented as high accumulation of zinc in ZIF-8 incubated cells lead to high ROS level and cellular inflammation, ultimately inducing necrocytosis. For better understanding of the bio-effect of ZIF-8, ZnO NPs and Zn 2+ incubated HepG2 cells were evaluated in the same way. Higher accumulation of zinc in larger part of the cell population was found in ZIF-8 incubated cells than that in ZnO NPs incubated cells. It demonstrated higher bioavailability for ZIF-8 over ZnO NPs. While, in drug delivery application, the possible risk of the remained intracellular ZIF-8 cannot be ignored.
Na Liu,Yipeng Wang,Fei Ge,Shixiang Liu,Huaixian Xiao
The interaction of nanoparticles with coexisting chemicals affects the fate and transport of nanoparticles, as well as their combined effects on aquatic organisms. Here, we evaluated the joint effect of ZnO nanoparticle (nano-ZnO) and cetyltrimethyl ammonium chloride (CTAC) on the growth of Chlorella vulgaris and explored the possible mechanism. Results showed that an antagonistic effect of nano-ZnO and CTAC (0.1, 0.2 and 0.3 mg L −1 ) was found because CTAC stop nano-ZnO being broken down into solution zinc ions (Zn 2+ ). In the presence of CTAC, the zinc (including nano-ZnO and released Zn 2+ ) showed a higher adsorption on bound extracellular polymeric substances (B-EPS) but lower accumulation in the algal cells. Moreover, we directly demonstrated that nano-ZnO was adsorbed on the algal B-EPS and entered into the algal cells by transmission electron microscope coupled with energy dispersive X-ray (TEM-EDX). Hence, these results suggested that the combined system of nano-ZnO and CTAC exhibited an antagonistic effect due to the inhibition of CTAC on dissolution of nano-ZnO and accumulation of the zinc in the algal cells.
To explore toxic mechanisms of nano-ZnO on marine microalgae, algal growth inhibition test was carried out, and total Zn in the cell and total dissolved Zn in f/2 medium were determined. It was found that nano-ZnO was more toxic than bulk-ZnO on marine microalgae Skeletonema costatum . No matter under nano-ZnO or bulk-ZnO treatment, accumulation of intracellular Zn had a good linear correlation with growth inhibition ratio (IR). The total Zn content in the cell of microalgae was the dominant toxic mechanism of ZnO. Intracellular total Zn could be an indispensable parameter to indicate the toxic effects of nano-ZnO. Higher intracellular total Zn under nano-ZnO treatment than bulk-ZnO resulted in more toxicity of nano-ZnO on microalgae. Compared with Zn 2+ released by nano-ZnO into medium, lipid peroxidation (MDA level) injury, aggregation of nano-ZnO and transmembrane process of nano-ZnO also contributed to toxicity of nano-ZnO on Skeletonema costatum . The accumulation of intracellular Zn provides a new insight into toxic mechanisms of nano-ZnO.
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