In this study, a novel slow release carrier for the controlled release of citric acid (CA), hydroxypropyl chitosan-graft-carboxymethyl-β-cyclodextrin (HPCS-g-CMCD) was synthesized by the grafting reaction of carboxymethyl-β-cyclodextrin (CMCD) with hydroxypropyl chitosan (HPCS), and the structural characteristics of HPCS-g-CMCD were confirmed by FT-IR, TGA, and NMR. Based on HPCS- g -CMCD and CA, slow release citric acid (SRCA) was prepared by a spray drying method. HPCS- g -CMCD carrier has a better slow release performance for CA compared to HPCS and CMCD, and CA release mechanism was attributed to a Fickian diffusion. Furthermore, the release behavior of uranium in contaminated soil could be effectively controlled by SRCA. The effects of SRCA on improving the phytoremediation capacity in uranium-contaminated soil were investigated using Brassica juncea , which were grown in pots containing soil with uranium at 56 mg kg −1 . After 50 days of growth, 5 mmol kg −1 of CA, SRCA I, SRCA II, and SRCA III was applied, respectively. The results showed that slow release citric acid could enhance the uptake of uranium in Indian mustard. Uranium concentration in the root with SRCA I treatment was increased by 80.25% compared to the control, and the uranium removal efficiency of the SRCA I treatment was 1.66-fold greater than that of the control. Simultaneously, the leaching loss of uranium in SRCA I-treated soil was decreased by 37.35% compared to CA-treated soil. As a promising remediation strategy, SRCA-assisted phytoremediation may provide a kind of feasible technology with low leaching risk for remediation of uranium-contaminated soils.
Liqun Huang,Ge Sun,Wenli Xu,Shufang Li,Xiujun Qin,Quan An,Zhongwen Wang,Jianguo Li
The objective of this study was to explore the endocytosis mechanisms of uranium uptake in HK-2 cells and its toxic effects. Our results demonstrated that uranium exposure impairs redox homeostasis and increases the permeability of the cell membrane and mitochondrial membrane, which may induce cell apoptosis by cytochrome-c leakage . Alkaline phosphatase activity increased after uranium exposure, which may be involved in the process of intracellular mineralisation of uranium, leading to severe cell necrosis. Furthermore, our findings demonstrated that the clathrin-mediated endocytosis process contributed substantially to uranium uptake in HK-2 cells and the total uranium uptake was highly correlated with cell viability, reaching a high correlation coefficient (r = −0.853) according to Pearson correlation analysis. In conclusion, the uptake of uranium into mammalian cells was mainly facilitated by the clathrin-mediated endocytosis pathway and induced dose-dependent cellular toxicity, including redox homeostasis imbalance, membrane injury, cell apoptosis and necrosis.
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