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An optimized selective sequential extraction (SSE) procedure was developed to assess the arsenic (As) partitioning in copper slag. The potential As species in copper slag are partitioned into the readily soluble As, dissolvable arsenates, sparingly soluble arsenates, As residing in sulfides, arsenopyrite and metal As, as well as As incorporated into glassy silicates. The inductively coupled plasma atomic emission spectrometry (ICP-AES), scanning electronic microscopy (SEM), transmission electron microscope (TEM), X-ray diffractometry (XRD) and Fourier transform infrared spectroscopy (FTIR) were used to characterize the leachates and residues produced from the operation scheme. The selectivity and recovery of extractants were evaluated through single-phase extraction procedures. Partitioning data of As in slag samples show good agreement with the reported works and the total As recovery of each operation is over 90%. This suggests that the optimized SEE scheme can be reliably employed for As partitioning in As-bearing byproducts from copper smelting.

Drug resistance is a critical factor responsible for the recurrence of non-small cell lung cancer (NSCLC). Previous studies suggest that curcumin acts as a chemosensitizer and radiosensitizer in human malignancies, but the underlying mechanism remains elusive. In the present study, we explored how curcumin regulates the expression of miR-142-5p and sensitizes NSCLC cells to crizotinib. We found that miR-142-5p is significantly downregulated in NSCLC tissue samples and cell lines. Curcumin could increase crizotinib cytotoxicity by epigenetically restoring the expression of miR-142-5p. Furthermore, curcumin treatment suppressed the expression of DNA methylation-related enzymes, including DNMT1, DNMT3A, and DNMT3B, in NSCLC cells. In addition, the upregulation of miR-142-5p expression increased crizotinib cytotoxicity and induced apoptosis in tumor cells in a similar manner to that of curcumin. Strikingly, miR-142-5p overexpression suppressed crizotinib-induced autophagy in A549 and H460 cells. Mechanistically, miR-142-5p inhibited autophagy in lung cancer cells by targeting Ulk1. Overexpression of Ulk1 abrogated the miR-142-5p-induced elevation of crizotinib cytotoxicity in A549 and H460 cells. Collectively, our findings demonstrate that curcumin sensitizes NSCLC cells to crizotinib by inactivating autophagy through the regulation of miR-142-5p and its target Ulk1.