Herein, biochar was prepared using rice straw, and it served as the peroxymonosulfate (PMS) activator to degrade naphthalene (NAP). The results showed that pyrolysis temperature has played an important role in regulating biochar structure and properties. The biochar prepared at 900°C (BC900) had the best activation capacity and could remove NAP in a wide range of initial pH (5-11). In the system of BC900/PMS, multi-reactive species were produced, in which 1O2 and electron transfer mainly contributed to NAP degradation. In addition, the interference of complex groundwater components on the NAP removal rate must get attention. Cl- had a significant promotional effect but risked the formation of chlorinated disinfection by-products. HCO3-, CO32-, and humic acid (HA) had an inhibitory effect; surfactants had compatibility problems with the BC900/PMS system, which could lead to unproductive consumption of PMS. Significantly, the BC900/PMS system showed satisfactory remediation performance in spiked natural groundwater and soil, and it could solve the problem of persistent groundwater contamination caused by NAP desorption from the soil. Besides, the degradation pathway of NAP was proposed, and the BC900/PMS system could degrade NAP into low or nontoxic products. These suggest that the BC900/PMS system has promising applications in in-situ groundwater remediation.
Guangsangon E (GSE) is a novel Diels-Alder adduct isolated from leaves of Morus alba L, a traditional Chinese medicine widely applied in respiratory diseases. It is reported that GSE has cytotoxic effect on cancer cells. In our research, we investigated its anticancer effect on respiratory cancer and revealed that GSE induces autophagy and apoptosis in lung and nasopharyngeal cancer cells. We first observed that GSE inhibits cell proliferation and induces apoptosis in A549 and CNE1 cells. Meanwhile, the upregulation of autophagosome marker LC3 and increased formation of GFP-LC3 puncta demonstrates the induction of autophagy in GSE-treated cells. Moreover, GSE increases the autophagy flux by enhancing lysosomal activity and the fusion of autophagosomes and lysosomes. Next, we investigated that endoplasmic reticulum (ER) stress is involved in autophagy induction by GSE. GSE activates the ER stress through reactive oxygen species (ROS) accumulation, which can be blocked by ROS scavenger NAC. Finally, inhibition of autophagy attenuates GSE-caused cell death, termed as "autophagy-mediated cell death." Taken together, we revealed the molecular mechanism of GSE against respiratory cancer, which demonstrates great potential of GSE in the treatment of representative cancer.