Degradation of ciprofloxacin and inactivation of ciprofloxacin resistant E. faecium during UV -LED (275 nm)/chlorine process

Ciprofloxacin and ciprofloxacin-resistant bacteria are emerging concerns that threaten public health due to the heavy use of antibiotics and the development of bacterial resistance in water environments. In this study, we examined an energy-efficient treatment driven by a UV-LED/chlorine reaction with UV-LED chip emitting UV275 nm to remove ciprofloxacin and ciprofloxacin-resistant bacteria in water. Ciprofloxacin degradation during the UV-LED/chlorine reaction followed pseudo-first-order kinetics, and the excessive chlorine dosage has a negative effect on ciprofloxacin removal. Alkaline pH showed the best efficiency for ciprofloxacin removal, and the reactive chlorine species (RCS) played a major role at alkaline pH values. The cleavages of piperazine, cyclopropyl, and quinolone moieties are considered as the principal degradation reactions in the UV-LED/chlorine reaction. Seven byproducts (m/z = 362.9262, 306.1246, 289.0995, 288.1504, 263.0825, 147.0657, and 1183.9977), two chlorinated compounds (chloroform and chlorate) and two anions (formate and nitrate ions) were observed as the identified byproducts. Toxicity of tentatively identified byproducts were estimated by using quantitative structure activity relationship (QSAR). The complete detoxification of was achieved when applying UV-LED/chlorine process into hospital wastewater containing CIP. The UV-LED/chlorine process showed the best disinfection ability of E. faecium compared to UV-LED photolysis, chlorination, and UV-LED/H2O2 reactions. A significantly lower EE/O value (6.63 × 10−2 kWh/m3/order) during the UV-LED/chlorine reaction was also observed. Our results indicate that the UV-LED/chlorine process can effectively degrade ciprofloxacin and inactivate ciprofloxacin-resistant bacteria.N

SERTAD1 Sensitizes Breast Cancer Cells to Doxorubicin and Promotes Lysosomal Protein Biosynthesis

Acquired chemoresistance of tumor cells is an unwanted consequence of cancer treatment. Overcoming chemoresistance is particularly important for efficiently improving cancer therapies. Here, using multiple lines of evidence, we report the suppressive role of SERTAD1 in apoptosis/anoikis. Among various breast cancer cell lines, higher SERTAD1 expression was found in MCF7 and MDA-MB-231 in suspension than in adherent cell culture. We revealed an unexpected phenomenon that different types of cell deaths were induced in response to different doses of doxorubicin (Dox) in breast cancer cells, presumably via lysosomal membrane permeabilization. A low dose of Dox highly activated autophagy, while a high dose of the chemotherapy induced apoptosis. Inhibition of SERTAD1 promoted the sensitivity of breast cancer cells to Dox and paclitaxel, leading to a significant reduction in tumor volumes of xenograft mice. Simultaneously targeting cancer cells with Dox and autophagy inhibition successfully induced higher apoptosis/anoikis. The novel role of SERTAD1 in maintaining cellular homeostasis has also been suggested in which lysosomal contents, including LAMP1, LAMP2, CTSB, and CTSD, were reduced in SERTAD1-deficient cells