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The development of facile, sensitive, and robust methods for the detection of metal ions is fascinating for chemists because traditional strategies for their detection usually involve complicated instrumentation and critical sample preparation procedures. In this work, bicinchoninic acid was used in a specific reaction with Cu(I) for the spectrophotometric determination of various metal ions. The optimization of experimental parameters led to the establishment of a simple, fast, and accurate analytical method. Mn(II), Co(II), and Fe(II) can be detected at submicromolar levels using this method. Calibration graphs for Mn(II), Co(II), and Fe(II) are rectilinear within the range of 8–40, 15–150, and 15–150 μM, respectively. The detection limit for Mn(II), Co(II), and Fe(II) were 0.83, 1.4, and 1.9 mg/L, respectively, and the relative standard deviation did not exceed 2.5% for five replicates. The bathocuproine reaction demonstrated that Cu(II) can be reduced to Cu(I) by Mn(II). Then bicinchoninic acid can bind to Cu(I), creating a purple-colored product at 562 nm. The method has been successfully applied to evaluate the reaction process and stability of metal-organic frameworks. Moreover, the results were found to be in satisfactory agreement with those acquired by using the inductively coupled plasma mass spectrometry technique, which will open up a new avenue for using the proposed strategy as a conventional method to detect metal ions in scientific research. [ABSTRACT FROM AUTHOR]

The natural product dehydrocurvularin (DSE2) is a fungal-derived macrolide with potent anticancer activity, but the mechanism is still unclear. We found that DSE2 effectively inhibited the growth of gastric cancer cells and induced the apoptosis by activating Poly(ADP-ribose) polymerase 1 (PARP-1) and caspase-3. Pharmacological inhibition and genetic knockdown with PARP-1 or caspase-3 suppressed DSE2-induced apoptosis. PARP-1 was previously reported to be cleaved into fragments during apoptosis. However, PARP-1 was barely cleaved in DSE2-induced apoptosis. DSE2 induced PARP-1 activation as indicated by rapid depletion of NAD+ and the concomitant formation of poly(ADP-ribosylated) proteins (PARs). Interestingly, the PARP-1 inhibitor (Olaparib) attenuated the cytotoxicity of DSE2. Moreover, the combination of Olaparib and Z-DEVD-FMK (caspase-3 inhibitor) further reduced the cytotoxicity. It has been shown that PARP-1 activation triggers cytoplasm-nucleus translocation of apoptosis-inducing factor (AIF). Caspase-3 inhibitors inhibited PARP-1 activation and suppressed PARP-1-induced AIF nuclear translocation. These results indicated that DSE2-induced caspase-3 activation may occur before PARP-1 activation. The ROS inhibitor, N-acetyl-cysteine, significantly inhibited the activation of caspase-3 and PARP-1, indicating that ROS overproduction contributed to DSE2-induced apoptosis. Using an in vivo approach, we further found that DSE2 significantly inhibited gastric tumor growth and promoted translocation of AIF to the nucleus. In conclusion, DSE2 induces gastric cell apoptosis by activating caspase-3 and PARP-1, and shows potent antitumor activity against human gastric carcinoma in vitro and in vivo. [ABSTRACT FROM AUTHOR]