Multifunctional SERS chip mediated by black phosphorus@gold-silver nanocomposites inserted in bilayer membrane for in-situ detection and degradation of hazardous materials.

Self-cleaning surface-enhanced Raman scattering (SERS) substrates dependent on versatile two-dimensional semiconductors offer an efficient channel for the sensitive monitoring and timely degradation of hazardous molecules. Herein, a kind of sophisticated SERS-active nanocomposites was developed by incorporating Au-Ag nanoparticles onto black phosphorus (BP) nanosheets via photo-induced self-reduction. Combining the substantial electromagnetic "hot spots" triggered by bimetallic plasma coupling effect and the efficient charge transfer from BP to probe molecules, the proposed nanocomposites featured attractive SERS enhancement, facilitating a limit of detection down to 4.5 × 10-10 M. Attributed to the remarkable restriction of electron-hole recombination stemming from "Schottky contact", the photocatalytic activity of BP was prominently boosted, demonstrating a complete degradation time as short as 65 min. Furthermore, the disgusting instability of BP was considerably hindered by inserting the nanocomposites into various bilayer matrices with diverse hardness and viscosity inspired by cling film principle. Moreover, a significantly elevated collection rate high to 93.1% for in-situ detection was also achieved by the as-manufactured flexible SERS chips based on tape. This study illustrates a clear perspective for the development of versatile BP-based SERS chips which might facilitate sensitive analysis and treatment of perilous contaminants in complicated real-life scenarios.

Naja mossambica mossambica Cobra Cardiotoxin Targets Mitochondria to Disrupt Mitochondrial Membrane Structure and Function.

Cobra venom cardiotoxins (CVCs) can translocate to mitochondria to promote apoptosis by eliciting mitochondrial dysfunction. However, the molecular mechanism(s) by which CVCs are selectively targeted to the mitochondrion to disrupt mitochondrial function remains to be elucidated. By studying cardiotoxin from Naja mossambica mossambica cobra (cardiotoxin VII4), a basic three-fingered S-type cardiotoxin, we hypothesized that cardiotoxin VII4 binds to cardiolipin (CL) in mitochondria to alter mitochondrial structure/function and promote neurotoxicity. By performing confocal analysis, we observed that red-fluorescently tagged cardiotoxin rapidly translocates to mitochondria in mouse primary cortical neurons and in human SH-SY5Y neuroblastoma cells to promote aberrant mitochondrial fragmentation, a decline in oxidative phosphorylation, and decreased energy production. In addition, by employing electron paramagnetic resonance (EPR) and protein nuclear magnetic resonance (¹H-NMR) spectroscopy and phosphorescence quenching of erythrosine in model membranes, our compiled biophysical data show that cardiotoxin VII4 binds to anionic CL, but not to zwitterionic phosphatidylcholine (PC), to increase the permeability and formation of non-bilayer structures in CL-enriched membranes that biochemically mimic the outer and inner mitochondrial membranes. Finally, molecular dynamics simulations and in silico docking studies identified CL binding sites in cardiotoxin VII4 and revealed a molecular mechanism by which cardiotoxin VII4 interacts with CL and PC to bind and penetrate mitochondrial membranes.