Search

Aiming to construct a direct Z-scheme binary heterostructure for efficient degradation of the organic dye Rhodamine B (RhB), ZnWO4 nanorods decorated with SnS nanodots were rationally designed and prepared via a facile two-step route. Morphological observation and structural study showed that ultra-fine SnS nanodots were anchored on the surface of ZnWO4 nanorods to form an intimate contact between the two components. Such a special structure provided SnS/ZnWO4 nanocomposites with significantly enhanced light harvesting capacity, revealed by the results of UV-vis diffuse reflection spectroscopy (DRS). Photoluminescence (PL) analysis in combination with electrochemical measurements demonstrated that the recombination of photoactivated charge carriers was efficiently inhibited and the transfer of photoactivated charge carriers was successfully achieved due to the introduction of SnS. The degradation rate over SnS/ZnWO4 nanocomposites reached a maximum value at SnS content of 9 wt%. The significantly enhanced photoactivity of SnS/ZnWO4 nanocomposites was imputed to the synergistic effect of the promoted light absorption ability and effective photogenerated charge carriers' transfer and separation. [ABSTRACT FROM AUTHOR]

Lead is a heavy metal known to be toxic to both animals and plants. Nitric oxide (NO) was reported to participate in plant responses to different heavy metal stresses. In this study, we analyzed the function of exogenous and endogenous NO in Pb-induced toxicity in tobacco BY-2 cells, focusing on the role of NO in the generation of reactive oxygen species (ROS) as well as Pb 2+ and Ca 2+ fluxes using non-invasive micro-test technology (NMT). Pb treatment induced BY-2 cell death and rapid NO and ROS generation, while NO burst occurred earlier than ROS accumulation. The elimination of NO by 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) resulted in a decrease of ROS, and the supplementation of NO by sodium nitroprusside (SNP) caused an increased accumulation of ROS. Furthermore, the addition of exogenous NO stimulated Pb 2+ influx, thus promoting Pb uptake in cells and aggravating Pb-induced toxicity in cells, whereas the removal of endogenous NO produced the opposite effect. Moreover, we also found that both exogenous and endogenous NO enhanced Pb-induced Ca 2+ effluxes and calcium homeostasis disorder. These results suggest that exogenous and endogenous NO played a critical regulatory role in BY-2 cell death induced by Pb stress by promoting Pb 2+ influx and accumulation and disturbing calcium homeostasis.