Development of LaxCa1-xMnO3 materials for Bezaktiv Blue removal in aqueous media.

In this work, mixed oxides of LaxCa1-xMnO3 perovskite type (x = 0, 0.5 and 1.0) were synthesized through modified proteic method using collagen and calcination process at 700 °C/2 h in order to remove the commercial textile dye Bezaktiv Blue S-MAX from water. Oxides were characterized using X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), N2 physisorption, scanning electron microscopy (SEM) and point of zero charge (PZC) techniques while the dye only by the first two techniques. The XRD showed that perovskite monophase was obtained for x = 0.5 and 1.0. However, for x = 0, the low crystalline perovskite phase was obtained in the midst of precursor oxides. FTIR showed the adsorption process did not damage the adsorbents structure. The successful obtained materials have meso and macroporous with slit or cavity shape, rough surface and particles with varying sizes. The pseudo-second-order model was the one that best fit the kinetic data. The process must occur through electrostatic surface interactions between the adsorbent surface and the dye molecule. For the equilibrium study, Langmuir isotherm is the most suitable when using LaMnO3 adsorbent, while Freundlich isotherm was better suited when used the other two materials. The adsorbents were termally regenerated and reused five times. The best performance was exhibited by LaMnO3.

Effect of overexpression of citrus 9-cis-epoxycarotenoid dioxygenase 3 (CsNCED3) on the physiological response to drought stress in transgenic tobacco.

9-cis-epoxycarotenoid dioxygenase (NCED) encodes a key enzyme in abscisic acid (ABA) biosynthesis. Little is known regarding the regulation of stress response by NCEDs at physiological levels. In the present study, we generated transgenic tobacco overexpressing an NCED3 ortholog from citrus (CsNCED3) and investigated its relevance in the regulation of drought stress tolerance. Wild-type (WT) and transgenic plants were grown under greenhouse conditions and subjected to drought stress for 10 days. Leaf predawn water potential (Ψwleaf), stomatal conductance (gs), net photosynthetic rate (A), transpiration rate (E), instantaneous (A/E) and intrinsic (A/gs) water use efficiency (WUE), and in situ hydrogen peroxide (H2O2) and abscisic acid (ABA) production were determined in leaves of irrigated and drought-stressed plants. The Ψwleaf decreased throughout the drought stress period in both WT and transgenic plants, but was restored after re-watering. No significant differences were observed in gs between WT and transgenic plants under normal conditions. However, the transgenic plants showed a decreased (P ≤ 0.01) gs on the 4th day of drought stress, which remained lower (P ≤ 0.001) than the WT until the end of the drought stress. The A and E levels in the transgenic plants were similar to those in WT; therefore, they exhibited increased A/gs under drought conditions. No significant differences in A, E, and gs values were observed between the WT and transgenic plants after re-watering. The transgenic plants had lower H2O2 and higher ABA than the WT under drought conditions. Our results support the involvement of CsNCED3 in drought avoidance.

Electronegative LDL induction of apoptosis in macrophages: involvement of Nrf2.

The aim of this study was to determine the apoptotic pathways and mechanisms involved in electronegative LDL [LDL(-)]-induced apoptosis in RAW 264.7 macrophages and the role of Nrf2 in this process. Incubation of RAW 264.7 macrophages with LDL(-) for 24 h resulted in dose-dependent cell death. Activated caspases were shown to be involved in the apoptosis induced by LDL(-); incubation with the broad caspase inhibitor z-VAD prevented apoptosis in LDL(-)-treated cells. CD95 (Fas), CD95 ligand (FasL), CD36 and the tumor necrosis factor (TNF) ligand Tnfsf10 were overexpressed in LDL(-)-treated cells. However, Bax, Bcl-2 and Mcl-1 protein levels remained unchanged after LDL(-) treatment. LDL(-) promoted hyperpolarization of the mitochondrial membrane, elevated reactive oxygen species (ROS) production and translocation of Nrf2 to the nucleus, a process absent in cells treated with native LDL. Elicited peritoneal macrophages from Nrf2-deficient mice exhibited an elevated apoptotic response after challenge with LDL(-), together with an increase in the production of ROS in the absence of alterations in CD36 expression. These results provide evidence that CD36 expression induced by LDL(-) is Nrf2-dependent. Also, it was demonstrated that Nrf2 acts as a compensatory mechanism of LDL(-)-induced apoptosis in macrophages.