Oxidative Treatments of Pesticides in Rainwater Runoff by HOCl, O3, and O3/H2O2: Effects of pH, Humic Acids and Inorganic Matters

This study systematically investigated the oxidative treatment of five selected pesticides, alachlor (ALA), carbendazim (CAR), diuron (DIU), pyrimethanil (PYR), and tebuconazole (TEB), by comparing their relative reactivities as a function of three different oxidative treatment processes (i.e., chlorine (HOCl), ozone (O3), and ozone/hydrogen peroxide (O3/H2O2)) under various oxidant dosages, reaction times, and pH conditions. For oxidative treatment, pesticide standards were spiked into rainwater. The removal efficiency of the selected pesticides varied considerably depending on the oxidative treatment processes. HOCl, O3, and O3/H2O2 treatments were highly effective at eliminating CAR (>80%) and PYR (>99%), while they were not significantly effective in removing TEB (<20%). In the case of DIU, HOCl (81%) was shown to be more effective than O3 (24%) and O3/H2O2 (49%). The removal efficiency of ALA was in the order of O3/H2O2 (49%) > O3 (20%) > HOCl (8.5%). The effect of increasing the solution pH from 5.0 to 9.0 on pesticide degradation varied between the oxidative treatment processes. Additionally, NH4+, NO2−, and humic acid in rainwater significantly inhibited pesticide degradation.

Zeta Potential of Cellulose Nanoparticles as a Function of pH

In this work, we obtained dispersions of nanosized cellulose particles and measured the zeta potential of particles at pH from 1 to 14. It was found that CNF retains sedimentation stability at pH from 3 to 11. At the same time, CNF obtained by acid treatment with homogenization has the maximum zeta potential about -62 mV at pH = 6. CNF obtained by oxidative treatment with homogenization has a maximum zeta potential of about -46 mV at pH = 7. CNC obtained by oxidative treatment with homogenization retains sedimentation stability at pH from 4 to 11 and has a maximum zeta potential of about -73 mV at pH =4.

PARP-1 activation after oxidative insult promotes energy stress-dependent phosphorylation of YAP1 and reduces cell viability

Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that catalyze the transfer of ADP-ribose units from NAD+ to several target proteins involved in cellular stress responses. Using WRL68 (HeLa derivate) cells, we previously showed that PARP-1 activation induced by oxidative stress after H2O2 treatment lead to depletion of cellular NAD+ and ATP, which promoted cell death. In this work, LC–MS/MS-based phosphoproteomics in WRL68 cells showed that the oxidative damage induced by H2O2 increased the phosphorylation of YAP1, a transcriptional co-activator involved in cell survival, and modified the phosphorylation of other proteins involved in transcription. Genetic or pharmacological inhibition of PARP-1 in H2O2-treated cells reduced YAP1 phosphorylation and degradation and increased cell viability. YAP1 silencing abrogated the protective effect of PARP-1 inhibition, indicating that YAP1 is important for the survival of WRL68 cells exposed to oxidative damage. Supplementation of NAD+ also reduced YAP1 phosphorylation, suggesting that the loss of cellular NAD+ caused by PARP-1 activation after oxidative treatment is responsible for the phosphorylation of YAP1. Finally, PARP-1 silencing after oxidative treatment diminished the activation of the metabolic sensor AMPK. Since NAD+ supplementation reduced the phosphorylation of some AMPK substrates, we hypothesized that the loss of cellular NAD+ after PARP-1 activation may induce an energy stress that activates AMPK. In summary, we showed a new crucial role of PARP-1 in the response to oxidative stress in which PARP-1 activation reduced cell viability by promoting the phosphorylation and degradation of YAP1 through a mechanism that involves the depletion of NAD+.