Sorption kinetics studies of herbicides, using different models, are an important tool for determining the mechanisms and kinetic parameters that explain the bioavailability and environmental behavior of these compounds. However, little is known about the combined effects of fertilizers and herbicides and how it could modify these processes on the soil. The aim of this study was to evaluate the sorption kinetics of diuron and 2,4-D in an Andisol treated with urea using various kinetic models. The experiments were carried out in batch, independently for each herbicide, with urea application in an equivalent dose of 200 kg N ha −1 and artificial pH modifications. The results showed no differences in sorption kinetics due to urea for diuron; however 2,4-D showed differences with urea and changes in pH conditions. The data fitted well with the pseudo-second-order model (R 2 > 0.996), showing a maximum soil adsorption capacity of 11.9, 10.8, and 9.61 mg kg −1 for diuron, 2,4-D, and 2,4-D-urea, respectively. The initial adsorption rate was similar for both herbicides, but a significant increase in the rate constant was observed for 2,4-D at acid pH. We conclude from the Elovich and Weber-Morris models that both herbicides were adsorbed mainly during the first stage, followed by lower adsorption in the slower second stage. According to these models, mass transfer across the boundary layer, and to a lesser degree intraparticle diffusion mechanisms, controlled sorption kinetics for both herbicides. The results suggest that urea application could influence sorption process of acid herbicides for pH changes in soils.

The oxidized low-density lipoprotein receptor 1 (LOX-1) is one of the most important receptors for modified LDLs, such as oxidated (oxLDL) and acetylated (acLDL) low-density lipoprotein. LOX-1 and oxLDL are fundamental in atherosclerosis, where oxLDL/LOX1 promotes ROS generation and NF-κB activation inducing the expression of IL-6, a STAT3 activator. Furthermore, LOX-1/oxLDL function has been associated with other diseases, such as obesity, hypertension, and cancer. In prostate cancer (CaP), LOX-1 overexpression is associated with advanced stages, and its activation by oxLDL induces an epithelial-mesenchymal transition, increasing angiogenesis and proliferation. Interestingly, enzalutamide-resistant CaP cells increase the uptake of acLDL. Enzalutamide is an androgen receptor (AR) antagonist for castration-resistant prostate cancer (CRPC) treatment, and a high percentage of patients develop a resistance to this drug. The decreased cytotoxicity is promoted in part by STAT3 and NF-κB activation that induces the secretion of the pro-inflammatory program and the expression of AR and its splicing variant AR-V7. Here, we demonstrate for the first time that oxLDL/LOX-1 increases ROS levels and activates NF-κB, inducing IL-6 secretion and the activation of STAT3 in CRPC cells. Furthermore, oxLDL/LOX1 increases AR and AR-V7 expression and decreases enzalutamide cytotoxicity in CRPC. Thus, our investigation suggests that new factors associated with cardiovascular pathologies, such as LOX-1/oxLDL, may also promote important signaling axes for the progression of CRPC and its resistance to drugs used for its treatment.

Maytenus disticha (Hook F.), belonging to the Celastraceae family, is an evergreen shrub, native of the central southern mountains of Chile. Previous studies demonstrated that the total extract of M. disticha (MD) has an acetylcholinesterase inhibitory activity along with growth regulatory and insecticidal activities. β-Dihydroagarofurans sesquiterpenes are the most active components in the plant. However, its activity in cancer has not been analyzed yet. Here, we demonstrate that MD has a cytotoxic activity on breast (MCF-7), lung (PC9), and prostate (C4-2B) human cancer cells with an IC50 (µg/mL) of 40, 4.7, and 5 µg/mL, respectively, an increasing Bax/Bcl2 ratio, and inducing a mitochondrial membrane depolarization. The β-dihydroagarofuran-type sesquiterpene (MD-6), dihydromyricetin (MD-9), and dihydromyricetin-3-O-β-glucoside (MD-10) were isolated as the major compounds from MD extracts. From these compounds, only MD-6 showed cytotoxic activity on MCF-7, PC9, and C4-2B with an IC50 of 31.02, 17.58, and 42.19 µM, respectively. Furthermore, the MD-6 increases cell ROS generation, and MD and MD-6 induce a mitochondrial superoxide generation and apoptosis on MCF-7, PC9, and C4-2B, which suggests that the cytotoxic effect of MD is mediated in part by the β-dihydroagarofuran-type that induces apoptosis by a mitochondrial dysfunction.