2,4-Dichlorophenoxyacetic acid promotes S-nitrosylation and oxidation of actin affecting cytoskeleton and peroxisomal dynamics.

2,4-Dichlorophenoxyacetic acid (2,4-D) is a synthetic auxin used as a herbicide to control weeds in agriculture. A high concentration of 2,4-D promotes leaf epinasty and cell death. In this work, the molecular mechanisms involved in the toxicity of this herbicide are studied by analysing in Arabidopsis plants the accumulation of reactive oxygen species (ROS) and nitric oxide (NO), and their effect on cytoskeleton structure and peroxisome dynamics. 2,4-D (23 mM) promotes leaf epinasty, whereas this process was prevented by EDTA, which can reduce ·OH accumulation. The analysis of ROS accumulation by confocal microscopy showed a 2,4-D-dependent increase in both H2O2 and O2·(-), whereas total NO was not affected by the treatment. The herbicide promotes disturbances on the actin cytoskeleton structure as a result of post-translational modification of actin by oxidation and S-nitrosylation, which could disturb actin polymerization, as suggested by the reduction of the F-actin/G-actin ratio. These effects were reduced by EDTA, and the reduction of ROS production in Arabidopsis mutants deficient in xanthine dehydrogenase (Atxdh) gave rise to a reduction in actin oxidation. Also, 2,4-D alters the dynamics of the peroxisome, slowing the speed and shortening the distances by which these organelles are displaced. It is concluded that 2,4-D promotes oxidative and nitrosative stress, causing disturbances in the actin cytoskeleton, thereby affecting the dynamics of peroxisomes and some other organelles such as the mitochondria, with xanthine dehydrogenase being involved in ROS production under these conditions. These structural changes in turn appear to be responsible for the leaf epinasty.

Regulation of epinasty induced by 2,4-dichlorophenoxyacetic acid in pea and Arabidopsis plants.

The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) causes uncontrolled cell division and malformed growth in plants, giving rise to leaf epinasty and stem curvature. In this study, mechanisms involved in the regulation of leaf epinasty induced by 2,4-D were studied using different chemicals involved in reactive oxygen species (ROS) accumulation (diphenyleniodonium, butylated hydroxyanisole, EDTA, allopurinol), calcium channels (LaCl3), protein phosphorylation (cantharidin, wortmannin) and ethylene emission/perception (aminoethoxyvinyl glycine, AgNO3). The effect of these compounds on the epinasty induced by 2,4-D was analysed in shoots and leaf strips from pea plants. For further insight into the effect of 2,4-D, studies were also made in Arabidopsis mutants deficient in ROS production (rbohD, rbohF, xdh), ethylene (ein 3-1, ctr 1-1, etr 1-1), abscisic acid (aba 3.1), and jasmonic acid (coi 1.1, jar 1.1, opr 3) pathways. The results suggest that ROS production, mainly ·OH, is essential in the development of epinasty triggered by 2,4-D. Epinasty was also found to be regulated by Ca2+, protein phosphorylation and ethylene, although all these factors act downstream of ROS production. The use of Arabidopsis mutants appears to indicate that abscisic and jasmonic acid are not involved in regulating epinasty, although they could be involved in other symptoms induced by 2,4-D.

Oxidative stress and arsenic toxicity: role of NADPH oxidases.

The effect of arsenic (25 and 50 µM As for 1 and 5d) was analysed in wild type (WT) and Arabidopsis thaliana (L.) Heynh plants deficient in NADPH oxidase C (AtrbohC). The content of H(2)O(2) and malondialdehyde (MDA) increased with the As concentration, while the opposite effect was found for NO in WT and AtrbohC plants. The As treatment reduced catalase and increased glutathione reductase activities to the same extent in WT and AtrbohC plants, although the induction of all SOD isoforms (mainly CuZn-SODs) was observed in WT plants, the opposite effects being found in AtrbohC plants. Glycolate oxidase (H(2)O(2) producers) considerably increased with the concentration and time of treatment with As in WT and AtrbohC mutants. Arsenic induced the uptake and translocation of P, S, Cu, Zn, and Fe in WT plants, while in AtrbohC plants the opposite trend was noted and the uptake of As became considerably lower than in WT plants. These results suggest that As causes oxidative stress by inducing glycolate oxidase, while NADPH oxidase does not appear to participate in ROS overproduction but could be critical in regulating antioxidant defences as well as the transport and translocation of As and macro/micronutrients.

Mortality from renal dysfunction in heart transplant patients: creatinine versus glomerular filtration rate.

INTRODUCTION: One of the most common, significant problems after heart transplantation (HT) is the development of renal dysfunction. In recent years, the glomerular filtration rate (GFR) has replaced the serum creatinine as the standard parameter for its determination. Our objective was to analyze which renal function parameter (creatinine or GFR) at 1 year after HT better classified patients who will die during follow-up. PATIENTS AND METHODS: The study included 316 consecutive HT patients surviving at least 1 year after transplantation. Creatinine and GFR were determined by the Modification of Diet in Renal Disease Study (MDRD4) equation. Mortality during the follow-up was analyzed to compare both parameters using receiver operating characteristic curves. RESULTS: Over a mean follow-up of 6±3 years, 97 patients died (30.7%). At 1 year after HT, the patients who succumbed displayed a significantly higher mean creatinine value (1.63±0.65 vs 1.41±0.64 mg/dL; P=.004) and a more decreased GFR (53.8 vs 60.8 mL/min/1.73 m2; P=.006). Both groups had the same area under the curve, 0.61 (95% confidence interval: 0.54-0.68; P=.002). CONCLUSION: Among our population, GFR calculated by the abbreviated MDRD4 equation did not provide any additional prognostic value to serum creatinine at 1 year after HT to predict long-term mortality.

[Paraquat poisoning: report of two cases and literature review]. / Intoxicación por paraquat: presentación de dos casos y revisión de la literatura.

Cases of poisoning with pesticides, especially suicidal ones, continue to be an important therapeutic problem. The heribicide paraquat (1.1' dimethyl-4.4' bipyridylium dichloride) is the second cause of pesticide poisoning in our country, which is associated with a high mortality rate. We report two cases of suicidal ingestion of paraquat who developed multiorgan failure with a lethal outcome. We also present a brief review of the literature, mainly focused on the different therapeutic options.