Cadmium and arsenic-induced-stress differentially modulates Arabidopsis root architecture, peroxisome distribution, enzymatic activities and their nitric oxide content

In plant cells, cadmium (Cd) and arsenic (As) exert toxicity mainly by inducing oxidative stress through an imbalance between the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), and their detoxification. Nitric oxide (NO) is a RNS acting as signalling molecule coordinating plant development and stress responses, but also as oxidative stress inducer, depending on its cellular concentration. Peroxisomes are versatile organelles involved in plant metabolism and signalling, with a role in cellular redox balance thanks to their antioxidant enzymes, and their RNS (mainly NO) and ROS. This study analysed Cd or As effects on peroxisomes, and NO production and distribution in the root system, including primary root (PR) and lateral roots (LRs). Arabidopsis thaliana wild-type and transgenic plants enabling peroxisomes to be visualized in vivo, through the expression of the 35S-cyan fluorescent protein fused to the peroxisomal targeting signal1 (PTS1) were used. Peroxisomal enzymatic activities including the antioxidant catalase, the H2O2-generating glycolate oxidase, and the hydroxypyruvate reductase, and root system morphology were also evaluated under Cd/As exposure. Results showed that Cd and As differently modulate these activities, however, catalase activity was inhibited by both. Moreover, Arabidopsis root system was altered, with the pollutants differently affecting PR growth, but similarly enhancing LR formation. Only in the PR apex, and not in LR one, Cd more than As caused significant changes in peroxisome distribution, size, and in peroxisomal NO content. By contrast, neither pollutant caused significant changes in peroxisomes size and peroxisomal NO content in the LR apex

Jasmonic acid methyl ester induces xylogenesis and modulates auxin-induced xylary cell identity with NO Involvement

In Arabidopsis basal hypocotyls of dark-grown seedlings, xylary cells may form from the pericycle as an alternative to adventitious roots. Several hormones may induce xylogenesis, as Jasmonic acid (JA), as well as indole-3-acetic acid (IAA) and indole-3-butyric acid (IBA) auxins, which also affect xylary identity. Studies with the ethylene (ET)-perception mutant ein3eil1 and the ET-precursor 1-aminocyclopropane-1-carboxylic acid (ACC), also demonstrate ET involvement in IBA-induced ectopic metaxylem. Moreover, nitric oxide (NO), produced after IBA/IAA-treatments, may affect JA signalling and interact positively/negatively with ET. To date, NO-involvement in ET/JA-mediated xylogenesis has never been investigated. To study this, and unravel JA-effects on xylary identity, xylogenesis was investigated in hypocotyls of seedlings treated with JA methyl-ester (JAMe) with/without ACC, IBA, IAA. Wild-type (wt) and ein3eil1 responses to hormonal treatments were compared, and the NO signal was quantified and its role evaluated by using NO-donors/scavengers. Ectopic-protoxylem increased in the wt only after treatment with JAMe(10 μM), whereas in ein3eil1 with any JAMe concentration. NO was detected in cells leading to either xylogenesis or adventitious rooting, and increased after treatment with JAMe(10 μM) combined or not with IBA(10 μM). Xylary identity changed when JAMe was applied with each auxin. Altogether, the results show that xylogenesis is induced by JA and NO positively regulates this process. In addition, NO also negatively interacts with ET-signalling and modulates auxin-induced xylary identity

Signalling Properties of Inositol Polyphosphates

Several studies have identified specific signalling functions for inositol polyphosphates (IPs) in different cell types and have led to the accumulation of new information regarding their cellular roles as well as new insights into their cellular production. These studies have revealed that interaction of IPs with several proteins is critical for stabilization of protein complexes and for modulation of enzymatic activity. This has not only revealed their importance in regulation of several cellular processes but it has also highlighted the possibility of new pharmacological interventions in multiple diseases, including cancer. In this review, we describe some of the intracellular roles of IPs and we discuss the pharmacological opportunities that modulation of IPs levels can provide

Infectious agents in atherosclerotic cardiovascular diseases through oxidative stress

Accumulating evidence demonstrates that vascular oxidative stress is a critical feature of atherosclerotic process, potentially triggered by several infectious agents that are considered as risk co-factors for the atherosclerotic cardiovascular diseases (CVDs). C. pneumoniae has been shown to upregulate multiple enzymatic systems capable of producing reactive oxygen species (ROS) such as NADPH oxidase (NOX) and cyclooxygenase in vascular endothelial cells, NOX and cytochrome c oxidase in macrophages as well as nitric oxide synthase and lipoxygenase in platelets contributing to both early and late stages of atherosclerosis. P. gingivalis seems to be markedly involved in the atherosclerotic process as compared to A. actinomycetemcomitans contributing to LDL oxidation and foam cell formation. Particularly interesting is the evidence describing the NLRP3 inflammasome activation as a new molecular mechanism underlying P. gingivalis-induced oxidative stress and inflammation. Amongst viral agents, immunodeficiency virus-1 and hepatitis C virus seem to have a major role in promoting ROS production, contributing, hence, to the early stages of atherosclerosis including endothelial dysfunction and LDL oxidation. In conclusion, oxidative mechanisms activated by several infectious agents during the atherosclerotic process underlying CVDs are very complex and not well-known, remaining, thus, an attractive target for future research

Nitric oxide alleviates cadmium- but not arsenic-induced damages in rice roots

Nitric oxide (NO) has signalling roles in plant stress responses. Cadmium (Cd) and arsenic (As) soil pollutants alter plant development, mainly the root-system, by increasing NO-content, triggering reactive oxygen species (ROS), and forming peroxynitrite by NO-reaction with the superoxide anion. Interactions of NO with ROS and peroxynitrite seem important for plant tolerance to heavy metal(oid)s, but the mechanisms underlying this process remain unclear. Our goal was to investigate NO-involvement in rice (Oryza sativa L.) root-system after exposure to Cd or As, to highlight possible differences in NO-behaviour between the two pollutants. To the aim, morpho-histological, chemical and epifluorescence analyses were carried out on roots of different origin in the root-system, under exposure to Cd or As, combined or not with sodium nitroprusside (SNP), a NO-donor compound. Results show that increased intracellular NO levels alleviate the root-system alterations induced by Cd, i.e., inhibition of adventitious root elongation and lateral root formation, increment in lignin deposition in the sclerenchyma/endodermis cell-walls, but, even if reducing As-induced endodermis lignification, do not recover the majority of the As-damages, i.e., enhancement of AR-elongation, reduction of LR-formation, anomalous tissue-proliferation. However, NO decreases both Cd and As uptake, without affecting the pollutants translocation-capability from roots to shoots. Moreover, NO reduces the Cd-induced, but not the As-induced, ROS levels by triggering peroxynitrite production. Altogether, results highlight a different behaviour of NO in modulating rice root-system response to the toxicity of the heavy metal Cd and the metalloid As, which depends by the NO-interaction with the specific pollutant

Cadmium and arsenic affect root development in Oryza sativa L. negatively interacting with auxin

Cadmium (Cd) and arsenic (As), non essential, but toxic, elements for animals and plants are frequently present in paddy fields. Oryza sativa L., a staple food for at least the half of world population, easily absorbs As and Cd by the root, and in this organ the pollutants evoke consistent damages, reducing/modifying the root system. Auxins are key hormones in regulating all developmental processes, including root organogenesis. Moreover, plants respond to environmental stresses, such as those caused by Cd and As, by changing levels and distribution of endogenous phytohormones. Even though the effects of Cd and As on the roots have been investigated in some species, it remains necessary to deepen the knowledge about the cross-talk between these toxic elements and auxin during root formation and development, in particular in agronomically important plants, such as rice. Hence, the research goal was to investigate the interactions between Cd and As, alone or combined, and auxin during the development of rice roots. To reach the aim, morphological, histological and histochemical analyses were carried out on seedlings, exposed or not to Cd and/or As, belonging to the wild type and transgenic lines useful for monitoring indole-3-acetic acid (IAA) localization, i.e., OsDR5:GUS, and IAA cellular influx and efflux, i.e., OsAUX1:GUS and OsPIN5b:GUS. Moreover, the transcript levels of the YUCCA2 and ASA2, IAA biosynthetic genes were also monitored in Cd and/or As exposed wild type seedlings. The results highlight that As and Cd affect cyto-histology and morphology of the roots. In particular, they alter the lateral root primordia organization and development with negative consequences on root system architecture. This is due to a disturbance of IAA biosynthesis and transport, as indicated by the altered expression of both ASA2 and YUCCA2 biosynthetic genes, and AUX1 and PIN5b transporter genes

The History of Armand Trousseau and Cancer-Associated Thrombosis

“Je suis perdu; une phlegmatia qui vient de se déclarer cette nuit, ne me laisse aucun doute sur nature de mon mal.” —Armand Trousseau “I am lost; a phlebitis which has declared itself this night leaves me no doubt about the nature of my illness.

Class II Phosphoinositide 3-Kinases Contribute to Endothelial Cells Morphogenesis

PMCID: PMC3539993This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Does accidental phoropter tilt have a significant effect on determination of correcting cylinder?

Does accidental phoropter tilt have a significant effect on determination of correcting cylinder