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Salt stress is a major abiotic stress that limits agricultural productivity in many regions of the world. To understand the molecular basis of the salt stress response, two wheat (Triticum durum Desf.) cultivars, Karim and Azizi, which are of agronomic significance in Tunisia, were grown under non-saline and saline conditions (100 mM). Leaves and roots of control and salt-stressed plants were harvested after 11 days of salt treatment. Karim cultivar may behave as a typical Na+ include, which compartmentalizes Na+ within the leaf cell vacuoles where it could be used as an osmoticum to lower the osmotic potential necessary for the maintenance of the plant hydric status. While, accumulation of K+ was greater in Karim cultivar compared to Azizi, in both organs, presenting an important manifestation of salinity tolerance. Significant changes in metabolism of antioxidative system were observed, with an increase in protein tyrosine nitration, which indicates that salinity stress induces a nitro-oxidative stress. [ABSTRACT FROM AUTHOR]

Abstract Leishmaniases are infectious diseases, caused by protozoa of the Leishmania genus. These drugs present high toxicity, long-term administration, many adverse effects and are expensive, besides the identification of resistant parasites. In this work, the antileishmanial activity of quinoline derivative salts (QDS) was evaluated, as well as the toxicity on mammalian cells and the mechanism of action of the most promising compound. Among the compound tested, only the compound QDS3 showed activity against promastigotes and amastigotes of Leishmania spp., being more active against the intracellular amastigotes of L. amazonensis -GFP (IC 50 of 5.48 μM). This value is very close to the one observed for miltefosine (IC 50 of 4.05 μM), used as control drug. Furthermore, the compound QDS3 exhibited a selective effect, being 40.35 times more toxic to the amastigote form than to the host cell. Additionally, promastigotes of L. amazonensis treated with this compound exhibited characteristics of cells in the process of apoptosis such as mitochondrial membrane depolarization, mitochondrial swelling, increase of ROS production, phosphatidylserine externalization, reduced and rounded shape, and cell cycle alteration. The integrity of the plasma membrane remained unaltered, excluding necrosis in treated promastigotes. The compound QDS3 inhibited the formation of autophagic vacuoles, which may have contributed to parasite death by preventing autophagic mechanisms in the removal of damaged organelles, intensifying the damage caused by the treatment, highlighting the antileishmanial effect of this compound. In addition, treatment with QDS3 induced increased ROS levels in L. amazonensis -infected macrophages, but not in uninfected host cell. These data reinforce that the induction of oxidative stress is one of the main toxic effects caused by the treatment with the compound QDS3 in L. amazonensis , causing irreversible damage and triggering a selective death of intracellular parasites. Data shown here confirm the biological activity of quinoline derivatives and encourage future in vivo studies with this compound in the murine model. Highlights • Organic salts were screened as potential antileishmanial agents. • The quinoline derivative salt (QDS3) exhibited the best antileishmanial effect. • QDS3 induced apoptosis in promastigotes of L. amazonensis. • This compound inhibited the formation of autophagic vacuoles. • The oxidative stress can be the key event in the induction of apoptosis. [ABSTRACT FROM AUTHOR]

We previously reported an alfalfa half-sib family, HS-B, with improved salt tolerance, compared to parental plants, P-B. In this study, we conducted additional experiments to address potential physiological mechanisms that may contribute to salt tolerance in HS-B. Vegetatively propagated HS-B and P-B plants were treated with a nutrient solution (control) or a nutrient solution containing NaCl ( EC = 12 dS/m). Shoots and roots were harvested at various time points after treatment for quantification of proline, soluble sugar, and H2O2 using spectrophotometers. Subcellular localization and quantification of Na in roots were conducted using a Na+-specific dye under a confocal microscope. HS-B produced 86 and 89% greater shoot and root dry biomass, respectively, compared to parental plants, P-B, under salinity in the greenhouse. Under saline conditions the HS-B shoots accumulated 115% and roots 55% more soluble sugars than P-B counterparts. The non-saline HS-B shoots, however, showed 72% less soluble sugars than the non-saline P-B plants. Under saline conditions HS-B accumulated 39% less proline in shoots, while roots accumulated 56% more proline, compared to their P-B parents. HS-B plants also showed a greater reduction of stomatal conductance under mild saline stress. HS-B shoots and roots contained 3-4 times less reactive oxygen species (H2O2) after salt treatment compared to P-B plants. Sodium localization and distribution analysis using Na+-specific dye revealed HS-B plants accumulated 88% and 48% less Na+ in stele and xylem vessels compared to P-B. The study provides insights into the potential mechanisms that may contribute to salt tolerance in HS-B: maintaining RWC by accumulating soluble sugars while reducing transpiration, maintaining healthy status by reducing oxidative stresses, and preventing salt toxicity by reducing accumulation of Na+ inside root cells and xylem. [ABSTRACT FROM AUTHOR]

Key points Recent studies have shown that high salt (HS) intake leads to endothelial dysfunction and impaired vascular reactivity in different vascular beds in both animal and human models, due to increased oxidative stress., The objective of this study was to assess vascular response to flow-induced dilatation (FID) and to elucidate the role of vascular oxidative stress/antioxidative capacity in middle cerebral arteries (MCAs) of HS-fed rats in vitro., The novelty of this study is in demonstrating impaired flow-induced dilatation of MCAs and down-regulation of vascular antioxidant genes with HS intake, leading to increased levels of oxidative stress in blood vessels and peripheral lymph organs, which together contribute to impaired FID., In addition, results show increased oxidative stress in leukocytes of peripheral lymph organs, suggesting the occurrence of inflammatory processes due to HS intake., Recirculation of leukocytes might additionally increase vascular oxidative stress in vivo., Abstract The aim of this study was to determine flow-induced dilatation (FID) and the role of oxidative stress/antioxidative capacity in isolated, pressurized middle cerebral arteries (MCAs) of high salt (HS)-fed rats. Healthy male Sprague-Dawley rats (11 weeks old) were fed low salt (0.4% NaCl; LS group) or high salt (4% NaCl; HS group) diets for 1 week. Reactivity of MCAs in response to stepwise increases in pressure gradient (Δ10-Δ100 mmHg) was determined in the absence or presence of the superoxide dismutase (SOD) mimetic TEMPOL and/or the nitric oxide synthases (NOS) inhibitor Nω-nitro- l-arginine methyl ester ( l-NAME). mRNA levels of antioxidative enzymes, NAPDH-oxidase components, inducible (iNOS) and endothelial nitric oxide synthases (eNOS) were determined by quantitative real-time PCR. Blood pressure (BP), antioxidant enzymes activity, oxidative stress in peripheral leukocytes, lipid peroxidation products and the antioxidant capacity of plasma were measured for both groups. FID was reduced in the HS group compared to the LS group. The presence of TEMPOL restored dilatation in the HS group, with no effect in the LS group. Expression of glutathione peroxidase 4 (GPx4) and iNOS in the HS group was significantly decreased; oxidative stress was significantly higher in the HS group compared to the LS group. HS intake significantly induced basal reactive oxygen species production in the leukocytes of mesenteric lymph nodes and splenocytes, and intracellular production after stimulation in peripheral lymph nodes. Antioxidant enzyme activity and BP were not affected by HS diet. Low GPx4 expression, increased superoxide production in leukocytes, and decreased iNOS expression are likely to underlie increased oxidative stress and reduced nitric oxide bioavailability, leading to impairment of FID in the HS group without changes in BP values. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Recent data would suggest pre-menopausal insulin resistant women are more prone to diastolic dysfunction than men, yet it is unclear why. We and others have reported that transgenic (mRen2)27 (Ren2) rats overexpressing the murine renin transgene are insulin resistant due to oxidative stress in insulin sensitive tissues. As increased salt intake promotes inflammation and oxidative stress, we hypothesized that excess dietary salt would promote diastolic dysfunction in transgenic females under conditions of excess tissue Ang II and circulating aldosterone levels. Materials/methods: For this purpose we evaluated cardiac function in young female Ren2 rats or age-matched Sprague–Dawley (SD) littermates exposed to a high (4%) salt or normal rat chow intake for three weeks. Results: Compared to SD littermates, at 10weeks of age, female Ren2 rats fed normal chow showed elevations in left ventricular (LV) systolic pressures, LV and cardiomyocyte hypertrophy, and displayed reductions in LV initial filling rate accompanied by increases in 3-nitrotyrosine content as a marker of oxidant stress. Following 3weeks of a salt diet, female Ren2 rats exhibited no further changes in LV systolic pressure, insulin resistance, or markers of hypertrophy but exaggerated increases in type 1 collagen, 3-nitrotryosine content, and diastolic dysfunction. These findings occurred in parallel with ultrastructural findings of pericapillary fibrosis, increased LV remodeling, and mitochondrial biogenesis. Conclusion: These data suggest that a diet high in salt in hypertensive female Ren2 rats promotes greater oxidative stress, maladaptive LV remodeling, fibrosis, and associated diastolic dysfunction without further changes in LV systolic pressure or hypertrophy. [Copyright &y& Elsevier]

Abstract: This study describes the transcriptional analysis of antioxidant and immune defense genes in gills tissue of disk abalone exposed to thermal, salinity and hypoxia-related stress, using quantitative real-time PCR. Results showed that manganese superoxide dismutase (MnSOD), copper zinc superoxide dismutase (CuZnSOD), catalase (CAT), thioredoxin peroxidase (TPx), selenium dependant glutathione peroxidase (SeGPx), and thioredoxin-2 (TRx-2) transcripts were expressed differently in gills, and that they respond collectively as a classical enzymatic antioxidant defense system in abalone. Comparative analysis of expression profiles indicated that CAT, TPx and SeGPx transcripts were significantly up-regulated (p <0.05) by all three physical stress conditions — thermal (28 °C), salinity (25‰) and hypoxia — relative to levels in respective controls. In contrast, CuZnSOD and TRx-2 transcription were down-regulated in response to thermal stress. Interestingly, all the antioxidant transcripts exhibited significant up-regulation in response to salinity-related stress. Meanwhile, hypoxia caused up-regulation of the MnSOD, CAT, TPx and SeGPx, but not the CuZnSOD and TRx-2 transcripts. One of the most significant outcomes was the more than 10-fold induction of SeGPx, suggesting that SeGPx is a potential biomarker gene among antioxidant enzymes, under conditions of physical stress. The effects of physical stress on the transcriptional responses of immune functional genes namely suppressor of cytokine signaling-2 (SOCS-2) and myxovirus resistance (Mx) were investigated. We observed that salinity and hypoxia increase both the SOCS-2 and Mx transcripts, while thermal stress at 28 °C exerts less of an effect, producing mixed transcriptional responses (both up and down regulation). Based upon these results, we postulate that abalones utilize antioxidant and immune defense mechanisms together to overcome physical stresses. [Copyright &y& Elsevier]

Abstract: The present work describes a two-stage approach to analyzing combustion-generated samples for their potential to produce oxidant stress. This approach is illustrated with the two commonly encountered transition metals, copper and iron. First, their abilities to generate hydroxyl radical were measured in a cell-free, phosphate-buffered saline solution containing ascorbate and/or citrate. Second, their abilities to induce heme oxygenase-1 in cultured human epidermal keratinocytes were assessed in cell culture. Combustion-generated copper oxide nanoparticles were active in both assays and were found to be soluble in culture medium. Depletion of glutathione in the cells or loading the cells with ascorbate greatly increased heme oxygenase-1 induction in the presence of copper. By contrast, iron oxide nanoparticles were active in the phosphate-buffered saline but not in cell culture, and they aggregated in culture medium. Soluble salts of copper and iron exhibited the same contrast in activities as the respective combustion-generated particles. The results suggest that the capability of combustion-generated environmental samples to produce oxidant stress can be screened effectively in a two step process, first in phosphate-buffered saline with ascorbate and subsequently in epithelial cell culture for those exhibiting activity initially. The results also point to an unanticipated interaction in cells of oxidant stress-generating metals with an antioxidant (ascorbate) that is usually missing in culture medium formulations. Thus, ascorbate supplementation of cultured human cells is likely to improve their ability to model the in vivo effects of particulate matter containing copper and other redox-active metals. [Copyright &y& Elsevier]

In this study we examined the short- and long-term impact of early life dietary sodium (Na) on prenatally programmed hypertension. Hypertension was induced in rat offspring by a maternal low protein (LP) diet. Control and LP offspring were randomized to a high (HS), standard (SS), or low (LS) Na diet after weaning. On the SS diet, the LP pups developed hypertension by 6 weeks of age. The development of hypertension was prevented by the LS diet and exacerbated by the HS diet. Kidney nitrotyrosine content, a measure of oxidative stress, was reduced by the LS diet compared with the HS diet. The modified diets had no effect on control pups. A group of animals on the SS diet was followed up to 51 weeks of age after an early life 3-week exposure to the HS or LS diet. This brief early exposure of LP animals to the LS diet prevented the later development of hypertension and ameliorated the nephrosclerosis observed after early exposure to the HS diet. The LP offspring with early exposure to LS diet had lost their salt-sensitivity when challenged with the HS diet at the age of 43–49 weeks. No effect of early life dietary Na was observed in control animals. These results show that hypertension in this model is salt sensitive and may, in part, be mediated by salt-induced renal oxidative stress and that there may exist a developmental window which allows postnatal “reprogramming” of the hypertension. [ABSTRACT FROM AUTHOR]

Abstract: Some medicinal plants need to be cultivated commercially in order to meet the ever-increasing demand for medicinal plants for the indigenous systems of medicine as well as for the pharmaceutical industry; in this regard, it seems significant to test the important medicinal plants for their salt-tolerance capacity, with a view to exploiting the saline lands for medicinal plant cultivation. Phyllanthus amarus plants were grown in the presence of NaCl in order to study the effect of NaCl (80 mM NaCl) in the induction of oxidative stress in terms of lipid peroxidation (TBARS content), H2O2 content, osmolyte concentration, proline(PRO)-metabolizing enzymes, and antioxidant enzyme activities. Groundwater was used for irrigation of control plants. Plants were uprooted randomly on 90 days after sowing (DAS). NaCl-stressed plants showed increased TBARS, H2O2, glycine betaine (GB), and PRO contents, whereas NaCl uptake decreased proline oxidase (PROX) activity and increased γ-glutamyl kinase (γ-GK) activity when compared to control. The antioxidant enzymes superoxide dismutase (SOD), peroxidase (POX) and catalase (CAT) were increased under salinity. To cite this article: C.A. Jaleel et al., C. R. Biologies 330 (2007). [Copyright &y& Elsevier]

The molecular pathophysiology of hypertension is probably like a jigsaw puzzle of different but overlapping sets of factors and pathways that vary from one patient or one group of patients to another. Mitochondrial and metabolic abnormalities could be crucial pieces of this puzzle. [ABSTRACT FROM AUTHOR]