scholarly journals Oxidative damages induced by short-term exposure to cadmium in bean plants: Protective role of salicylic acid

2013 ◽  
Vol 85 ◽  
pp. 32-38 ◽  
Author(s):  
Issam Saidi ◽  
Marwa Ayouni ◽  
Amina Dhieb ◽  
Yassine Chtourou ◽  
Wided Chaïbi ◽  
...  
Heart ◽  
2010 ◽  
Vol 96 (24) ◽  
pp. 1990-1996 ◽  
Author(s):  
J.-B. Henrotin ◽  
M. Zeller ◽  
L. Lorgis ◽  
Y. Cottin ◽  
M. Giroud ◽  
...  

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 648-648
Author(s):  
Niraj R. Joshi ◽  
Sudip Banerjee ◽  
Raktim Mukherjee ◽  
Shail Chaube ◽  
A.V. Ramachandran

HortScience ◽  
2011 ◽  
Vol 46 (2) ◽  
pp. 260-264 ◽  
Author(s):  
Mason T. MacDonald ◽  
Rajasekaran R. Lada ◽  
Alex I. Martynenko ◽  
Martine Dorais ◽  
Steeve Pepin ◽  
...  

Needle loss after harvest is a major problem for Atlantic Canada's Christmas tree and greenery industry. Ethylene is a signal for abscission in balsam fir, but preliminary studies have suggested that the role of ethylene may be influenced by length of exposure. Short-term and long-term ethylene exposure experiments were conducted. Branches were exposed to ethylene for 24 h (short-term) or continuously (long-term) at concentrations of 0 to 1000 ppm. The response variables measured were needle retention duration (NRD), average water use (AWU), and xylem pressure potential (XPP). Short-term exposure to any concentration of ethylene delayed needle abscission by 30 to 40 days. In contrast, long-term exposure to all concentrations of ethylene accelerated abscission, most evident by a 21-day decrease in NRD at 1000 ppm ethylene. There was a 60% decrease in NRD, 160% decrease (more negative) in XPP, and 80% increase in AWU as a result of long-term exposure to ethylene. Overall, our results demonstrate an opposite effect of short-term and long-term ethylene exposure, which suggests that short-term exposure to ethylene might help to precondition balsam fir and delay needle abscission during postharvest handling.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1415.1-1415
Author(s):  
F. Ingegnoli ◽  
T. Ubiali ◽  
T. Schioppo ◽  
V. Longo ◽  
S. Iodice ◽  
...  

Background:Air pollution is believed to cause oxidative stress and systemic inflammation, that could trigger autoimmunity in rheumatoid arthritis (RA). Several epidemiological studies investigated the possible role of air pollution in the outbreak of RA with controversial results. As far as we know, studies on the effects on disease activity of short-term exposure have not been published.Objectives:To evaluate the impact of short-term exposure to air pollutants (daily mean PM10, PM2.5, NO2and O3) on disease activity in patients with RA.Methods:Consecutive patients with RA (ACR/EULAR Criteria 2010) resident in Lombardy (Italy) were enrolled. In each patient Disease Activity Score on 28 joints (DAS28), Simple Disease Activity Index (SDAI) were assessed. Daily PM10, PM2.5, NO2and O3concentrations, estimated by Regional Environmental Protection Agency at municipality resolution, were used to assign short-term exposure from day of visit back to 14 days. Multivariable linear regression models were performed to identify the day of the pollutants independently associated with disease activity indices, adjusting for the variables significant at the univariate analysis. β coefficients were reported for 1 μg/m3increments of pollutants’ concentrations.Results:422 RA patients were enrolled in the study between January and June 2018: 81.5% females, mean age 58.2±13.3 years, mean disease duration 16.1±11.5 years, 27.3% current smokers, 59.5% RF positivity, 54.5% ACPA positivity. Sparse punctual statistically significant negative associations emerged at the multivariate analysis between PM10, PM2.5, NO2and the outcomes, although with very low estimates, whereas positive associations resulted for O3.Afterwards patients were stratified in 3 subgroups according to their ongoing treatment (no therapy, n=25, conventional synthetic Disease Modifying anti-Rheumatic Drugs -DMARDs-, n=108 and biological or targeted synthetic DMARDs, n=289). A statistical significance was found by analysing the influence of therapy on the interaction between PM2.5and DAS28 (Figure below): a positive trend between PM2.5and DAS28 appeared in the first two groups (no therapy, 0.013±0.007, p=0.06 and csDMARDs, 0.006±0.004, p=0.17), whereas a statistically significant inverse association was seen in the b/tsDMARDs group (-0.005±0.002, p=0.01). Therapy interaction was particularly evident in several days before the visit also for O3.Conclusion:The changes of the outcome measures related to the increase of the pollutants’ levels did not reach the minimal clinically important difference, therefore air pollution seems barely relevant on disease activity once the loss of tolerance is established in RA. O3and PM/NO2always exhibit an opposite performance having inversely proportional atmospheric concentrations, whereas the biological role of this substance is still matter of debate and will need further understanding. Therapy seems to be able to interact with the relation between air pollutants and the parameters considered.Disclosure of Interests:Francesca Ingegnoli: None declared, Tania Ubiali: None declared, Tommaso Schioppo: None declared, Valentina Longo: None declared, Simona Iodice: None declared, Ennio Giulio Favalli Consultant of: Consultant and/or speaker for BMS, Eli-Lilly, MSD, UCB, Pfizer, Sanofi-Genzyme, Novartis, and Abbvie, Speakers bureau: Consultant and/or speaker for BMS, Eli-Lilly, MSD, UCB, Pfizer, Sanofi-Genzyme, Novartis, and Abbvie, Orazio De Lucia: None declared, Antonella Murgo: None declared, Valentina Bollati: None declared, Roberto Caporali Consultant of: AbbVie; Gilead Sciences, Inc.; Lilly; Merck Sharp & Dohme; Celgene; Bristol-Myers Squibb; Pfizer; UCB, Speakers bureau: Abbvie; Bristol-Myers Squibb; Celgene; Lilly; Gilead Sciences, Inc; MSD; Pfizer; Roche; UCB


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1112-1112
Author(s):  
Cornelia Fischer ◽  
Brigitte Spath ◽  
Ali Amirkhosravi ◽  
Walter Fiedler ◽  
Carsten Bokemeyer ◽  
...  

Abstract Abstract 1112 Acute myelogenous leukemia (AML) may be complicated by DIC. TF plays a critical role in AML-associated coagulopathy, and induction of apoptosis significantly increases TF PCA on leukemic blasts, mainly via phosphatidylserine (PS) membrane exposure. However, PDI, a thiol isomerase with oxidoreductase and chaperone activity, has also been implicated in cellular TF regulation. Particularly, PDI inhibitors have been shown to exert antithrombotic activity in animal models. Besides its predominant localization in the endoplasmic reticulum, PDI is present on cell surfaces, where it may represent a promising therapeutic target. We investigated the effect of PDI inhibitors on the expression of TF PCA by leukemic HL60 and THP1 cells to explore their potential as anticoagulant drugs for the prevention and/or treatment of AML-associated DIC. Using a fluorescence-based insulin reduction assay, we confirmed inhibition of recombinant human PDI by bacitracin and quercetin-3-rutinoside (also known as rutin and recently shown to be a specific PDI inhibitor) with IC50 values of 0.6 mM and 14 μM, respectively, showing >95% inhibition at 1 mM (bacitracin) and 50 μM (rutin). Significant insulin reductase activity was observed on HL60 cells, and this activity was inhibited by 75% and 49% using 1 mM bacitracin and 100 μM rutin, respectively, suggesting the presence of additional, PDI-independent thiol isomerase activity. Short-term treatment with 100 μM rutin for 15 min also inhibited TF PCA on HL60 cells by 37%. Importantly, the inhibitory effect of rutin on cell-associated PDI and TF activity was completely abolished by cell washing, confirming previous evidence that rutin is a reversible PDI inhibitor. When HL60 cells were exposed to rutin (100 μM) for 24 hrs, cell-associated TF PCA was increased 2.3-fold (P<0.01), an effect that was accompanied by enhanced PS exposure, as assessed by annexin V-FITC binding (positive cells, 32±11 vs. 10±4%; P<0.01), and increased PCA of cellular microparticles (MPs) isolated from culture supernatants, as evidenced by the thrombin generation parameters lag phase (LP, 14±1 vs. 19±4 min), peak thrombin (PT, 55±17 vs. 22±14 nM), and area under the curve (AUC, 1193±329 vs. 476±347 nM*min; P<0.01). Interestingly, treatment with 100 μM rutin also resulted in a 1.7-fold increase in total cellular TF antigen (P=0.07). The effects of long-term incubation with bacitracin (1 mM) were even more pronounced, involving an 8.3-fold and 4.6-fold increase in cell-associated TF PCA and total cellular TF antigen, respectively. PS exposure (45±9%) and shedding of procoagulant MPs (LP, 7±1 min; PT, 175±49 nM; AUC, 2756±402 nM*min) were also significantly increased. While neither short-term nor long-term exposure to rutin affected TF PCA on THP1 cells, co-incubation with rutin dose-dependently (10–100 μM) inhibited daunorubicin-induced TF PCA in this cell model, an effect that could not be explained by decreased PS exposure. Importantly, both the reaction pattern of HL60 and that of THP1 cells were reproduced ex vivo using myeloblasts from AML patients. In summary, our findings suggest a highly complex and context-dependent role of PDI in leukemic-cell TF PCA expression. While short-term exposure to rutin can reversibly inhibit both PDI and TF activity, long-term exposure may result in significantly increased cellular TF PCA and MP shedding, pointing to a possible role of PDI in PS homeostasis, cytoskeleton rearrangement, and/or TF recycling. In addition, induction of leukemic-cell apoptosis and necrosis by cytotoxic drugs, which is associated with an early loss in membrane integrity and enhanced accessibility of cytoplasmic enzymes, may involve an additional role of (intracellular) PDI in the efficient presentation of TF PCA by AML blasts. Disclosures: No relevant conflicts of interest to declare.


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