scholarly journals Nitrogenous Nutrition Affects Uptake of Arsenic and Defense Enzyme Responses in Wheat

2021 ◽  
Vol 30 (3) ◽  
pp. 2213-2231
Author(s):  
Marína Maglovski ◽  
Ľubomír Rybanský ◽  
Marek Bujdoš ◽  
Lubomír Adamec ◽  
Monika Bardáčová ◽  
...  
Keyword(s):  
2012 ◽  
Vol 18 (3) ◽  
pp. 359
Author(s):  
Jia LI ◽  
Delin XU ◽  
Hai LONG ◽  
Guangbing DENG ◽  
Zhifen PAN ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Lorenzo Di Cesare Mannelli ◽  
Matteo Zanardelli ◽  
Laura Micheli ◽  
Carla Ghelardini

Peroxisomes provide glial cells with protective functions against the harmful effects of H2O2on neurons and peroxisome impairment results in nervous lesions. Agonists of theγ-subtype of the Peroxisome-Proliferator-Activated-Receptors (PPAR) have been proposed as neuroprotective agents in neurodegenerative disorders. Nevertheless, the role of PPAR-γalterations in pathophysiological mechanisms and the relevance of peroxisome functions in the PPAR-γeffects are not yet clear. In a primary cell culture of rat astrocytes, the irreversible PPAR-γantagonist GW9662 concentration-dependently decreased the activity of catalase, the most important antioxidant defense enzyme in peroxisomes. Catalase functionality recovered in a few days and the PPAR-γagonist rosiglitazone promoted reversal of enzymatic damage. The reversible antagonist G3335 reduced both the activity and expression of catalase in a rosiglitazone-prevented manner. G3335 reduced also the glutathione reductase expression, indicating that enzyme involved in glutathione regeneration was compromised. Neither the PPAR-αtarget gene Acyl-Coenzyme-A-oxidase-1 nor the mitochondrial detoxifying enzyme NADH:ubiquinone-oxidoreductase (NDFUS3) was altered by PPAR-γinhibition. In conclusion, PPAR-γinhibition induced impairment of catalase in astrocytes. A general decrease of the antioxidant defenses of the cell suggests that a PPAR-γhypofunction could participate in neurodegenerative mechanisms through peroxisomal damage. This series of experiments could be a useful model for studying compounds able to restore peroxisome functionality.


Blood ◽  
2005 ◽  
Vol 106 (10) ◽  
pp. 3594-3601 ◽  
Author(s):  
Margaret E. Tome ◽  
David B. F. Johnson ◽  
Lisa M. Rimsza ◽  
Robin A. Roberts ◽  
Thomas M. Grogan ◽  
...  

AbstractDiffuse large B-cell lymphoma (DLBCL) is a heterogeneous disease in which approximately 40% of the patients respond well to current chemotherapy, but the prognosis for the other 60% is poor. The Leukemia/Lymphoma Molecular Profiling Project (LLMPP) used microarray technology to define a molecular profile for each of 240 patients with DLBCL and develop a molecular outcome predictor score that accurately predicted patient survival. Data from our laboratory and others suggest that alterations in antioxidant defense enzyme levels and redox environment can be oncogenic and affect the response to glucocorticoid treatment, one of the components of combination chemotherapy regimens for lymphoma. The goal of the current study was to reanalyze the LLMPP microarray data to determine whether the levels of antioxidant defense enzymes and redox proteins were correlated with prognosis in DLBCL. We found that patients with DLBCL with the worst prognosis, according to the outcome predictor score, had decreased expression of catalase, glutathione peroxidase, manganese superoxide dismutase, and VDUP1, a protein that inhibits thioredoxin activity. The data suggest that the patients with the worst prognosis combine a decrease in antioxidant defense enzyme expression with an increase in thioredoxin system function (the redox signature score).


2018 ◽  
Vol 8 ◽  
Author(s):  
E. Patrick Fuerst ◽  
Matthew S. James ◽  
Anne T. Pollard ◽  
Patricia A. Okubara
Keyword(s):  
Wild Oat ◽  

2018 ◽  
Vol 391 (11) ◽  
pp. 1237-1245 ◽  
Author(s):  
Xia Zhu ◽  
Ya-qin Cheng ◽  
Qian Lu ◽  
Lei Du ◽  
Xiao-xing Yin ◽  
...  

2020 ◽  
Vol 21 (20) ◽  
pp. 7759
Author(s):  
Paola Leonetti ◽  
Sergio Molinari

Two wild-type field populations of root-knot nematodes (Mi-Vfield, Mj-TunC2field), and two isolates selected for virulence in laboratory on resistant tomato cultivars (SM2V, SM11C2), were used to induce a resistance reaction in tomato to the soil-borne parasites. Epigenetic and metabolic mechanisms of resistance were detected and compared with those occurring in partially or fully successful infections. The activated epigenetic mechanisms in plant resistance, as opposed to those activated in infected plants, were detected by analyzing the methylated status of total DNA, by ELISA methods, and the expression level of key genes involved in the methylation pathway, by qRT-PCR. DNA hypo-methylation and down-regulation of two methyl-transferase genes (CMT2, DRM5), characterized the only true resistant reaction obtained by inoculating the Mi-1.2-carrying resistant tomato cv Rossol with the avirulent field population Mi-Vfield. On the contrary, in the roots into which nematodes were allowed to develop and reproduce, total DNA was generally found to be hyper-methylated and methyl-transferase genes up-loaded. DNA hypo-methylation was considered to be the upstream mechanism that triggers the general gene over-expression observed in plant resistance. Gene silencing induced by nematodes may be obtained through DNA hyper-methylation and methyl-transferase gene activation. Plant resistance is also characterized by an inhibition of the anti-oxidant enzyme system and activation of the defense enzyme chitinase, as opposed to the activation of such a system and inhibition of the defense enzyme glucanase in roots infested by nematodes.


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