scholarly journals Role of hydrogen peroxide and the redox state of ascorbate in the induction of antioxidant enzymes in pea leaves under excess light stress

2004 ◽  
Vol 31 (4) ◽  
pp. 359 ◽  
Author(s):  
Jose A. Hernández ◽  
Carolina Escobar ◽  
Gary Creissen ◽  
Phil M. Mullineaux

In this work we used two different pea cultivars, JI281 is a semidomesticated land race of pea from Ethiopia whereas JI399 is a typical domesticated pea variety. Exposure of pea leaves to excess light (EL) for 1 h caused a reversible photoinhibition of photosynthesis as showed by changes in Fv / Fm. Although little difference existed between the two pea genotypes with respect to photoinhibition, after 60 min of EL the decline in Fv / Fm was higher in JI281 than in JI399 leaves. As a consequence of EL, H2O2 increased in both pea cultivars, whereas lipid peroxidation and protein oxidation slightly increased, although differences between cultivars were minimal. The redox state of ascorbate shifted towards its oxidized form under EL stress in both cultivars. Transcript levels of genes coding antioxidant enzymes varied with EL in both cultivars, but the response was more pronounced in JI399. The induction observed during EL was maintained or increased after the stress period, as occurred for cytGR and chlMDHAR. GR protein accumulation and activity correlated with the transcript accumulation in JI399, but not in JI288. In this work, a possible role for H2O2 and redox status of ascorbate in the photoxidative stress signalling is discussed.

2021 ◽  
Vol 22 (12) ◽  
pp. 6183
Author(s):  
Delia Acevedo-León ◽  
Lidia Monzó-Beltrán ◽  
Segundo Ángel Gómez-Abril ◽  
Nuria Estañ-Capell ◽  
Natalia Camarasa-Lillo ◽  
...  

The role of oxidative stress (OS) in cancer is a matter of great interest due to the implication of reactive oxygen species (ROS) and their oxidation products in the initiation of tumorigenesis, its progression, and metastatic dissemination. Great efforts have been made to identify the mechanisms of ROS-induced carcinogenesis; however, the validation of OS byproducts as potential tumor markers (TMs) remains to be established. This interventional study included a total of 80 colorectal cancer (CRC) patients and 60 controls. By measuring reduced glutathione (GSH), its oxidized form (GSSG), and the glutathione redox state in terms of the GSSG/GSH ratio in the serum of CRC patients, we identified significant changes as compared to healthy subjects. These findings are compatible with the effectiveness of glutathione as a TM. The thiol redox state showed a significant increase towards oxidation in the CRC group and correlated significantly with both the tumor state and the clinical evolution. The sensitivity and specificity of serum glutathione levels are far above those of the classical TMs CEA and CA19.9. We conclude that the GSSG/GSH ratio is a simple assay which could be validated as a novel clinical TM for the diagnosis and monitoring of CRC.


2017 ◽  
Vol 86 (4) ◽  
Author(s):  
Ewelina Ratajczak ◽  
Karl Josef Dietz

Peroxiredoxins (Prx) are important regulators of the redox status of tree seeds during maturation and long-term storage. Thioredoxins (Trx) are redox transmitters and thereby regulate Prx activity. Current research is focused on the association of Trx with Prx in tree seeds differing in the tolerance to desiccation. The results will allow for better understanding the regulation of the redox status in orthodox, recalcitrant, and intermediate seeds. The findings will also elucidate the role of the redox status during the loss of viability of sensitive seeds during drying and long-term storage.


2014 ◽  
Vol 369 (1640) ◽  
pp. 20130228 ◽  
Author(s):  
Eiri Heyno ◽  
Gilles Innocenti ◽  
Stéphane D. Lemaire ◽  
Emmanuelle Issakidis-Bourguet ◽  
Anja Krieger-Liszkay

In photosynthetic organisms, sudden changes in light intensity perturb the photosynthetic electron flow and lead to an increased production of reactive oxygen species. At the same time, thioredoxins can sense the redox state of the chloroplast. According to our hypothesis, thioredoxins and related thiol reactive molecules downregulate the activity of H 2 O 2 -detoxifying enzymes, and thereby allow a transient oxidative burst that triggers the expression of H 2 O 2 responsive genes. It has been shown recently that upon light stress, catalase activity was reversibly inhibited in Chlamydomonas reinhardtii in correlation with a transient increase in the level of H 2 O 2 . Here, it is shown that Arabidopsis thaliana mutants lacking the NADP–malate dehydrogenase have lost the reversible inactivation of catalase activity and the increase in H 2 O 2 levels when exposed to high light. The mutants were slightly affected in growth and accumulated higher levels of NADPH in the chloroplast than the wild-type. We propose that the malate valve plays an essential role in the regulation of catalase activity and the accumulation of a H 2 O 2 signal by transmitting the redox state of the chloroplast to other cell compartments.


2012 ◽  
Vol 169 (10) ◽  
pp. 929-939 ◽  
Author(s):  
Alessio Fini ◽  
Lucia Guidi ◽  
Francesco Ferrini ◽  
Cecilia Brunetti ◽  
Martina Di Ferdinando ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 435
Author(s):  
Elena Kalinina ◽  
Maria Novichkova

S-glutathionylation and S-nitrosylation are reversible post-translational modifications on the cysteine thiol groups of proteins, which occur in cells under physiological conditions and oxidative/nitrosative stress both spontaneously and enzymatically. They are important for the regulation of the functional activity of proteins and intracellular processes. Connecting link and “switch” functions between S-glutathionylation and S-nitrosylation may be performed by GSNO, the generation of which depends on the GSH content, the GSH/GSSG ratio, and the cellular redox state. An important role in the regulation of these processes is played by Trx family enzymes (Trx, Grx, PDI), the activity of which is determined by the cellular redox status and depends on the GSH/GSSG ratio. In this review, we analyze data concerning the role of GSH/GSSG in the modulation of S-glutathionylation and S-nitrosylation and their relationship for the maintenance of cell viability.


Author(s):  
Lyudmila P. Kuzmina ◽  
Anastasiya G. Khotuleva ◽  
Evgeniy V. Kovalevsky ◽  
Nikolay N. Anokhin ◽  
Iraklij M. Tskhomariya

Introduction. Various industries widely use chrysotile asbestos, which determines the relevance of research aimed at the prevention of asbestos-related diseases. It is promising to assess the role of specific genes, which products are potentially involved in the development and regulation of certain links in the pathogenesis of asbestosis, forming a genetic predisposition to the disease. The study aims to analyze the presence of associations of genetic polymorphism of cytokines and antioxidant enzymes with asbestosis development. Materials and methods. Groups were formed for examination among employees of OJSC "Uralasbest" with an established diagnosis of asbestosis and without lung diseases. For each person included in the study, dust exposure doses were calculated considering the percentage of time spent at the workplace during the shift for the entire work time. Genotyping of single nucleotide polymorphisms of cytokines IL1b (rs16944), IL4 (rs2243250), IL6 (rs1800795), TNFα (rs1800629) and antioxidant enzymes SOD2 (rs4880), GSTP1 (rs1610011), CAT (rs1001179) was carried out. Results. The authors revealed the associations of polymorphic variants A511G IL1b gene (OR=2.457, 95% CI=1.232-4.899) and C47T SOD2 gene (OR=1.705, 95% CI=1.055-2.756) with the development of asbestosis. There was an increase in the T allele IL4 gene (C589T) frequency in persons with asbestosis at lower values of dust exposure doses (OR=2.185, 95% CI=1.057-4.514). The study showed the associations of polymorphism C589T IL4 gene and C174G IL6 gene with more severe asbestosis, polymorphism A313G GSTP1 gene with pleural lesions in asbestosis. Conclusion. Polymorphic variants of the genes of cytokines and antioxidant enzymes, the protein products directly involved in the pathogenetic mechanisms of the formation of asbestosis, contribute to forming a genetic predisposition to the development and severe course of asbestosis. Using the identified genetic markers to identify risk groups for the development and intense period of asbestos-related pathology will optimize treatment and preventive measures, considering the organism's characteristics.


2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.


2019 ◽  
Vol 25 (16) ◽  
pp. 1889-1912 ◽  
Author(s):  
Rosario Pastor ◽  
Josep A. Tur

Background: Antioxidant supplementation has become a common practice among athletes to theoretically achieve a reduction in oxidative stress, promote recovery and improve performance. Objective: To assess the effect of antioxidant supplements on exercise. Methods: A systematic literature search was performed up to January 2019 in MEDLINE via EBSCO and Pubmed, and in Web of Sciences based on the following terms: “antioxidants” [Major] AND “exercise” AND “adaptation”; “antioxidant supplement” AND “(exercise or physical activity)” AND “(adaptation or adjustment)” [MesH]. Thirty-six articles were finally included. Results: Exhaustive exercise induces an antioxidant response in neutrophils through an increase in antioxidant enzymes, and antioxidant low-level supplementation does not block this adaptive cellular response. Supplementation with antioxidants appears to decrease oxidative damage blocking cell-signaling pathways associated with muscle hypertrophy. However, upregulation of endogenous antioxidant enzymes after resistance training is blocked by exogenous antioxidant supplementation. Supplementation with antioxidants does not affect the performance improvement induced by resistance exercise. The effects of antioxidant supplementation on physical performance and redox status may vary depending on baseline levels. Conclusion: The antioxidant response to exercise has two components: At the time of stress and adaptation through genetic modulation processes in front of persistent pro-oxidant situation. Acute administration of antioxidants immediately before or during an exercise session can have beneficial effects, such as a delay in the onset of fatigue and a reduction in the recovery period. Chronic administration of antioxidant supplements may impair exercise adaptations, and is only beneficial in subjects with low basal levels of antioxidants.


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