scholarly journals Antichagasic Activity of Komaroviquinone Is Due to Generation of Reactive Oxygen Species Catalyzed by Trypanosoma cruzi Old Yellow Enzyme

2005 ◽  
Vol 49 (12) ◽  
pp. 5123-5126 ◽  
Author(s):  
Nahoko Uchiyama ◽  
Zakayi Kabututu ◽  
Bruno K. Kubata ◽  
Fumiyuki Kiuchi ◽  
Michiho Ito ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Life Cycle ◽  
Trypanosoma Cruzi ◽  
Reductase Activity ◽  
Reactive Oxygen ◽  
Semiquinone Radical ◽  
Oxygen Species ◽  
Old Yellow Enzyme ◽  
Interesting Candidate

ABSTRACT A novel potent trypanocidal diterpene, komaroviquinone, was reduced by Trypanosoma cruzi old yellow enzyme (TcOYE) to its semiquinone radical. The reductase activity in trypanosome lysates was completely immunoabsorbed by anti-TcOYE antibody. Since TcOYE is expressed throughout the T. cruzi life cycle, komaroviquinone is an interesting candidate for developing new antichagasic drugs.

The production of reactive oxygen species enhanced with the reduction of menadione by active thioredoxin reductase

Metallomics ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1490-1497 ◽  
Author(s):  
Jing Li ◽  
Xin Zuo ◽  
Ping Cheng ◽  
Xiaoyuan Ren ◽  
Shibo Sun ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Molecular Oxygen ◽  
Thioredoxin Reductase ◽  
Reactive Oxygen ◽  
Semiquinone Radical ◽  
Ros Production ◽  
Oxygen Species ◽  
Reduction Mechanism ◽  
Radical Intermediate ◽  
Electron Reduction

TXNRD1 participates in the ROS production with menadione by a one-electron reduction mechanism. TXNRD1 transfers electrons from NADPH to menadione to yield a semiquinone radical intermediate, which reacts with molecular oxygen to generate ROS.

scholarly journals Proline Modulates the Trypanosoma cruzi Resistance to Reactive Oxygen Species and Drugs through a Novel D, L-Proline Transporter

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e92028 ◽  
Author(s):  
Melisa Sayé ◽  
Mariana R. Miranda ◽  
Fabio di Girolamo ◽  
María de los Milagros Cámara ◽  
Claudio A. Pereira
Keyword(s):  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Reactive Oxygen ◽  
Oxygen Species

Lymphokine-activated killer cell susceptibility in epirubicin-resistant and parental human non-small cell lung cancer (NSCLC)

Biologia ◽  
2007 ◽  
Vol 62 (2) ◽  
Author(s):  
Aysun Ozkan
Keyword(s):  
Reactive Oxygen Species ◽  
Defense Mechanism ◽  
Reductase Activity ◽  
Combined Treatment ◽  
Killer Cell ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Negative Control ◽  
Lak Cells ◽  
Oxygen Species

AbstractThe aim of this study was to evaluate that: (i) epirubicin-HCl (EPI) and lymphokine-activated killer (LAK) cells cytotoxicity may be mediated by free radical generation; and (ii) resistant H1299 cells may be more sensitive to combined treatment of LAK cells plus EPI than the LAK or EPI treatment alone. Viability of H1299 cells treated with EPI, LAK and LAK plus EPI was measured using the MTT test. Amount of glutathione (GSH), protein content and enzymatic activity were measured by spectrophotometer. Glutathione S-transferase (GST)-pi expression in the cells was determined by western blot analysis. LAK plus EPI combined treatment increased susceptibility of H1299 WT and H1299 EPI(R) (300-fold EPI resistant) cells to LAK cell cytotoxicity. The resistance of H1299 EPI(R) cells to EPI appears to be associated with a developed tolerance to free radicals, most likely because of a 2-fold increase in NADPH-dependent-cytochrome-P450 reductase (NADPH-CYP reductase) activity, 11-fold GST activity and 11-and 7-fold augmented selenium dependent and independent glutathione peroxidase (GSH-Px) activity, respectively. Amount of GST-pi in H1299 EPI(R) cells is statistically different from negative control and H1299 WT (p < 0.01). It is proposed that production of reactive oxygen species and hydrogen peroxide by the treatment of EPI and LAK cells can cause cytotoxicity of H1299 WT and H1299 EPI(R) cells. Superoxide dismutase, catalase, GSH-Px, GST, NADPH-CYP reductase and GSH must be considered as part of the intracellular antioxidant defense mechanism of H1299 WT and H1299 EPI(R) cells against reactive oxygen species. Combined treatment of EPI plus LAK cells caused the increasing cytotoxicity on the H1299 EPI(R) cells.

Induction of NADPH oxidase activity and reactive oxygen species production by a single Trypanosoma cruzi antigen

2010 ◽  
Vol 40 (13) ◽  
pp. 1531-1538 ◽  
Author(s):  
Natalia Guiñazú ◽  
Eugenio Antonio Carrera-Silva ◽  
María Cecilia Becerra ◽  
Andrea Pellegrini ◽  
Inés Albesa ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Nadph Oxidase Activity ◽  
Species Production

scholarly journals Priming with γ-Aminobutyric Acid against Botrytis cinerea Reshuffles Metabolism and Reactive Oxygen Species: Dissecting Signalling and Metabolism

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1174
Author(s):  
Henry Christopher Janse van Rensburg ◽  
Wim Van den Ende
Keyword(s):  
Reactive Oxygen Species ◽  
Nitrate Reductase ◽  
Botrytis Cinerea ◽  
Reductase Activity ◽  
Reactive Oxygen ◽  
Aminobutyric Acid ◽  
Guaiacol Peroxidase ◽  
Oxygen Species ◽  
Biotic Stresses ◽  
Ros Burst

The stress-inducible non-proteinogenic amino acid γ-aminobutyric acid (GABA) is known to alleviate several (a)biotic stresses in plants. GABA forms an important link between carbon and nitrogen metabolism and has been proposed as a signalling molecule in plants. Here, we set out to establish GABA as a priming compound against Botrytis cinerea in Arabidopsis thaliana and how metabolism and reactive oxygen species (ROS) are influenced after GABA treatment and infection. We show that GABA already primes disease resistance at low concentrations (100 µM), comparable to the well-characterized priming agent β-Aminobutyric acid (BABA). Treatment with GABA reduced ROS burst in response to flg22 (bacterial peptide derived from flagellum) and oligogalacturonides (OGs). Plants treated with GABA showed reduced H2O2 accumulation after infection due to increased activity of catalase and guaiacol peroxidase. Contrary to 100 µM GABA treatments, 1 mM exogenous GABA induced endogenous GABA before and after infection. Strikingly, 1 mM GABA promoted total and active nitrate reductase activity whereas 100 µM inhibited active nitrate reductase. Sucrose accumulated after GABA treatment, whereas glucose and fructose only accumulated in treated plants after infection. We propose that extracellular GABA signalling and endogenous metabolism can be separated at low exogenous concentrations.

scholarly journals Galectin-1-deficient mice are protected against Trypanosoma cruzi infection through altered neutrophil migration and production of reactive oxygen species and nitric oxide

2020 ◽  
Author(s):  
Thalita Bachelli Riul ◽  
Helioswilton Sales de Campos ◽  
Djalma de Souza Lima-Junior ◽  
Ana Elisa Caleiro Seixas Azzolini ◽  
Cristina Ribeiro de Barros Cardoso ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Neutrophil Migration ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Infection Site ◽  
Neutrophil Accumulation

SUMMARYTrypanosoma cruzi is an intracellular parasite that causes Chagas disease that affects millions of people worldwide. Many cellular and molecular aspects of this neglected disease are not fully understood. Prior studies have shown that galectin-1 (Gal-1), a β-galactoside-binding protein that regulates leukocyte recruitment to the inflammatory site, and promotes T. cruzi infection, but the mechanism is unclear. Here, we report that C57BL/6 mice lacking Gal-1 (Lgals1−/−) exhibited lower parasitemia and higher survival rates than their wildtype (WT) counterparts when infected with T. cruzi Y strain. Two weeks after infection, Lgals1−/− mice displayed greater neutrophil accumulation in infection site and heart tissue than WT mice. In T. cruzi-infected Lgals1−/− mice, infiltrated neutrophils produced increased levels of reactive oxygen species (ROS), while macrophages and neutrophils produced increased levels of nitric oxide (NO), which reduced replication and viability of parasites in vitro and downregulated IL-1β production. Pharmacological inhibition of NADPH oxidase and NO synthase during early in vivo infection reversed the protective effect of Gal-1 deficiency in Lgals1−/− mice. Together, our findings demonstrate that lacking Gal-1 favors neutrophil migration to the infection site and increases production of ROS and NO, thereby controlling the early steps of T. cruzi infection by reducing parasitemia and prolonging survival of infected mice.

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