A5069264330- Trypanosoma species research and implications
- Research on Leishmaniasis Studies
- Parasites and Host Interactions
- Nitric Oxide and Endothelin Effects
- Helminth infection and control
- Sulfur Compounds in Biology
- Coccidia and coccidiosis research
- Synthesis and Biological Evaluation
- Redox biology and oxidative stress
- Agricultural safety and regulations
- Hemoglobin structure and function
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Molecular Sensors and Ion Detection
- Polyamine Metabolism and Applications
- Adenosine and Purinergic Signaling
- Insect and Pesticide Research
- Parasitic Infections and Diagnostics
- Glutathione Transferases and Polymorphisms
- Biochemical effects in animals
- Biochemical and Molecular Research
- Mass Spectrometry Techniques and Applications
- Mosquito-borne diseases and control
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Metal-Catalyzed Oxygenation Mechanisms
- Lysosomal Storage Disorders Research
Universidad de la República de Uruguay
2015-2024
Universidad de Montevideo
2017
Instituto Nacional de Higiene, Epidemiología y Microbiología
2002
Macrophage-derived radicals generated by the NADPH oxidase complex and inducible nitric-oxide synthase (iNOS) participate in cytotoxic mechanisms against microorganisms. Nitric oxide ((•)NO) plays a central role control of acute infection Trypanosoma cruzi, causative agent Chagas disease, we have proposed that much its action relies on macrophage-derived peroxynitrite (ONOO(-) + ONOOH) formation, strong oxidant arising from reaction (•)NO with superoxide radical (O(2)(-)). Herein, shown...
ABSTRACT The potential of different parasite proteinases for use as vaccine candidates against fascioliasis in sheep was studied by vaccinating animals with the cathepsin L CL1 and CL2 leucine aminopeptidase (LAP) purified from adult flukes. In first trial, were immunized or mean protection levels obtained 33 34%, respectively. Furthermore, a significant reduction egg output observed vaccinated either (71%) (81%). second trial performed to determine protective two assayed together, well...
Trypanosoma cruzi undergo PCD (programmed cell death) under appropriate stimuli, the mechanisms of which remain to be established. In present study, we show that stimulation in T. epimastigotes by FHS (fresh human serum) results rapid (<1 h) externalization phosphatidylserine and depletion low molecular mass thiols dihydrotrypanothione glutathione. Concomitantly, enhanced generation oxidants was established EPR immuno-spin trapping radicals using DMPO (5,5-dimethylpyrroline-N-oxide)...
There is increasing evidence that Trypanosoma cruzi antioxidant enzymes play a key immune evasion role by protecting the parasite against macrophage-derived reactive oxygen and nitrogen species. Using T. transformed to overexpress peroxiredoxins TcCPX (T. cytosolic tryparedoxin peroxidase) TcMPX mitochondrial peroxidase), we found both cell lines readily detoxify cytotoxic diffusible species generated in vitro or released activated macrophages. Parasites TcAPX ascorbate-dependent...
Tobacco smoke is known to cause nitric oxide ((*)NO) inactivation and endothelial dysfunction. In this work we evaluated the interplay between (.)NO superoxide (O(2)(*-)) radicals consequent impact on (*)NO bioavailability nitroxidative stress in bovine aortic cells exposed cigarette extract (CSE) smokers. Bovine presence of CSE triggered O(2)(*-) production as indicated by spin-trapping electron paramagnetic resonance experiments. was produced both extracellulary (3.4 vs. 1.0...
Until recently, a capacity for apoptosis and synthesis of nitric oxide *NO) were viewed as exclusive to multicellular organisms. The existence these processes in unicellular parasites was recently described, with their biological significance remaining be elucidated. We have evaluated L-arginine metabolism Trypanosoma cruzi the context human serum-induced apoptotic death. Apoptosis evidenced by induction DNA fragmentation inhibition [3H]thymidine incorporation, which inhibited caspase...
The epimastigote stage of Trypanosoma cruzi undergoes PCD (programmed cell death) when exposed to FHS (fresh human serum). Although it has been known for over 30 years that complement is responsible FHS-induced death, the link between activation and triggering not established. We have previously shown mitochondrion participates in orchestration this model. Several changes mitochondrial function were described, particular was mitochondrion-derived O(2)(*-) (superoxide radical) necessary PCD....
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, presents a variable clinical course, varying from asymptomatic to serious debilitating pathologies with cardiac, digestive or cardio-digestive impairment. Previous studies using two clonal T. cruzi populations, Col1.7G2 (T. I) and JG II) demonstrated that there was differential tissue distribution of these parasites during infection in BALB/c mice, predominance heart. To date little is known about mechanisms determine this...
Increased production of reactive nitrogen (RNS) and oxygen (ROS) species its detrimental effect to mitochondria are associated with endothelial dysfunction. This study was designed determine the a peroxynitrite flux, promoted by 1,3-morpholinosydnonimine (SIN-1), in mitochondrial function some redox homeostasis parameters bovine aortic cells (BAEC). Moreover, diphenyl diselenide (PhSe)2, simple organic selenium compound, preventing peroxynitrite-mediated cytotoxicity also investigated. Our...
Significance In Chagas disease (CD), macrophages are the first line of defense against its causative agent, Trypanosoma cruzi . Here, we show that superoxide radical (O 2 •− ), a reactive species produced during phagocytosis, diffuses toward T. , causing toxicity. Much O permeation involves protonation inside acidic phagosome. To deal with host-derived oxidants, contains broad antioxidant enzyme armamentarium. Herein, generated parasites overexpressing cytosolic dismutase (Fe-SODB) and...
Chagas disease (CD), caused by the protozoa Trypanosoma cruzi, is a chronic illness in which parasites persist host-infected tissues for years. T. cruzi invasion cardiomyocytes elicits production of pro-inflammatory mediators [TNF-α, IL-1β, IFN-γ; nitric oxide (·NO)], leading to mitochondrial dysfunction with increased superoxide radical (O2·-), hydrogen peroxide (H2O2) and peroxynitrite generation. We hypothesize that these redox may control parasite proliferation through induction...