Evidence map›Paper›PMID 25671543›Full record

ArticlePloS one2015

Proliferation and differentiation of Trypanosoma cruzi inside its vector have a new trigger: redox status.

Natália P Nogueira, Francis M S Saraiva, Pedro E Sultano, Paula R B B Cunha, Gustavo A T Laranja, Graça A Justo, Kátia C C Sabino, Marsen G P Coelho, Ana Rossini, Georgia C Atella and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 93 citations in OpenAlex.

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  19. Structural New Data for Mitochondrial Peroxiredoxin FromFrontiers in cellular and infection microbiology · 2022
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  20. Influence ofInternational journal of molecular sciences · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Natália P NogueiraLaboratório de Interação Tripanossomatídeos e Vetores-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Francis M S SaraivaLaboratório de Interação Tripanossomatídeos e Vetores-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Pedro E SultanoLaboratório de Interação Tripanossomatídeos e Vetores-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Paula R B B CunhaLaboratório de Bioquímica de Lipídeos e Lipoproteínas-Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), Universidade Federal do Rio de Janeiro (UFRJ)-Rio de Janeiro, Brasil.
Gustavo A T LaranjaLaboratório de Interação Tripanossomatídeos e Vetores-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Graça A JustoLaboratório de Imunologia Aplicada à Bioquímica de Proteínas e Produtos Naturais-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Kátia C C SabinoLaboratório de Imunologia Aplicada à Bioquímica de Proteínas e Produtos Naturais-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Marsen G P CoelhoLaboratório de Imunologia Aplicada à Bioquímica de Proteínas e Produtos Naturais-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Ana RossiniLaboratório de Toxicologia e Biologia Molecular, Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil.
Georgia C AtellaInstituto Nacional de Ciência e Tecnologia-Entomologia Molecular (INCT-EM)-Rio de Janeiro, Brasil; Laboratório de Bioquímica de Lipídeos e Lipoproteínas-Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), Universidade Federal do Rio de Janeiro (UFRJ)-Rio de Janeiro, Brasil.
Marcia C PaesLaboratório de Interação Tripanossomatídeos e Vetores-Departamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes (IBRAG), Universidade do Estado do Rio de Janeiro (UERJ), Rio de Janeiro, Brasil; Instituto Nacional de Ciência e Tecnologia-Entomologia Molecular (INCT-EM)-Rio de Janeiro, Brasil.
Universidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BRInstituto Nacional de Ciência e Tecnologia em Entomologia Molecular · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trypanosoma cruzi proliferate and differentiate inside different compartments of triatomines gut that is the first environment encountered by T. cruzi. Due to its complex life cycle, the parasite is constantly exposed to reactive oxygen species (ROS). We tested the influence of the pro-oxidant molecules H2O2 and the superoxide generator, Paraquat, as well as, metabolism products of the vector, with distinct redox status, in the proliferation and metacyclogenesis. These molecules are heme, hemozoin and urate. We also tested the antioxidants NAC and GSH. Heme induced the proliferation of epimastigotes and impaired the metacyclogenesis. β-hematin, did not affect epimastigote proliferation but decreased parasite differentiation. Conversely, we show that urate, GSH and NAC dramatically impaired epimastigote proliferation and during metacyclogenesis, NAC and urate induced a significant increment of trypomastigotes and decreased the percentage of epimastigotes. We also quantified the parasite loads in the anterior and posterior midguts and in the rectum of the vector by qPCR. The treatment with the antioxidants increased the parasite loads in all midgut sections analyzed. In vivo, the group of vectors fed with reduced molecules showed an increment of trypomastigotes and decreased epimastigotes when analyzed by differential counting. Heme stimulated proliferation by increasing the cell number in the S and G2/M phases, whereas NAC arrested epimastigotes in G1 phase. NAC greatly increased the percentage of trypomastigotes. Taken together, these data show a shift in the triatomine gut microenvironment caused by the redox status may also influence T. cruzi biology inside the vector. In this scenario, oxidants act to turn on epimastigote proliferation while antioxidants seem to switch the cycle towards metacyclogenesis. This is a new insight that defines a key role for redox metabolism in governing the parasitic life cycle.

Indexed as

AcetylcysteineAnimalsAntioxidantsCell CycleCell ProliferationHemeHydrogen PeroxideInsect VectorsOxidation-ReductionRhodniusTrypanosoma cruziUric AcidAcetylcysteineAntioxidantsHemeHydrogen PeroxideUric Acid

Identifiers

PMID25671543
PMCPMC4324650
OpenAlexW2019255623

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.