ArticleParasites & vectors2022
Trypanosoma cruzi iron superoxide dismutases: insights from phylogenetics to chemotherapeutic target assessment.
Article in Parasites & vectors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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3 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Distribution, host origin, and transmission cycles of Trypanosoma cruzi genotypes in the State of Rio Grande do Norte, Brazil.Revista da Sociedade Brasileira de Medicina Tropical · 2025Pooled it
- Selection, Identification, and Transcript Expression Analysis of Antioxidant Enzyme Genes inAntioxidants (Basel, Switzerland) · 2023Article
- TriTrypDB: An integrated functional genomics resource for kinetoplastida.PLoS neglected tropical diseases · 2023Article
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Authors and funding
11 authors at 3 institutions in 1 country.
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Abstract
backgroundComponents of the antioxidant defense system in Trypanosoma cruzi are potential targets for new drug development. Superoxide dismutases (SODs) constitute key components of antioxidant defense systems, removing excess superoxide anions by converting them into oxygen and hydrogen peroxide. The main goal of the present study was to investigate the genes coding for iron superoxide dismutase (FeSOD) in T. cruzi strains from an evolutionary perspective.
methodsIn this study, molecular biology methods and phylogenetic studies were combined with drug assays. The FeSOD-A and FeSOD-B genes of 35 T. cruzi strains, belonging to six discrete typing units (Tcl-TcVI), from different hosts and geographical regions were amplified by PCR and sequenced using the Sanger method. Evolutionary trees were reconstructed based on Bayesian inference and maximum likelihood methods. Drugs that potentially interacted with T. cruzi FeSODs were identified and tested against the parasites.
resultsOur results suggest that T. cruzi FeSOD types are members of distinct families. Gene copies of FeSOD-A (n = 2), FeSOD-B (n = 4) and FeSOD-C (n = 4) were identified in the genome of the T. cruzi reference clone CL Brener. Phylogenetic inference supported the presence of two functional variants of each FeSOD type across the T. cruzi strains. Phylogenetic trees revealed a monophyletic group of FeSOD genes of T. cruzi TcIV strains in both distinct genes. Altogether, our results support the hypothesis that gene duplication followed by divergence shaped the evolution of T. cruzi FeSODs. Two drugs, mangafodipir and polaprezinc, that potentially interact with T. cruzi FeSODs were identified and tested in vitro against amastigotes and trypomastigotes: mangafodipir had a low trypanocidal effect and polaprezinc was inactive.
conclusionsOur study contributes to a better understanding of the molecular biodiversity of T. cruzi FeSODs. Herein we provide a successful approach to the study of gene/protein families as potential drug targets.
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