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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Mitochondrial behavior during nuclear and mitochondrial DNA repair in Trypanosoma cruzi epimastigotes

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Author(s):
Antonio Salgado Martins, Tamires Marco [1] ; Peloso, Eduardo de Figueiredo [2] ; Costa-Silva, Hellida Marina [3] ; Rajao, Matheus Andrade [3] ; Van Houten, Bennet [4, 5] ; Machado, Carlos Renato [3] ; Gadelha, Fernanda Ramos [1]
Total Authors: 7
Affiliation:
[1] Univ Estadual Campinas, Dept Bioquim & Biol Tecidual, Campinas, SP - Brazil
[2] UNIFAL, Dept Bioquim, Inst Ciencias Biomed, Alfenas, MG - Brazil
[3] ICB UFMG, Dept Bioquim & Imunol, Belo Horizonte, MG - Brazil
[4] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA - USA
[5] Univ Pittsburgh, Hillman Canc Ctr, Canc Inst, Pittsburgh, PA - USA
Total Affiliations: 5
Document type: Journal article
Source: Experimental Parasitology; v. 219, DEC 2020.
Web of Science Citations: 0
Abstract

Different genotoxic agents can lead to DNA single- and double-strand breaks, base modification and oxidation. As most living organisms, Trypanosoma cruzi is subjected to oxidative stress during its life cycle; thus, DNA repair is essential for parasite survival and establishment of infection. The mitochondrion plays important roles beyond the production of ATP. For example, it is a source of signaling molecules, such as the superoxide anion and H2O2. Since T. cruzi has only one mitochondrion, the integrity of this organelle is pivotal for parasite viability. H2O2 and methyl methanesulfonate cause DNA lesions in T. cruzi that are repaired by different DNA repair pathways. Herein, we evaluate mitochondrial involvement during the repair of nuclear and mitochondrial DNA in T. cruzi epimastigotes incubated with these two genotoxic agents under conditions that induce repairable DNA damage. Overall, in both treatments, an increase in oxygen consumption rates and in mitochondrial H2O2 release was observed, as well as maintenance of ATP levels compared to control. Interestingly, these changes coincided with DNA repair kinetics, suggesting the importance of the mitochondrion for this energy-consuming process. (AU)

FAPESP's process: 12/21594-3 - Role of mitochondria on Trypanosoma cruzi survival treated with H2O2 concentration that induce DNA damage
Grantee:Tamires Marco Antonio
Support Opportunities: Scholarships in Brazil - Scientific Initiation