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

Autor: Marco Antônio Salgado Martins T; Departamento de Bioquímica e Biologia Tecidual, UNICAMP, Campinas, SP, Brazil., de Figueiredo Peloso E; Departamento de Bioquímica, Instituto de Ciências Biomédicas, UNIFAL, Alfenas, MG, Brazil., Costa-Silva HM; Departamento de Bioquímica e Imunologia, ICB - UFMG, Belo Horizonte, Minas Gerais, Brazil., Rajão MA; Departamento de Bioquímica e Imunologia, ICB - UFMG, Belo Horizonte, Minas Gerais, Brazil., Van Houten B; Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine and the University of Pittsburgh Cancer Institute, Hillman Cancer Center, Pittsburgh, PA, United States., Machado CR; Departamento de Bioquímica e Imunologia, ICB - UFMG, Belo Horizonte, Minas Gerais, Brazil., Ramos Gadelha F; Departamento de Bioquímica e Biologia Tecidual, UNICAMP, Campinas, SP, Brazil. Electronic address: frgad@unicamp.br.
Jazyk: angličtina
Zdroj: Experimental parasitology [Exp Parasitol] 2020 Dec; Vol. 219, pp. 108016. Date of Electronic Publication: 2020 Oct 06.
DOI: 10.1016/j.exppara.2020.108016
Abstrakt: 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 H 2 O 2 . Since T. cruzi has only one mitochondrion, the integrity of this organelle is pivotal for parasite viability. H 2 O 2 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 H 2 O 2 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.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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