ArticleParasites & vectors2020
DNA double-strand breaks in the Toxoplasma gondii-infected cells by the action of reactive oxygen species.
Article in Parasites & vectors, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- A Toxoplasma gondii-derived ROP38 protein engages Ser15/Thr18-linked p53 activation and DNA damage-associated apoptotic signaling in human cancer cells.Cell communication and signaling : CCS · 2026Article
- ZBP1 mediated restriction of Toxoplasma gondii in both the early acute and chronic brain stages of infection.ImmunoHorizons · 2026Article
- Atovaquone-proguanil and reduced digestive cancer risk: aGut microbes · 2025Article
- The impacts of chronic infections on shaping cellular senescence.Immunity & ageing : I & A · 2025Review
- Brazilian Red Propolis and Its Active Constituent 7-O-methylvestitol Impair Early and Late Stages ofMicroorganisms · 2025Article
- Molecular Characterization, Oxidative Stress-Mediated Genotoxicity, and Hemato-Biochemical Changes in Domestic Water Buffaloes Naturally Infected withPathogens (Basel, Switzerland) · 2025Article
- Toxoplasma gondii infection induces early host cell cycle arrest and DNA damage in primary human host cells by a MYR1-dependent mechanism.Communications biology · 2024Article
- Metabolic changes inmBio · 2024Article
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Article
- Metabolic changes to host cells withbioRxiv : the preprint server for biology · 2023Article
- PP2Acα-B'/PR61 Holoenzyme of Toxoplasma gondii Is Required for the Amylopectin Metabolism and Proliferation of Tachyzoites.Microbiology spectrum · 2023Article
- Artemisinin derivatives induce oxidative stress leading to DNA damage and caspase-mediated apoptosis in Theileria annulata-transformed cells.Cell communication and signaling : CCS · 2023Article
- Cyto-genotoxicity of crystalline and amorphous niobium (V) oxide nanoparticles in CHO-K1 cells.Toxicology research · 2022Article
- Disruption of Toxoplasma gondii-Induced Host Cell DNA Replication Is Dependent on Contact Inhibition and Host Cell Type.mSphere · 2022Article
- The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity.International journal of molecular sciences · 2022Review
- Host autophagy limitsFrontiers in microbiology · 2022Article
- Modulation of autophagy as a therapeutic strategy forFrontiers in cellular and infection microbiology · 2022Review
- Oxidative Stress as a Possible Target in the Treatment of Toxoplasmosis: Perspectives and Ambiguities.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundToxoplasma gondii is an obligate parasite of all warm-blooded animals around the globe. Once infecting a cell, it manipulates the host's DNA damage response that is yet to be elucidated. The objectives of the present study were three-fold: (i) to assess DNA damages in T. gondii-infected cells in vitro; (ii) to ascertain causes of DNA damage in T. gondii-infected cells; and (iii) to investigate activation of DNA damage responses during T. gondii infection.
methodsHeLa, Vero and HEK293 cells were infected with T. gondii at a multiplicity of infection (MOI) of 10:1. Infected cells were analyzed for a biomarker of DNA double-strand breaks (DSBs) γH2AX at 10 h, 20 h or 30 h post-infection using both western blot and immunofluorescence assay. Reactive oxygen species (ROS) levels were measured using 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA), and ROS-induced DNA damage was inhibited by a ROS inhibitor N-acetylcysteine (NAC). Lastly, DNA damage responses were evaluated by detecting the active form of ataxia telangiectasia mutated/checkpoint kinase 2 (ATM/CHK2) by western blot.
resultsγH2AX levels in the infected HeLa cells were significantly increased over time during T. gondii infection compared to uninfected cells. NAC treatment greatly reduced ROS and concomitantly diminished γH2AX in host cells. The phosphorylated ATM/CHK2 were elevated in T. gondii-infected cells.
conclusionsToxoplasma gondii infection triggered DNA DSBs with ROS as a major player in host cells in vitro. It also activated DNA damage response pathway ATM/CHK2. Toxoplasma gondii manages to keep a balance between survival and apoptosis of its host cells for the benefit of its own survival.
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