FB2026_03 , released September 17, 2026
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Citation
González-Marín, B., Calderón-Segura, M.E., Sekelsky, J. (2023). ATM/Chk2 and ATR/Chk1 Pathways Respond to DNA Damage Induced by Movento[®] 240SC and Envidor[®] 240SC Keto-Enol Insecticides in the Germarium of Drosophila melanogaster.  Toxics 11(9): 754.
FlyBase ID
FBrf0257673
Publication Type
Research paper
Abstract
DNA damage response (DDR) pathways in keto-enol genotoxicity have not been characterized, and few studies have reported genotoxic effects in non-target organisms. The present study shows that concentrations of 11.2, 22.4, 37.3 mg/L of Movento[®] 240SC and 12.3, 24.6, 41.1 mg/L of Envidor[®] 240SC for 72 h oral exposure induced DSBs by significantly increasing the percentage of γH2AV expression in regions 2b and 3 from the germarium of wild type females of Drosophila melanogaster Oregon R, compared to the control group (0.0 mg/L of insecticides), via confocal immunofluorescence microscopy. The comparison between both insecticides' reveals that only the Envidor[®] 240SC induces concentration-dependent DNA damage, as well as structural changes in the germarium. We determined that the DDR induced by Movento[®] 240SC depends on the activation of the ATM[tefu], Chk1[grp] and Chk2[lok] kinases by significantly increasing the percentage of expression of γH2AV in regions 2b and 3 of the germarium, and that ATR[mei-29D] and p53[dp53] kinases only respond at the highest concentration of 37.3 mg/L of Movento[®] 240SC. With the Envidor[®] 240SC insecticide, we determined that the DDR depends on the activation of the ATR[mei-29D]/Chk1[grp] and ATM[tefu]/Chk2[lok] kinases, and p53[dp53] by significantly increasing the percentage of expression of γH2AV in the germarium.
PubMed ID
PubMed Central ID
PMC10535977 (PMC) (EuropePMC)
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Toxics
    Title
    Toxics
    ISBN/ISSN
    2305-6304
    Data From Reference
    Chemicals (3)
    Genes (6)
    Human Disease Models (1)