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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

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 fo...

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Detalles Bibliográficos
Autores principales: González-Marín, Berenyce, Calderón-Segura, María Elena, Sekelsky, Jeff
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10535977/
https://www.ncbi.nlm.nih.gov/pubmed/37755764
http://dx.doi.org/10.3390/toxics11090754
Descripción
Sumario: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.