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

• Published in: Toxics (Basel) Vol. 11; no. 9; p. 754
• Main Authors: González-Marín, Berenyce, Calderón-Segura, María Elena, Sekelsky, Jeff
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 06.09.2023; MDPI
• Subjects: Antibodies; Apoptosis; Carcinogens; Cell cycle; CHK1 protein; Damage; Deoxyribonucleic acid; DNA; DNA damage; DNA damage response; DNA repair; Drosophila germarium; Drosophila melanogaster; Fruit flies; Genotoxicity; Immunofluorescence; Insecticides; Insects; keto-enol insecticides; Kinases; Lipid peroxidation; Lipids; Microscopy; Nontarget organisms; Ovaries; Oxidative stress; Pesticides; Yeast; Oregon; United States > US; Mexico; DNA damage response; Drosophila germarium; keto-enol insecticides
• ISSN: 2305-6304; 2305-6304
• DOI: 10.3390/toxics11090754

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 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 , and kinases by significantly increasing the percentage of expression of γH2AV in regions 2b and 3 of the germarium, and that and 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 and kinases, and by significantly increasing the percentage of expression of γH2AV in the germarium.