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Bisphenol A induced oxidative stress mediated genotoxicity in Drosophila melanogaster
- Anet, Antony, Olakkaran, Shilpa, Kizhakke Purayil, Anupama, Hunasanahally Puttaswamygowda, Gurushankara
- Journal of hazardous materials 2019 v.370 pp. 42-53
- Drosophila melanogaster, antioxidant activity, bisphenol A, catalase, comet assay, eggs, food intake, genotoxicity, glutathione, glutathione transferase, heterozygosity, larvae, lethal concentration 50, lipid peroxidation, models, mutagens, oxidative stress, reactive oxygen species, rearing, superoxide dismutase, tail
- This study investigates Bisphenol A (BPA) induced oxidative stress that mediates the genotoxicity in in vivo model Drosophila melanogaster. The calculated LC50 for BPA was 12.35 μg/mL. The strains of D. melanogaster were reared in 0.1, 1.0, 2.5 and 5.0 μg/mL BPA treated food media from the embryonic stage (egg); oxidative stress and genotoxicity parameters were analyzed. Food intake analysis confirmed that BPA is not an anti feedant for Drosophila larvae and it consumed BPA containing food. Increased reactive oxygen species (ROS) and lipid peroxidation (LPO) and depletion of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione-s-transferase (GST) antioxidant activities were observed in BPA treated groups compared to control. Positive single spots/wing frequencies were observed in standard (ST) and high bioactivation (HB) crosses of marker heterozygous (MH; mwh/flr3) and balancer heterozygous (BH; mwh/TM3) genotype flies indicating BPA is mutagenic and not recombinogenic. A significant increase in tail length and % tail DNA in Comet assay after BPA treatment reveals that BPA has a potential to induce the genotoxicity. Present study suggests that BPA exposure induces oxidative stress, which could be one of the possible mechanisms for induction of genotoxicity.