## 4 Discussion
On the other hand, [PERSON] et al. [86] investigated the ameliorative effects of flavonoid antioxidant luteolin on BPA-induced toxicity in _D. melanogaster_. The results confirmed BPA-induced oxidative stress imbalance and behavioural deficits in flies. On the other hand, luteolin increased the survival rate and augmented antioxidant markers in flies, as well as ameliorating BPA-induced oxidative degeneration. This provides further insight into the antioxidative and chemopreverities properties of luteolin against BPA-induced toxicity. [PERSON] and coworkers [87] investigated the ameliorating effect of tetravalent cerium oxide nanoparticles, which is analogous to that of luteolin [86], and confirmed that BPA induced lipid peroxidation and ROS formation. Also, BPA exposure at millimolar doses induced micronuclelei formation and impeded nucleocytoplasmic transport, whereas CeO\({}_{2}\) nanoparticles improved dynamic and sexual behaviour abnormalities and ameliorated oxidative stress induced by BPA. [PERSON] [88] and coworkers analyzed the effects of BPA on _D. melanogaster_ during the embryonic period. It was shown that a 1 mM dose of BPA had an effect on developmental, behaviouristic and biochemical markers. The pupal eclosion rate decreased. Moreover, the F\({}_{1}\) flies also developed behaviouristic changes in sexual, dynamic and social behaviour as a result of BPA's interference with the dopaminergic system, in a similar manner to the human phenotypes ASD and ADHD, induced by oxidative stress. [PERSON] et al. [89] mention that BPA has been linked to behavioural changes in children, and has been shown to impact neurodevelopmental processes in animal models. BPA in concentrations up to 2 mM induces hyperactivity in larvae, increases grooming in adults and reduces sexual behaviour. Moreover, behavioural changes are highly dependent on the genetic background, suggesting that BPA may elicit a gene-environment interaction with _gFmr1_, causing fragile X syndrome and autism spectrum disorder. [PERSON] and coauthors [90] exposed _D. melanogaster_ to concentrations of 0.0035 g/mL, which corresponds to nearly 15.3 mM, and 0.005 g/mL (nearly 21.9 mM). The feeding rate, foraging path, climbing ability and frequency of courtship displays were reduced for both females and males at 15.3 mM, whereas for the higher concentrations, up to 21.9 mM, only treated females, and not males, exhibited significantly reduced climbing behaviour. A study by [PERSON] and coauthors [91] exposed _D. melanogaster_ to doses up to 2.2 mM, confirming negative geotaxis in the climbing reflex, indicating the negative effect of BPA for motorics in mago, which may also be manifested in higher organisms. Exposure to other bisphenolic compounds has also been evaluated at millimolar concentrations. For example, in [92], exposure of _Drosophila melanogaster_ to 1 mM bisphenol F (BPF) caused failure in the regulation of neurodevelopmentally important genes, including _dFmr1_, in FXS-model strains, as well as other genes linked to synapse formation and neuronal protection. This may link the genotoxicity and neurotoxicity of not only BPA, but also BPF, to developmental retardations and autism spectrum disorder. In [93], [PERSON] and coworkers exposed the aquatic midge _Chironomus riparus_ to the BPA alternative bisphenol S (BPS) at concentrations up to 500 ug/L, and the BPS exposure caused crucial alterations in genes, including _EcR_, _ERR_, _EP4_, _cyp18a1_, _lsp70_, _lsp40_, _cyp4g_, _GPx_ and GST, related to the ecodotysone pathway. These alterations showed the possibility for BPS to cause crucial developmental changes in an invertebrate model. In [94], various bisphenols, including BPA, BPS and BPF, were tested on _Drosophila melanogaster_ for their possible genetically induced neurotoxic effects. The concentrations used were up to 12 mM for BPA, whereas those for BPF reached 25 mM.