## 4 Discussion  
BPA is currently recognized as an endocrine disruptor. EDCs are defined by the World Health Organization (WHO) as \"an exogenous substance or mixture that alters function(s) of the endocrine system and consequently causes adverse health effects in an intact organism, or its progeny, or (sub)populations\" [5; 63; 64; 65; 66; 67; 5; 7; 5; 10]. They can interfere with hormonal function in several ways: by affecting hormone biosynthesis directly, or by affecting their metabolism, transport and/or action mechanism. They can also act on a genomic and epigenomic level, altering gene expression or genomic imprinting. A lot of EDCs are thus known to cause alterations in fetal development and the typical feedback mechanisms of the endocrine system, often with transgenerational effects [11; 12; 13; 14; 66; 67; 68; 69]. Chemicals such as BPA are nowadays a major concern worldwide, mainly because they may cause bioaccumulation and reproductive toxicity. Several groups of investigators have concluded, from studies in several animals, that BPA can cause disorders in the development of various organs of the body, such as the male and female reproductive tract, the prostate, the mammary gland, tissues and organs involved in metabolism, and even the brain (causing neurobehavioral changes). Human studies have also shown an association between exposure to BPA and a variety of diseases, including various types of cancer, infertility problems (low counts and quality of sperm) and worsening of asthma, among others [68]. In this study, _Drosophila melanogaster_ was used as a model organism to evaluate the biological, behavioural and genotoxic effects caused by exposure to BPA and explore its potential mechanisms of action. Our results showed that, when it comes to longevity, BPA caused no significant changes in mean survival after acute exposure. However, individuals are continuously exposed to BPA, so chronic treatment was applied in the following two generations. We then observed that chronic exposure to BPA during larval development exhibited greater toxicity than acute exposure, having a greater impact on maximal longevity in the early stages of life. This suggests that BPA may have a more relevant effect on earlier deaths, and that it is on those deaths that greater emphasis should be placed in future studies. The results also show that parental chronic treatments can also affect offspring's longevity, and that chronic exposure to BPA during successive generations increasingly affects the survival of individuals, leading to increasing variations in their longevity. Non-monotonic dose-response curves (NMDRCs) were obtained in both generations, which is common in studies involving EDCs such as BPA. In fact, according to [PERSON] [69], NMDRCs are common in the BPA literature, occurring in more than 20% of all experiments and in at least one endpoint in more than 30% of all studies. Similar conclusions regarding the ability of EDCs to produce NMDRCs have been  
Figure 8: The mean basal damage observed in the Comet assay and its significance for \(p<0.05\), obtained by Student’s \(t\)-test. The results are plotted as mean + SEM when compared to the control. Legend: \(\bullet\)—\(p<0.05\); \(\bullet\)—\(p<0.005\). made by the World Health Organization, the United Nations Environment Programme, the Endocrine Society, and several other scientists [11; 12; 13; 14; 15; 69]. In a study by [PERSON] et al. [70] the nematode _Caenorhabditis elegans_ was used to evaluate several parameters, including lifespan, after a chronic exposure to BPA (10 days, from L4 larvae to day 10 adults) in a long-term, low-concentration experiment. Their results, contrary to ours, showed no significant effects following exposure, which could have been due to the fact that the concentrations they used ranged between 0.0001 and 10 \(\upmu\)M, concentrations much lower than the ones used in this study.