## 4 Discussion  
_Drosophila melanogaster (D.m.)_ possesses numerous genes and detoxification mechanisms similar to those found in humans [58]. Hence, it should be used to understand the physiological aspects of metals, as an essential indicator for determining toxicity levels of \(Cu^{2+}\) and \(Pb^{2+}\), and to assess the toxic impact of heavy metals.  
Although it has beneficial effects on organisms, high concentrations of \(Cu^{2+}\) indicate negative effects, manifested by an inhibition of proliferation resulting in the reduction in larvae, pupae, and adult number. The \(Cu^{2+}\) toxicity phenomenon was proved using the _Oregon_-R genotype at concentrations of 0.50-2 mM range [59; 60]. Other studies reveled an inhibition of proliferation in \(Cu^{2+}\) depending on the sex (0.40 mM for females and 0.75 mM for males [46]).  
The application of the \(D.m.\) research model revealed inhibitory effects for \(Pb^{2+}\) concentrations, similar to results previously recorded by other researchers [61].  
The onset of oxidative stress at concentrations of 0.20 mM \(Pb^{2+}\) along with a mutagenic effect (manifesting as wing spots of 0.40 mM) was demonstrated [62].  
As our study and others suggest, genetic factors play an important and decisive role in assessing heavy metal toxicity levels. Research indicates the possibility of developing genotypes with enhanced tolerance to \(Cu^{2+}\) at concentrations of up to 50 mM, with survival  
Figure 5: Comparative study of the toxic effects on _Drosophila melanogaster (D.m.)_ at different concentrations of lead and copper: (**A**)—larvae stage III, (**B**)—pupae, (**C**)—adult. “**”—\(p<0.05\), “**”—\(p<0.01\), “**”—**”—Significant at \(p<0.001\).  
rates exceeding 75% [63]. This stands in contrast to other genotypes, which exhibit survival rates of less than 18%.  
The application of the \(D.m.\) model provided valuable insights into both acute and chronic toxicity, owing to the rapidity of its life cycle and the ease with which multiple generations can be generated and observed [64].  
Comparatively, our results suggest that \(Cu^{2+}\) effects impact more then \(Pb^{2+}\), with a greater reduction in adult number. This pronounced effect of \(Cu^{2+}\) over \(Pb^{2+}\) was also observed in plants [65]. This result may be understandable in itself, as copper (CuSO4) is often used as an antimicrobial and antibacterial agent, playing a homeostatic role, whereas lead accumulation presents a markedly different toxicological profile.  
Both \(Cu^{2+}\) and \(Pb^{2+}\) can induce the production of reactive oxygen species (ROS), causing oxidative stress [66; 67]. Consequently, ROS induces programmed cell death (PCD) [68; 69].  
Also, the levels of glutathione (GSH), an antioxidant and essential compound for cellular detoxification, can be significantly affected by exposure to copper and lead. GSH acts as a cytoplasmic buffer to counteract high concentrations of copper ions, facilitating their utilization in metabolic processes, maintaining copper homeostasis, and aiding in its detoxification [70; 71].  
On the other hand, in the case of \(Pb^{2+}\), GSH transforms lead ions into a less toxic form. However, prolonged or high concentrations of exposure to lead can overcome the capacity of the GSH detoxification system. Other research revealed that individuals chronically exposed to high levels of lead (50 \(\upmu\)g/dL) had lower GSH levels compared to the control group (1.5 \(\upmu\)g/dL) [72].  
Utilizing the \(D.m.\) research model, we discovered that the _white vestigial_ genotype exhibited increased susceptibility, possibly due to the presence of \"\(\upmu\)g\" genes involved in the translation elongation process (TEF), which could impair detoxification mechanisms. The acute effects of copper were evident across all genotypes, indicating differing detoxification mechanisms compared to lead.