p-Coumaric acid potential in restoring neuromotor function and oxidative balance through the Parkin pathway in a Parkinson disease-like model in Drosophila melanogaster.

p-Coumaric acid is a significant phenolic compound known for its potent antioxidant activity. Thus, this study investigated the effects of p-coumaric acid on the behavioral and neurochemical changes induced in Drosophila melanogaster by exposure to rotenone in a Parkinson disease (PD)-like model. The flies were divided into four groups and maintained for seven days on different diets: a standard diet (control), a diet containing rotenone (500 µM), a control diet to which p-coumaric acid was added on the fourth day (0.3 µM), and a diet initially containing rotenone (500 µM) with p-coumaric acid added on the fourth day (0.3 µM). Exposure to p-coumaric acid ameliorated locomotor impairment and reduced mortality induced by rotenone. Moreover, p-coumaric acid normalized oxidative stress markers (ROS, TBARS, SOD, CAT, GST, and NPSH), mitigated oxidative damage, and reflected in the recovery of dopamine levels, AChE activity, and cellular viability post-rotenone exposure. Additionally, p-coumaric acid restored the immunoreactivity of Parkin and Nrf2. The results affirm that p-coumaric acid effectively mitigates PD-like model-induced damage, underscoring its antioxidant potency and potential neuroprotective effect.

Sex-specific changes in oxidative stress parameters and longevity produced by Bisphenol F and S compared to Bisphenol A in Drosophila melanogaster.

Female and male Drosophila melanogaster were exposed separately for seven days to Bisphenol A (BPA), Bisphenol F (BPF), and Bisphenol S (BPS) at concentrations of 0.25, 0.5, and 1 mM. We observed that males exposed to 0.5 and 1 mM BPS showed lower catalase (CAT) activity and higher superoxide dismutase (SOD) and reactive species (RS); CAT activity decreased for BPF 0.5 and 1 mM. Nevertheless, BPA 0.5 and 1 mM decreased CAT activity, increased RS and lipid peroxidation (LPO), and reduced mitochondrial viability. None of the bisphenols altered the cell viability of male flies, although BPA 0.5 and 1 mM reduced longevity. In female flies, BPA and BPS 0.5 and 1 mM increased RS and LPO levels and decreased CAT activity and glutathione-S-transferase (GST), which may have contributed to lower mitochondrial and cell viability. Furthermore, BPS decreased SOD activity at the 1 mM concentration, and BPA reduced the SOD activity at concentrations of 0.5 and 1 mM. In the BPF 1 mM group, there was a reduction in GST activity and an increase in RS and LPO levels. The toxicological effects were different between sexes, and BPA was more harmful than BPF and BPS in male flies. Thus, our findings showed that females were more susceptible to oxidative cell damage when exposed to BPA and BPS than to BPF, and daily exposure to BPA and BPS at all concentrations reduced female longevity, as well as in BPF 1 mM.

Oxidative stress and decreased dopamine levels induced by imidacloprid exposure cause behavioral changes in a neurodevelopmental disorder model in Drosophila melanogaster.

Neurodevelopmental disorders, such as Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD) are responsible for behavioral deficits in children. Imidacloprid is a nicotinic acetylcholine receptor agonist, capable of causing behavioral changes in Drosophila melanogaster, similar to the ADHD-like phenotypes. We assess whether behavioral damage induced by imidacloprid exposure in Drosophila melanogaster is associated with neurochemical changes and whether these changes are similar to those observed in neurodevelopmental disorders such as ASD and ADHD. The fruit flies were divided into four groups, exposed to either a standard diet (control) or a diet containing imidacloprid (200, 400 or 600 ρM) and allowed to mate for 7 days. After hatching, the progeny was subjected to in vivo and ex vivo tests. The ones exposed to imidacloprid showed an increase in hyperactivity, aggressiveness, anxiety and repetitive movements, as well as, a decrease in social interaction. Furthermore, exposure to imidacloprid decreased dopamine levels, cell viability and increased oxidative stress in the flies' progeny. These results demonstrated that the behavioral damage induced by imidacloprid exposure involves a reduction in dopamine levels and oxidative stress and that these neurochemical changes are in line with the events that occur in ASD and ADHD-like phenotypes in other models.