Neuroprotective effects of brown rice consumption in an iron-induced parkinsonism in Drosophila

Iron (Fe) accumulation and resultant oxidative stress play a significant role in the neuronal death observed in Parkinson's disease (PD). Brown rice (BR) possesses antioxidant properties able to reduce cellular oxidative damage. Thus, we hypothesized that BR may ameliorate Fe-induced parkinsonism due to oxidative stress.

Two - to three-day-old male flies were concurrently exposed to Fe (ferrous sulphate, 1 mM) and interventions, divided into eight groups: control; Fe; BR; white rice (WR); L-dopa (1 mM); Fe (1 mM) + BR; Fe (1 mM) + WR; and Fe (1 mM) + L-dopa (1 mM). The flies were exposed for 15 days to their respective diets, and their behavior, relevant biomarkers, and the expression of related genes were evaluated.

Chronic exposure to Fe caused cognitive and locomotor deficits by increasing Fe levels (p = 0.027) in flies' heads, as well as heightened aggression and grooming episodes (p < 0.001). The elevated iron levels induced changes consistent with oxidative stress, evidenced by increased MDA levels (p < 0.001), and reduced activity of catalase (p < 0.001) and glutathione peroxidase (GPx) (p < 0.001), along with decreased dopamine levels (p < 0.001). Additionally, there was dysregulation in the mRNA expression of malvolio, ferritin, Nrf2, DJ-1, GPx, and catalase (p < 0.05). BR prevented the Fe-induced effects (Fe + BR group) even more effectively than L-Dopa (p < 0.001).

The findings indicate that BR has the potential to mitigate Fe-induced ROS-mediated damage in a Drosophila model of PD-like disease by modulating key players in the Nrf2 signaling pathway.