Efeito do extrato de quinoa sobre um modelo experimental de doença de Parkinson em Drosophila melanogaster

Abstract

Parkinson's disease (PD) is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons of the substantia nigra in the central nervous system, in addition, changes in the cholinergic system are observed in this pathogenesis, and the neurotransmitters dopamine and acetylcholine exert important physiological functions. Oxidative stress appears to be an important factor contributing to PD development. Rotenone, a toxic compound I inhibitor of mitochondrial complex I in the electron transport chain, induces an increase in oxidative stress and consequently causes cellular damage, leading to the characteristic symptoms of PD. The medication used in the treatment of PD does not have a preventive effect and can still cause side effects. In this way, it becomes important to search for efficient natural treatments without side effects. Quinoa, an important source of bioactive compounds such as phenolic compounds, shows its antioxidant properties with protective action against cell damage, which protects against factors that can lead to the development of neurodegenerative diseases. Thus, the objective of this work was to evaluate the effect of quinoa extract on rotenone-induced Parkinson's disease experimental model in Drosophila melanogaster. Flies, males and females with 1 to 4 days old were separated into 4 groups and exposed for 7 days to the diet: control; quinoa extract (5.0 mg/mL); rotenone (500 μM) and rotenone (500 μM) + quinoa extract (5.0 mg/mL). The assessment of food consumption was performed on a single day and the survival rate was monitored every 24 hours for 7 days. After that, behavioral evaluations of negative geotaxis, open field and memory were performed. Then, biochemical evaluations of oxidative stress indicators, dopamine levels, activity of tyrosine hydroxylase and acetylcholinesterase enzymes were performed in the flies' heads. In behavioral tests, flies exposed to rotenone showed decreased survival, impaired locomotor activities and memory, as well as decreased levels of dopamine and activity of tyrosine hydroxylase and acetylcholinesterase enzymes. In the oxidative stress indicators, they decreased the activity of superoxide dismutase (SOD) and catalase (CAT) and increased the production of reactive species and TBARS. However, co-exposure to quinoa extract protected the toxicity caused by rotenone in behavioral and biochemical evaluations. This protection may be related to the phenolic compounds present in the quinoa extract, which have an antioxidant action mechanism and the ability to modulate some enzymes. These results show that it is a possible adjunct in the treatment of PD.