7-cloro-4-(Fenilselanil) Quinolina protege contra alterações comportamentais, oxidativas e colinérgicas induzidas pela exposição à acrilamida em Drosophila melanogaster

Abstract

Acrylamide (ACR) is a food contaminant formed when carbohydrate-rich foods are heated to high temperatures (above 120°C) and its formation occurs through the Maillard reaction. Several studies have reported that ACR can induce genotoxicity, carcinogenicity, and neurotoxicity. It is suggested that oxidative stress and alterations in the activity of the enzyme acetylcholinesterase (AChE) may be involved in the neurotoxicity caused by ACR, thus compounds with antioxidant and anticholinesterase properties such as 7-chloro-4-(phenylselanyl) quinoline (4-PSQ) can prevent or delay neurotoxicity caused by ACR. Therefore, the aim of this study was to evaluate whether 4-PSQ, an organic selenium compound, has a protective effect against ACR damage induction in Drosophila melanogaster. Adult flies (both sexes), between 1 and 3 days old, were divided into 4 groups of 50 flies each: Control; 4-PSQ (25 μM); ACR (5 mM) and ACR (5 mM). + 4-PSQ (25 μM). Flies were exposed to the diet for 4 days according to their respective groups. Flies exposed to ACR had reduced activity rate, locomotor activity, exploratory behavior, and an increase in acetylcholinesterase (AChE) activity. Neurotoxicity was also associated with a marked increase in the reactive species (RS), increased malondialdehyde (MDA) levels, decreased superoxide dismutase (SOD) activity, increased catalase (CAT) activity, increased glutathione S-transferase (GST) activity, and decreased cell viability in the head of flies compared to the control group. This study reveals, for the first time that co-treatment with 4-PSQ in Drosophila melanogaster decreased mortality and protected against locomotor deficits, AChE activity, reactive oxygen species (RS) and MDA levels, CAT, SOD and GST activity, and the cell viability. In conclusion, our results show the neuroprotective effect of 4-PSQ against ACR-induced toxicity.