Avaliação do efeito neuroprotetor da Quercetina em camundongos expostos a um herbicida à base de Glifosato

Abstract

As symptoms following exposure to pesticides such as glyphosate based herbicides (GBH’s) and those of neurological diseases such as depression are similar, it has been hypothesized that pesticide exposure has an association with neurological diseases. The aim of this study was to investigate whether quercetin use would protect against neurological changes following exposure to a subchronic low dose of a GBH. Forty adult male Swiss mice were divided into four treatment groups: Control, Glyphosate, Quercetin and Gly+Quer groups. According to the group, mice received 50 mg/kg of a GBH solution, 30 mg/kg of quercetin, and/or vehicles via gavage, for 30 days. The animals were subjected to behavioral tests, including open field (OF), elevated plus maze (EPM), forced swim test (FST) and sucrose preference test (PST). After euthanasia, hippocampal tissues were collected to measure oxidative stress markers such as reactive species (REs), total antioxidant capacity (FRAP), reduced glutathione (GSH), acetylcholinesterase activity (AChE) and for histological evaluation. The dorsal raphe nucleus was collected for neurotransmitter analysis of serotonin, dopamine and noradrenaline. The Glyphosate group showed anxious and depressive-like behavior in the EPM and FST tests, as well as expressed increased RE levels and decreased GSH levels in the hippocampus. The Quercetin group showed similar behavior as the Glyphosate group after treatment, with no alterations in the other parameters evaluated. However, the Gly+Quer group showed partial or total improvement in behavioral tests (EPM, FST) and reduced oxidative stress markers (REs and GSH). The results reveal that exposure to a subchronic low dose of glyphosate herbicide was capable of promoting alterations in the central nervous system. Furthermore, this study demonstrated the existence of an apparent quercetin paradox, the benefits of which could be enhanced by hormesis mechanisms.