Selenito de sódio previne neurotoxicidade induzida por paraquat em peixe-zebra (Danio rerio)

Abstract

Considering the sodium selenite (Na2SeO3) antioxidant properties and the involvement of oxidative and nitrosative stress events in neurotoxicity induced by paraquat (PQ) herbicide, this study investigated the potential protective effect of a Na2SeO3 diet on biochemical and behavioral parameters in zebrafish exposed to PQ. The fish were pretreated with a Na2SeO3 supplemented diet for 21 days and then, the PQ treatment (20 mg/kg) to induction of neurotoxicity model was intraperitoneally administered in a total of 6 injections for 16 days (one injection every 3 days). Among behavioral parameters analyzed, Na2SeO3 pretreatment attenuated locomotor damage as decrease of distance traveled, the increase in time spent on top area of the tank and the increase in the latency to fish to enter in the closer to conspecifics area (interaction group).. In addition, the Na2SeO3 pretreatment abolished the exacerbation of freezing behavior and even prevented agonistic behavior like anxiety and aggression. Regarding to oxidative damage, Na2SeO3 pretreatment prevented the increase in carbonylation of protein (CP), reactive oxygen species (ROS) and nitrite/nitrate NOx levels caused by PQ treatment. Na2SeO3 pretreatment also prevented the increase in antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx) and decrease in non-protein thiols levels (NPSH) induced by PQ treatment. The activation of the glutathione-S-tranferase (GST) enzyme by Na2SeO3 diet and PQ treatment was effective in preventing changes in levels of thiobarbituric reactive substances (TBARS). In conclusion, Na2SeO3 diet prevented behavioral changes and biochemical damage observed in PQ-treateds animals. Na2SeO3 pretreatment was beneficial because acts not only modulating the redox parameters, but also modulating phenotypes like anxiety and aggression in zebrafish PQ-treated. This study demonstrated for the first time that the zebrafish is an convenient organism model for "screening" of potential neuroprotective molecules against the neurotoxicity induced by PQ.