Estudo experimental dos efeitos da exposição repetida ao herbicida atrazina sobre a atividade neurocomportamental, biomarcadores do estresse oxidativo e sistema dopaminérgico
Carregando...
Data
2020-02-20
Autores
Título da Revista
ISSN da Revista
Título de Volume
Editor
Universidade Estadual Paulista (Unesp)
Resumo
O herbicida atrazina (ATR) é um praguicida usado intensivamente na agricultura, que persiste no meio ambiente e causa toxicidade em espécies não-alvo, inclusive seres humanos. Considerando o potencial da ATR para produzir efeitos no sistema nervoso central (SNC) e a falta de informações na literatura corrente sobre esse tipo de toxicidade, o objetivo deste projeto de pesquisa foi avaliar os efeitos da exposição subcrônica ao herbicida ATR sobre parâmetros neurocomportamentais específicos e estabelecer sua correlação com o estresse oxidativo (EO) em tecido cerebral de ratos e com o sistema dopaminérgico em regiões específicas do cérebro, nominalmente córtex pré-frontal (CPF), hipocampo (HIP) e corpo estriado. Ratos Wistar machos receberam solução salina (0,3 ml; controle - Ct), atrazina (ATR; 100 mg/kg), atrazina mais vitamin E (ATR; 100 mg/Kg + VE; 200 mg/kg), apenas vitamina E (VE; 200 mg/kg), atrazina mais levodopa (ATR; 100 mg/Kg + LEV; 20 mg/kg) e apenas levodopa (LEV; 20 mg/kg), por gavage, durante 28 dias. O comportamento foi avaliado utilizando arena de campo aberto (ACA), labirinto em cruz elevado (LCE) e hole-board (HB). O teste de estresse oxidativo no tecido cerebral avaliou os níveis de malondialdeído (MDA), capacidade antioxidante hidrofílica (CAH) e atividade das enzimas superóxido dismutase (SOD) e catalase (CAT). A dopamina (DA) foi quantificada por HPLC, em áreas cerebrais específicas (CPF, HIP e estriado). Exposição à ATR provocou ansiedade, diminuiu a coordenação motora e não alterou a atividade locomotora dos animais. A ATR não modificou os níveis de MDA, a CAH nem as atividades da SOD e CAT. No entanto, ATR+VE aumentou os níveis de MDA e a CAH enquanto a VE aumentou a atividade da SOD. Além disso, o tratamento com ATR não alterou os níveis de DA no estriado cerebral, mas aumentou sua concentração no CPF e no HIP. Como conclusão, observou-se que a exposição subcrônica ao herbicida ATR foi capaz de prejudicar parâmetros comportamentais específicos, principalmente aqueles relacionados a ansiedade e a coordenação motora. Esses prejuízos não estão relacionados com a indução de EO no tecido cerebral de ratos. Além disso, sugere-se atenção em situações de suplementação oral por VE, pois, quando combinada com substâncias do tipo praguicidas, pode exercer efeitos pró-oxidantes a nível de SNC. Adicionalmente a ATR foi capaz de causar perturbações nos sistemas dopaminérgicos cerebrais de ratos, principalmente nas regiões do CPF e HIP, não alterando os níveis de DA na região do estriado. Esses resultados reforçam a relação entre exposição à praguicidas e efeitos de neurotoxicidade.
Atrazine (ATR) herbicide is a pesticide used intensively in agriculture that persists in environment and causes toxicity on non-target species, include humans. Considering the potential of ATR to produce effects on the central nervous system (CNS) and the lack of information in the current literature about this type of toxicity, the aim of this research project was to evaluate the effects of subchronic exposure to ATR herbicide on specific neurobehavioral parameters and to establish its correlation with oxidative stress (OE) in rat brain tissue and with the dopaminergic system in specific brain regions, nominally prefrontal cortex (PFC), hippocampus (HIP) and striatum. Male Wistar rats received saline (0.3 ml; control - Ct), atrazine (ATR; 100 mg/kg), atrazine plus vitamin E (ATR; 100 mg/Kg + VE; 200 mg/kg) only vitamin E (VE; 200 mg/kg), atrazine plus levodopa (ATR; 100 mg/Kg + LEV; 20 mg/kg) and only levodopa (LEV; 20 mg/kg), via gavage, during 28 days. Behavior was assessed using open field arena (OF), elevated plus-maze (EPM) and hole-board (HB) apparatus. Oxidative stress assay in brain tissue evaluated malondialdehyde (MDA) levels, hydrophilic antioxidant capacity (HAC), and superoxide dismutase (SOD) and catalase (CAT) enzymes activity. Dopamine (DA) was quantified using HPLC, in specific brain areas (PFC, HIP and striatum). ATR exposure caused anxiety-like behavior, decreased motor coordination and did not alter the locomotor activity of the animals. ATR did not change the MDA levels, the HAC, or SOD and CAT activities. However, ATR+VE increased MDA levels and the HAC while VE increased SOD activity. Additionally, ATR treatment did not change DA levels in the striatum cerebral, but increased its concentration in PFC and HIP. As a conclusion, it was observed that subchronic exposure to ATR herbicide was able to impair specific behavioral parameters, especially those related to anxiety and motor coordination. These impairs are not related to OE induction in brain tissue of the rats. Moreover, attention is suggested in situations of oral VE supplementation, because, when combined with substances like pesticides, it can exert pro-oxidant effects in the CNS. Additionally, ATR was able to cause disturbances in the brain dopaminergic systems of rats, mainly in the regions of PFC and HIP, without altering the DA levels in the striatum region. These results reinforce to relation between pesticides exposure and neurotoxic effects.
Atrazine (ATR) herbicide is a pesticide used intensively in agriculture that persists in environment and causes toxicity on non-target species, include humans. Considering the potential of ATR to produce effects on the central nervous system (CNS) and the lack of information in the current literature about this type of toxicity, the aim of this research project was to evaluate the effects of subchronic exposure to ATR herbicide on specific neurobehavioral parameters and to establish its correlation with oxidative stress (OE) in rat brain tissue and with the dopaminergic system in specific brain regions, nominally prefrontal cortex (PFC), hippocampus (HIP) and striatum. Male Wistar rats received saline (0.3 ml; control - Ct), atrazine (ATR; 100 mg/kg), atrazine plus vitamin E (ATR; 100 mg/Kg + VE; 200 mg/kg) only vitamin E (VE; 200 mg/kg), atrazine plus levodopa (ATR; 100 mg/Kg + LEV; 20 mg/kg) and only levodopa (LEV; 20 mg/kg), via gavage, during 28 days. Behavior was assessed using open field arena (OF), elevated plus-maze (EPM) and hole-board (HB) apparatus. Oxidative stress assay in brain tissue evaluated malondialdehyde (MDA) levels, hydrophilic antioxidant capacity (HAC), and superoxide dismutase (SOD) and catalase (CAT) enzymes activity. Dopamine (DA) was quantified using HPLC, in specific brain areas (PFC, HIP and striatum). ATR exposure caused anxiety-like behavior, decreased motor coordination and did not alter the locomotor activity of the animals. ATR did not change the MDA levels, the HAC, or SOD and CAT activities. However, ATR+VE increased MDA levels and the HAC while VE increased SOD activity. Additionally, ATR treatment did not change DA levels in the striatum cerebral, but increased its concentration in PFC and HIP. As a conclusion, it was observed that subchronic exposure to ATR herbicide was able to impair specific behavioral parameters, especially those related to anxiety and motor coordination. These impairs are not related to OE induction in brain tissue of the rats. Moreover, attention is suggested in situations of oral VE supplementation, because, when combined with substances like pesticides, it can exert pro-oxidant effects in the CNS. Additionally, ATR was able to cause disturbances in the brain dopaminergic systems of rats, mainly in the regions of PFC and HIP, without altering the DA levels in the striatum region. These results reinforce to relation between pesticides exposure and neurotoxic effects.
Descrição
Palavras-chave
Atrazina, Neurotoxicidade, Comportamento, Estresse oxidativo, Sistema dopaminérgico, Atrazine, Neurotoxicity, Behavior, Oxidative stress, Dopaminergic system